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Hepatology 1998, 27:1463–1466.\nRubbia-Brandt L, Quadri R, Abid K, et al.: Hepatocyte steatosis is a cytopathic effect of hepatitis C virus genotype 3. J Hepatol 2000, 33:106–115.\nHourigan LF, Macdonald GA, Purdie D, et al.: Fibrosis in chronic hepatitis C correlates significantly with body mass index and steatosis. Hepatology 1999, 29:1215–1219.\nAdinolfi LE, Gambardella M, Andreana A, et al.: Steatosis accelerates the progression of liver damage of chronic hepatitis C patients and correlates with specific HCV genotype and visceral obesity. Hepatology 2001, 33:1358–1364.\nWestin J, Nordlinder H, Lagging M, et al.: Steatosis accelerates fibrosis development over time in hepatitis C virus genotype 3 infected patients. J Hepatol 2002, 37:837–842.\nCastera L, Hezode C, Roudot-Thoraval F, et al.: Worsening of steatosis is an independent factor of fibrosis progression in untreated patients with chronic hepatitis C and paired liver biopsies. Gut 2003, 52:288–292.\nPowell EE, Cooksley WG, Hanson R, et al.: The natural history of nonalcoholic steatohepatitis: a follow-up study of fortytwo patients for up to 21 years. Hepatology 1990, 11:74–80.\nWyatt J, Baker H, Prasad P, et al.: Steatosis and fibrosis in patients with chronic hepatitis C. J Clin Pathol 2004, 57:402–406.\nKaserer K, Fiedler R, Steindl P, et al.: Liver biopsy is a useful predictor of response to interferon therapy in chronic hepatitis C. Histopathology 1998, 32:454–461.\nPoynard T, Ratziu V, McHutchison J, et al.: Effect of treatment with peginterferon or interferon alfa-2b and ribavirin on steatosis in patients infected with hepatitis C. Hepatology 2003, 38:75–85. This large study confirms the causes, roles, and fate of steatosis in a treated cohort.\nAkuta N, Suzuki F, Tsubota A, et al.: Efficacy of interferon monotherapy to 394 consecutive naive cases infected with hepatitis C virus genotype 2a in Japan: therapy efficacy as consequence of tripartite interaction of viral, host and interferon treatment-related factors. J Hepatol 2002, 37:831–836.\nBjoro K, Bell H, Hellum KB, et al.: Effect of combined interferon-alpha induction therapy and ribavirin on chronic hepatitis C virus infection: a randomized multicentre study. Scand J Gastroenterol 2002, 37:226–232.\nPatton HM, Patel K, Behling C, et al.: The impact of steatosis on disease progression and early and sustained treatment response in chronic hepatitis C patients. J Hepatol 2004, 40:484–490.\nBressler BL, Guindi M, Tomlinson G, Heathcote J: High body mass index is an independent risk factor for nonresponse to antiviral treatment in chronic hepatitis C. Hepatology 2003, 38:639–644.\nMonto A, Alonzo J, Watson JJ, et al.: Steatosis in chronic hepatitis C: Relative contributions of obesity, diabetes mellitus, and alcohol. Hepatology 2002, 36:729–736.\nRubbia-Brandt L, Fabris P, Paganin S, et al.: Steatosis affects chronic hepatitis C progression in a genotype specific way. Gut 2004, 53:406–412.\nSanyal AJ, Contos MJ, Sterling RK, et al.: Nonalcoholic fatty liver disease in patients with hepatitis C is associated with features of the metabolic syndrome. Am J Gastroenterol 2003, 98:2064–2071.\nHui JM, Kench J, Farrell GC, et al.: Genotype-specific mechanisms for hepatic steatosis in chronic hepatitis C infection. J Gastroenterol Hepatol 2002, 17:873–881.\nHickman IJ, Powell EE, Prins JB, et al.: In overweight patients with chronic hepatitis C, circulating insulin is associated with hepatic fibrosis: implications for therapy. J Hepatol 2003, 39:1042–1048. In overweight but not lean patients with HCV, there was a significant increase in insulin levels with increasing fibrosis. This suggests that increased circulating insulin may be one factor responsible for the association between BMI and fibrosis in patients with chronic HCV.\nKumar D, Farrell GC, Fung C, George J: Hepatitis C virus genotype 3 is cytopathic to hepatocytes: reversal of hepatic steatosis after sustained therapeutic response. Hepatology 2002, 36:1266–1272. Reversal of steatosis after successful antiviral treatment provided proof of the role of viral factors in promoting steatosis in genotype 3-infected individuals.\nMoriya K, Yotsuyanagi H, Shintani Y, et al.: Hepatitis C virus core protein induces hepatic steatosis in transgenic mice. J Gen Virol 1997, 78:1527–1531.\nLerat H, Honda M, Beard MR, et al.: Steatosis and liver cancer in transgenic mice expressing the structural and nonstructural proteins of hepatitis C virus. Gastroenterology 2002, 122:352–365.\nPerlemuter G, Sabile A, Letteron P, et al.: Hepatitis C virus core protein inhibits microsomal triglyceride transfer protein activity and very low density lipoprotein secretion: a model of viral-related steatosis. FASEB J 2002, 16:185–194. This study proposes a mechanism for viral-induced steatosis, with core protein interfering with assembly and secretion of VLDL through a reduction in MTP activity.\nLonardo A, Adinolfi LE, Loria P, et al.: Steatosis and hepatitis C virus: mechanisms and significance for hepatic and extrahepatic disease. Gastroenterology 2004, 126:586–597.\nCardin R, Saccoccio G, Masutti F, et al.: DNA oxidative damage in leukocytes correlates with the severity of HCV-related liver disease: validation in an open population study. J Hepatol 2001, 34:587–592.\nFarinati F, Cardin R, Bortolami M, Rugge M: The mechanisms underlying hepatitis C virus genotype 3-mediated liver damage. J Hepatol 2003, 39:292–294.\nDay CP, James OF: Steatohepatitis: a tale of two \"hits\"? Gastroenterology 1998, 114:842–845.\nClouston AD, Powell EE: Interaction of non-alcoholic fatty liver disease with other liver diseases. Baillieres Best Pract Clin Gastroenterol 2002, 16:767–781.\nClouston AD, Jonsson JR, Purdie DM, et al.: Steatosis and chronic hepatitis C: analysis of fibrosis and stellate cell activation. J Hepatol 2001, 34:314–320.\nHickman IJ, Clouston AD, Macdonald GA, et al.: Effect of weight reduction on liver histology and biochemistry in patients with chronic hepatitis C. Gut 2002, 51:89–94.\nFeldstein AE, Canbay A, Angulo P, et al.: Hepatocyte apoptosis and fas expression are prominent features of human nonalcoholic steatohepatitis. Gastroenterology 2003, 125:437–443.\nWalsh MJ, Vanags DM, Clouston AD, et al.: Steatosis and liver cell apoptosis in chronic hepatitis C: a mechanism for increased liver injury. Hepatology 2004, 39:1230–1238.\nHui JM, Sud A, Farrell GC, et al.: Insulin resistance is associated with chronic hepatitis C virus infection and fibrosis progression. Gastroenterology 2003, 125:1695–1704.\nRatziu V, Munteanu M, Charlotte F, et al.: Fibrogenic impact of high serum glucose in chronic hepatitis C. J Hepatol 2003, 39:1049–1055.\nSvegliati-Baroni G, Ridolfi F, Di Sario A, et al.: Insulin and insulin-like growth factor-1 stimulate proliferation and type I collagen accumulation by human hepatic stellate cells: differential effects on signal transduction pathways. Hepatology 1999, 29:1743–1751.\nParadis V, Perlemuter G, Bonvoust F, et al.: High glucose and hyperinsulinemia stimulate connective tissue growth factor expression: a potential mechanism involved in progression to fibrosis in nonalcoholic steatohepatitis. Hepatology 2001, 34(4 Pt 1):738–744.\nSud A, Hui JM, Farrell GC, et al.: Improved prediction of fibrosis in chronic hepatitis C using measures of insulin resistance in a probability index. Hepatology 2004, 39:1239–1247.\nRomero-Gomez M, Castellano-Megias VM, Grande L, et al.: Serum leptin levels correlate with hepatic steatosis in chronic hepatitis C. Am J Gastroenterol 2003, 98:1135–1141.\nPiche T, Vandenbos F, Abakar-Mahamat A, et al.: The severity of liver fibrosis is associated with high leptin levels in chronic hepatitis C. J Viral Hepat 2004, 1:91–96.\nZhang BH, Hornsfield BP, Farrell GC: Chronic ethanol administration to rats decreases receptor-operated mobilization of intracellular ionic calcium in cultured hepatocytes and inhibits 1,4,5-inositol trisphosphate production: relevance to impaired liver regeneration. J Clin Invest 1996, 98:1237–1244.\nYang SQ, Lin HZ, Mandal AK, et al.: Disrupted signaling and inhibited regeneration in obese mice with fatty livers: implications for nonalcoholic fatty liver disease pathophysiology. Hepatology 2001, 34(4 Pt 1):694–706.\nRoskams T, Yang SQ, Koteish A, et al.: Oxidative stress and oval cell accumulation in mice and humans with alcoholic and nonalcoholic fatty liver disease. Am J Pathol 2003, 163:1301–1311.\nYang S, Koteish A, Lin H, et al.: Oval cells compensate for damage and replicative senescence of mature hepatocytes in mice with fatty liver disease. Hepatology 2004, 39:403–411. Hepatic progenitor cells and their fate may prove to have a central role in fibrosis and tumorigenesis in a range of liver diseases where steatosis impairs the normal regenerative programs of hepatocytes.\nGiambartolomei S, Covone F, Levrero M, Balsano C: Sustained activation of the Raf\u002FMEK\u002FErk pathway in response to EGF in stable cell lines expressing the Hepatitis C Virus (HCV) core protein. Oncogene 2001, 20:2606–2610.\nMichalopoulos GK, DeFrances MC: Liver regeneration. Science 1997, 276:60–66.\nSell S: Heterogeneity and plasticity of hepatocyte lineage cells. Hepatology 2001, 33:738–750.\nLewindon PJ, Pereira TN, Hoskins AC, et al.: The role of hepatic stellate cells and transforming growth factor-beta(1) in cystic fibrosis liver disease. Am J Pathol 2002, 160:1705–1715.\nRamm GA, Greco SA, Bridle KR, et al.: Monocyte chemotaxis protein-1, derived from hepatocytes isolated form bile ductligated rats, causes recruitment of hepatic stellate cells [abstract]. Hepatology 2002, 36(4 Part 2):260A.\nEzure T, Sakamoto T, Tsuji H, et al.: The development and compensation of biliary cirrhosis in interleukin-6-deficient mice. Am J Pathol 2000, 156:1627–1639.\nClouston AD, Jonsson JR, Letizia B, et al.: Fibrosis in chronic hepatitis C is associated with hepatic progenitor cell proliferation and a periportal ductular reaction, which is exacerbated by steatosis: a new model for disease progression. Hepatology 2003, 38(4 suppl 1):566A.\nHickman IJ, Jonsson JR, Prins JB, et al.: Modest weight loss and physical activity in overweight patients with chronic liver disease results in sustained improvements in alanine aminotransferase, fasting insulin, and quality of life. Gut 2004, 53:413–419. As an alternative therapy when antiviral treatment has failed, this preliminary trial of weight loss shows promise as an adjunct therapy for patients with chronic liver disease.\nOhata K, Hamasaki K, Toriyama K, et al.: Hepatic steatosis is a risk factor for hepatocellular carcinoma in patients with chronic hepatitis C virus infection. Cancer 2003, 97:3036–3043. Introducing a new role for steatosis in disease progression in HCV, this study may have implications for screening and treatment of steatosis in the long term.\nMoriya K, Nakagawa K, Santa T, et al.: Oxidative stress in the absence of inflammation in a mouse model for hepatitis C virus-associated hepatocarcinogenesis. Cancer Res 2001, 61:4365–4370. This transgenic study found that oxidative stress increased in aging mice and was a function of viral protein expression and not inflammation. The excess oxidative stress emerged as the antioxidant pathways became less efficient with age.\nKato T, Miyamoto M, Date T, et al.: Repeated hepatocyte injury promotes hepatic tumorigenesis in hepatitis C virus transgenic mice. Cancer Sci 2003, 94:679–685.",{"EN":95},"Steatosis is a common finding in chronic hepatitis C infection. It is associated with increased fibrogenesis and, in nongenotype 3 infection, with a reduced response to antiviral therapy. The steatosis is multifactorial; host factors, particularly excess body mass and insulin resistance, and viral cytopathic effects each play a variable role in different genotypes. How steatosis or the accompanying metabolic changes potentiate fibrosis remains enigmatic, but evidence is emerging that implicates oxidative stress, hyperinsulinemia, enhanced hepatocyte death, or altered regeneration programs. Tumorigenesis may also be increased. By reducing steatosis, and in some instances fibrosis, weight loss or other therapies targeting insulin resistance may have a role in those patients who have failed antiviral treatment.",{"EN":97},"Chronic hepatitis C and steatosis",{"VOID":99},"10.1007\u002Fs11901-004-0021-x","PUBLICATION","Author affiliation is blank","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11901-004-0021-x",[104,112,130],{"id":105,"sortIndex":65,"researcher":20,"roles":106,"affiliations":108,"properties":109},"61672dc1-9dfc-4640-badd-85b3a749a8cd",[107],"AUTHOR",[],{"title":110},{"VI":111},"Julie R. 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Mortality in the highly active antiretroviral therapy era: changing causes of death and disease in the HIV outpatient study. J Acquir Immune Defic Syndr. 2006;43:27–34.\nWeber R, Sabin C, Friis-Moller N, et al. Liver-related deaths in persons infected with the HIV: the D:A:D study. Arch Intern Med. 2006;166:1632–41.\nWyatt C, Malvestutto C, Coca S, et al. The impact of hepatitis C virus coinfection on HIV-related kidney disease: a systematic review and meta-analysis. AIDS. 2008;22:1799–807.\nPeters L, Grint D, Lundgren J, et al. HCV viremia increases the incidence of chronic kidney disease in HIV-infected patients. AIDS. 2012;26:1917–26.\nKakinami L, Block R, Adams M, Cohn S, Maliakkal B, Fisher S. Risk of cardiovascular disease in HIV, hepatitis C or HIV\u002FHCV patients compared to the general population. Int J Clin Pract. 2013;67:6–13.\nLo Re V, Teal V, Localio A, et al. Risk of hip fracture associated with HCV infection and HCV\u002FHIV coinfection. Hepatology. 2012;56:1688–98.\nSoriano V, Vispo E, Fernandez-Montero JV, Labarga P, Barreiro P. Update on HIV\u002FHCV coinfection. Curr HIV\u002FAIDS Rep. 2013. doi:10.1007\u002Fs11904-013-0169-5.\n• Soriano V, Sherman K, Rockstroh J, et al. Challenges and opportunities for hepatitis C drug development in HIV-HCV coinfected patients. AIDS. 2011;25:2197–208. This article summarises and discusses the major issues that may complicate the use of direct-acting antivirals in hepatitis C patients with HIV infection.\nNaggie S, Sulkowski M. Management of patients coinfected with HCV and HIV: a close look at the role for direct-acting antivirals. Gastroenterology. 2012;142:1324–34.\nBarreiro P, Vispo E, Labarga P, et al. Management and treatment of chronic hepatitis C in HIV patients. Semin Liver Dis. 2012;32:138–46.\nWitt M, Seaberg E, Darilay A, et al. Incident hepatitis C virus infection in men who have sex with men: a prospective cohort analysis, 1984-2011. Clin Infect Dis. 2013;57:77–84.\nSánchez C, Plaza Z, Vispo E, et al. Scaling up epidemics of acute hepatitis C and syphilis in HIV-infected men who have sex with men in Spain. Liver Int. 2013. doi:10.1111\u002Fliv.12212.\nMacías J, Berenguer J, Japón MA, et al. Fast fibrosis progression between repeated liver biopsies in patients coinfected with HIV\u002Fhepatitis C virus. Hepatology. 2009;50:1056–63.\nFernández-Montero JV, Soriano V. Management of hepatitis C in HIV and\u002For HBV co-infected patients. Best Pract Res Clin Gastroenterol. 2012;26:517–30.\nSoriano V, Puoti M, García-Gascó P, et al. Antiretroviral drugs and liver injury. AIDS. 2008;22:1–13.\nVispo E, Fernandez-Montero JV, Labarga P, Barreiro P, Soriano V. Low risk of liver toxicity using the most recently approved antiretroviral agents but still increased in HIV-HCV coinfected patients. AIDS. 2013;27:1187–8.\nLabarga P, Soriano V, Vispo ME, et al. Hepatotoxicity of antiretroviral drugs is reduced after successful treatment of chronic hepatitis C in HIV-infected patients. J Infect Dis. 2007;196:670–6.\nTorriani F, Rodriguez-Torres M, Rockstroh J, et al. Peginterferon alfa-2a plus ribavirin for chronic hepatitis C virus infection in HIV-infected patients. N Engl J Med. 2004;351:438–50.\nCarrat F, Bani-Sadr F, Pol S, et al. Pegylated interferon alfa-2b vs standard interferon alfa-2b plus ribavirin for chronic hepatitis C in HIV-infected patients: a randomized controlled trial. JAMA. 2004;292:2839–48.\nNuñez M, Miralles C, Berdun MA, et al. Role of weight-based ribavirin dosing and extended duration of therapy in chronic hepatitis C in HIV-infected patients: the PRESCO trial. AIDS Res Hum Retrovir. 2007;23:972–82.\nLabarga P, Barreiro P, da Silva A, et al. Comparison of high ribavirin induction versus standard ribavirin dosing, plus peginterferon-alfa for the treatment of chronic hepatitis C in HIV-infected patients: the PERICO trial. J Infect Dis. 2012;206:961–8.\nSoriano V, Puoti M, Peters M, et al. Care of patients coinfected with HIV and HCV: 2007 updated recommendations from the HCV-HIV international panel. AIDS. 2007;21:1073–89.\nEACS guidelines. (www.europeanaidsclinicalsociety.org). Updated version November 2012.\nMedrano J, Neukam K, Rallon N, et al. Modeling the probability of SVR to therapy with pegylated interferon plus ribavirin in patients coinfected with HCV and HIV. Clin Infect Dis. 2010;51:1209–16.\nMedrano J, de Ledinghen V, Taupin J-L et al. Baseline prediction of response to pegIFN-RBV in chronic hepatitis C using the Prometheus score. 63rd Annual Meeting of the American Association for the Study of Liver Diseases (AASLD 2012). Boston, Nov 9-13, 2012. Abstract 657.\n• Sulkowski M, Pol S, Mallolas J, et al. Boceprevir versus placebo with pegylated interferon alfa-2b and ribavirin for treatment of hepatitis C virus genotype 1 in patients with HIV: a randomised, double-blind, controlled phase 2 trial. Lancet Infect Dis. 2013;13:597–605. This is the pivotal study demonstrating the efficacy and safety of boceprevir in coinfected patients.\n• Sulkowski M, Sherman K, Dieterich D, et al. Telaprevir in combination with peginterferon and ribavirin for chronic HCV genotype 1 infection in HIV-infected patients. Ann Intern Med. 2013. doi:10.7326\u002F0003-4819-159-2-201307160-00654. This is the pivotal study demonstrating the efficacy and safety of telaprevir in coinfected patients.\nHulskotte E, Feng H, Xuan F, et al. Pharmacokinetic interactions between the hepatitis C virus protease inhibitor boceprevir and ritonavir-boosted HIV-1 protease inhibitors atazanavir, darunavir, and lopinavir. Clin Infect Dis. 2013;56:718–26.\nvan Heeswijk R, Beumont M, Kauffman R, et al. Review of drug interactions with telaprevir and antiretrovirals. Antivir Ther. 2013. doi:10.3851\u002FIMP2527.\nde Kanter C, Blonk M, Colbers A, et al. Lack of a clinically significant drug-drug interaction in healthy volunteers between the hepatitis C virus protease inhibitor boceprevir and the HIV integrase inhibitor raltegravir. Clin Infect Dis. 2013;56:300–6.\nCrauwels H, van Heeswijk R, Stevens M, et al. Clinical perspective on drug‑drug interactions with the non-nucleoside reverse transcriptase inhibitor rilpivirine. AIDS Rev. 2013;15:87–101.\nBenito JM, Sanchez-Parra C, Barreiro P, et al. Triple combination therapy for hepatitis C with telaprevir exhibits greater early antiviral activity than with boceprevir. Antivir Ther. 2013. doi:10.3851\u002FIMP2614.\nCachay E, Wyles D, Torriani F, et al. High incidence of serious adverse events in HIV-infected patients treated with a telaprevir-based HCV treatment regimen. AIDS. 2013 Jul 24. [Epub ahead of print].\nCotte L, Braun J, Lascoux-Combe C, et al. High early virological response with telaprevir-pegylated interferon-ribavirin in treatment-experienced HCV genotype 1\u002FHIV coinfected patients: ANRS HC26 TelapreVIH study. CROI 2013. March 3-6 2013. Atlanta, GA. Abstract 36.\nPoizot-Martin I, Bellissant E, Piroth L, et al. ANRS HC27 BocepreVIH interim analysis: high early virologic response with boceprevir + pegylated interferón + ribavirin in HCV\u002FHCV coinfected patients with previous failure to pegylated interferon + ribavirin. CROI 2013, Atlanta, GA. March 3-6 2013. Abstract 37.\nPoveda E, Vispo E, Barreiro P, et al. Predicted effect of direct-acting antivirals in the current HIV-HCV coinfected population in Spain. Antivir Ther. 2012;17:571–5.\nVispo E, Rallon N, Labarga P, Barreiro P, Benito JM, Soriano V. Different impact of IL28B polymorphisms on response to peginterferon plus ribavirin in HIV-positive patients infected with HCV subtypes 1a or 1b. J Clin Virol. 2012;55:58–61.\nBarreiro P, Cornelli B, Maida I, et al. Performance of boceprevir or telaprevir in triple therapy with peginterferon and ribavirin in routine clinical practice. EACS. 2013. doi:10.1016\u002FS1473-3099(13)70162-2.\nSoriano V, Labarga P, Fernández-Montero JV, et al. The changing face of hepatitis C in the new era of direct-acting antivirals. Antivir Res. 2013;97:36–40.\nDieterich D, Rockstroh J, Orkin C, et al. Simeprevir with pegylated interferon\u002Fribavirin in patients co-infected with chronic hepatitis C and HIV-1: week-24 interim analysis of the TMC435-C212 study. Program and abstracts of the 20th Conference on Retroviruses and Opportunistic Infections; March 3-6, 2013; Atlanta, GA. Abstract 154LB.\nDieterich D, Soriano V, Nelson M, et al. STARTVerso 4: high rates of early virologic response in hepatitis C virus genotype 1\u002FHIV co-infected patients treated with faldaprevir + pegylated interferon and ribavirin. Program and abstracts of the 20th Conference on Retroviruses and Opportunistic Infections; March 3-6, 2013; Atlanta, Georgia. Abstract 40LB.\nRockstroh J, Nelson M, Soriano V, et al. STARTVerso 4 Phase III trial of faldaprevir once-daily plus peginterferon alfa-2a and ribavirin in patients with HIV and HCV genotype 1 coinfection: end of treatment response. EACS, Brussels, Belgium. Oct 2013. (in press).\nSabo J, Kort J, Haschke M, et al. Pharmacokinetic interactions of darunavir\u002Fritonavir, efavirenz, and tenofovir with the HCV protease inhibitor faldaprevir in healthy volunteers. CROI 2013, Atlanta, GA. March 3-6 2013. Abstract 35.\nScheel T, Rice C. Understanding the hepatitis C virus life cycle paves the way for highly effective therapies. Nat Med. 2013;19:837–49.\nLok A, Gardiner D, Lawitz E, et al. Preliminary study of two antiviral agents for hepatitis C genotype 1. N Engl J Med. 2012;366:216–24.\nSuzuki Y, Ikeda K, Suzuki F, et al. Dual oral therapy with daclatasvir and asunaprevir for patients with HCV genotype 1b infection and limited treatment options. J Hepatol. 2013. doi:10.1016\u002Fj.jhep.2012.09.037.\nSoriano V, Vispo E, de Mendoza C, et al. Hepatitis C therapy with HCV NS5B polymerase inhibitors. Expert Opin Pharmacother. 2013;14:1161–70.\nLawitz E, Mangia A, Wyles D, et al. Sofosbuvir for previously untreated chronic hepatitis C infection. N Engl J Med. 2013;368:1878–87.\nJacobson I, Gordon S, Kowdley K, et al. Sofosbuvir for hepatitis C genotype 2 or 3 in patients without treatment options. N Engl J Med. 2013;368:1867–77.\nKowdley K, Lawitz E, Crespo I, et al. Sofosbuvir with pegylated interferon alfa-2a and ribavirin for treatment-naïve patients with hepatitis C genotype 1 infection (ATOMIC): an open-label, randomized, multicentre phase 2 trial. Lancet. 2013;381:2100–7.\nRodriguez-Torres M, Gonzalez A, Rodriguez J, et al. HIV\u002FHCV coinfected and HCV monoinfected patients have similar early HCV viral kinetics with the potent HCV nucleotide polymerase inhibitor sofosbuvir. ICAAC 2012, San Francisco, CA; Sept 9-12 2012 [abstract H-1921a].\nPoordad F, Lawitz E, Kowdley K, et al. Exploratory study of oral combination antiviral therapy for hepatitis C. N Engl J Med. 2013;368:45–53.\nGane E. Future perspectives: towards interferon-free regimens for HCV infection. Antivir Ther. 2012;17:1201–10.\nSulkowski M, Gardiner D, Rodriguez-Torres M, et al. High rate of sustained virologic response with the all-oral combination of daclatasvir (NS5A inhibitor) plus sofosbuvir (nucleotide NS5B inhibitor), with or without ribavirin, in treatment-naive patients chronically infected with HCV genotypes 1, 2, or 3. 63rd Annual Meeting of the American Association for the Study of Liver Diseases (AASLD 2012). Boston, November 9-13, 2012. Abstract LB-2.\nKowdley K, Lawitz E, Poordad F, et al. A 12-week interferon-free treatment regimen with ABT-450\u002Fr, ABT-267, ABT-333 and ribavirin achieves SVR rates (observed data) of 99% in treatment-naive patients and 93% in prior null responders with HCV genotype 1 infection. 63rd Annual Meeting of the American Association for the Study of Liver Diseases (AASLD 2012). Boston, November 9-13, 2012. Abstract LB-1.\nZeuzem S, Soriano V, Asselah T, et al. Interferon-free treatment with faldaprevir and BI 207127 for genotype 1 HCV infection. N Engl J Med. 2013;369:630–9.\nCohen M, Chen Y, McCauley M, et al. Prevention of HIV-1 infection with early antiretroviral therapy. N Engl J Med. 2011;365:493–505.\nBarreiro P, Duerr A, Beckerman K, Soriano V. Reproductive options for HIV-serodiscordant couples. AIDS Rev. 2006;8:158–70.\nThomas D. Global control of hepatitis C: where challenge meets opportunity. Nat Med. 2013;19:850–8.\nCenters for Disease Control and Prevention. Recommendations for the identification of chronic hepatitis C virus infection among persons born during 1945–1965. MMWR. 2012;61(RR-4):1–32.\nGrebely J, Matthews G, Lloyd A, et al. Elimination of hepatitis C virus infection among people who inject drugs through treatment as prevention: feasibility and future requirements. Clin Infect Dis. 2013 Jun 27. [Epub ahead of print].\nMartin N, Vickerman P, Grebely J, et al. HCV treatment for prevention among people who inject drugs: modeling treatment scale-up in the age of direct-acting antivirals. Hepatology. 2013. doi:10.1002\u002Fhep.26431.\nSoriano V, Perelson A, Zoulim F. Why are there different dynamics in the selection of drug resistance in HIV and hepatitis B and C viruses? J Antimicrob Chemother. 2008;62:1–4.\nRalston R, Jacobson I, Scull M. The conundrum of relapse in STAT-C therapy: does HCV play the Red Queen or Rip Van Winkle? Semin Liver Dis. 2011;31:410–9.\nRutter K, Hofer H, Beinhardt S, et al. Durability of SVR in chronic hepatitis C patients treated with peginterferon\u002Fribavirin in combination with a direct-acting antiviral. Aliment Pharmacol Ther. 2013;38:118–23.\nLawitz E, Poordad F, Kowdley K, et al. A phase 2a trial of 12-week interferon-free therapy with two direct-acting antivirals (ABT-450\u002Fr, ABT-072) and ribavirin in IL28B C\u002FC patients with chronic hepatitis C genotype 1. J Hepatol. 2013. doi:10.1016\u002Fj.jhep.2013.02.009.\nSoriano V, Vispo E, de Mendoza C, et al. Very late relapse after discontinuation of antiviral therapy for chronic hepatitis C. Antivir Ther. 2013. doi:10.3851\u002FIMP2659.\nDe Rosa F, Audagnotto S, Bargiacchi O, et al. Resolution of HCV infection after highly active antiretroviral therapy in a HIV-HCV coinfected patient. J Infect. 2006;53:e215–8.\nEndo T, Fujimoto K, Nishio M, et al. Case report: clearance of hepatitis C virus after changing the HAART regimen in a patient infected with hepatitis C virus and the HIV. J Med Virol. 2009;81:979–82.\nFalconer K, Gonzalez V, Reichard O, Sandberg J, Alaeus A. Spontaneous HCV clearance in HCV\u002FHIV-1 coinfection associated with normalized CD4 counts, low level of chronic immune activation and high level of T cell function. J Clin Virol. 2008;41:160–3.\nFialaire P, Payan C, Vitour D, et al. Sustained disappearance of hepatitis C viremia in patients receiving protease inhibitor treatment for HIV infection. J Infect Dis. 1999;180:574–5.\nPerez-Olmeda M, Garcia-Samaniego J, Soriano V. Hepatitis C viraemia in HIV-HCV co-infected patients having immune restoration with highly active antiretroviral therapy. AIDS. 2000;14:212.\nRanieri R, Santambrogio C, Veronelli A, Pontiroli A. Hepatitis C viremia persistently suppressed by HAART. Clin Infect Dis. 2003;36:1086–7.\nTorti C, Barnes E, Quiros-Roldan E, Puoti M, Carosi G, Klenerman P. Suppression of hepatitis C virus replication is maintained long term following HAART therapy, in an individual with HCV\u002FHIV co-infection. Antivir Ther. 2004;9:139–42.\nZeitoun J, Mallet V, Chaix ML, Viard J, Blanche S, Pol S. Stable recovery from HCV in HIV-HCV co-infection under antiretroviral therapy. J Clin Virol. 2007;40:71–3.\nWeissbrich B, Langmann P, Schubert J, Jassoy C, Klinker H. Resolution of HCV infection in a HIV-infected patient under HAART after several hepatitis flare-ups. Eur J Med Res. 2003;8:495–8.\nManfredi R, Dentale N, Calza L. Spontaneous clearance of chronic hepatitis C infection in a patient with a 20-year-old HIV-hepatitis C co-infection and chronic active hepatitis. Int J STD AIDS. 2012;23:e48–50.\nYokozaki S, Takamatsu J, Nakano I, et al. Immunologic dynamics in hemophiliac patients infected with hepatitis C virus and HIV: influence of antiretroviral therapy. Blood. 2000;96:4293–9.\nVispo E, Barreiro P, Plaza Z, et al. Spontaneous HCV clearance in HIV patients with chronic hepatitis C on antiretroviral therapy. EACS, Brussels, Belgium. Oct 2013 (in press).\nGuedj J, Dahari H, Rong L, et al. Modeling shows that the NS5A inhibitor daclatasvir has two modes of action and yields a shorter estimate of the hepatitis C virus half-life. Proc Natl Acad Sci U S A. 2013;110:3991–6.",{"EN":177},"Chronic hepatitis C virus (HCV) infection occurs globally in 20 % of HIV-seropositive patients. In coinfected individuals, HCV-related liver disease is a leading cause of morbidity and mortality. The advent of new direct-acting antivirals (DAA) has been particularly awaited for this population, in whom treatment with peginterferon plus ribavirin depicts limited efficacy and poor tolerability. However, pharmacologic interactions, drug resistance, medication adherence and pricing are major challenges using DAA in HIV\u002FHCV-coinfected patients. 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J Infect Dis 2000, 181:1528–1536.\nLechner F, Gruener NH, Urbani S, et al.: CD8+ T lymphocyte responses are induced during acute hepatitis C virus infection but are not sustained. Eur J Immunol 2000, 30:2479–2487.\nThimme R, Bukh J, Spangenberg HC, et al.: Viral and immunological determinants of hepatitis C virus clearance, persistence, and disease. Proc Natl Acad Sci U S A 2002, 99:15661–15668.\nGrakoui A, Shoukry NH, Woollard DJ, et al.: HCV persistence and immune evasion in the absence of memory T cell help. Science 2003, 302:659–662.\nShoukry NH, Grakoui A, Houghton M, et al.: Memory CD8+ T cells are required for protection from persistent hepatitis C virus infection. J Exp Med 2003, 197:1645–1655.\nThimme R, Oldach D, Chang KM, et al.: Determinants of viral clearance and persistence during acute hepatitis C virus infection. J Exp Med 2001, 194:1395–1406. CD4+ and CD8+ T-cell immunity during the natural course of acute hepatitis C.\nLechner F, Wong DK, Dunbar PR, et al.: Analysis of successful immune responses in persons infected with hepatitis C virus. J Exp Med 2000, 191:1499–1512.\nWedemeyer H, He XS, Nascimbeni M, et al.: Impaired effector function of hepatitis C virus-specific CD8+ T cells in chronic hepatitis C virus infection. J Immunol 2002, 169:3447–3458.\nGruener NH, Lechner F, Jung MC, et al.: Sustained dysfunction of antiviral CD8+ T lymphocytes after infection with hepatitis C virus. J Virol 2001, 75:5550–5558.\nErickson AL, Kimura Y, Igarashi S, et al.: The outcome of hepatitis C virus infection is predicted by escape mutations in epitopes targeted by cytotoxic T lymphocytes. Immunity 2001, 15:883–895.\nChang KM, Thimme R, Melpolder JJ, et al.: Differential CD4(+) and CD8(+) T-cell responsiveness in hepatitis C virus infection. Hepatology 2001, 33:267–276.\nScognamiglio P, Accapezzato D, Casciaro MA, et al.: Presence of effector CD8+ T cells in hepatitis C virus-exposed healthy seronegative donors. J Immunol 1999, 162:6681–6689.\nKoziel MJ, Wong DK, Dudley D, et al.: Hepatitis C virus-specific cytolytic T lymphocyte and T helper cell responses in seronegative persons. J Infect Dis 1997, 176:859–866.\nKubitschke AK, Bahr M, Aslan N, et al.: Induction of hepatitis C virus specific T cells by needle stick injury in the absence of HCV-viremia [abstract]. Hepatology 2003, 38:173A.\nHeller T, Sobao Y, Mizukoshi E, et al.: HCV exposure in humans: stimulation of cellular, but not humoral immune responses in the absence of detectable viremia [abstract]. Hepatology 2003, 38:182A.\nWedemeyer H, Mizukoshi E, Davis AR, et al.: Cross-reactivity between hepatitis C virus and influenza A virus determinantspecific cytotoxic T cells. J Virol 2001, 75:11392–11400.\nTakano S, Satomura Y, Omata M: Effects of interferon beta on non-A, non-B acute hepatitis: a prospective, randomized, controlled-dose study. Japan Acute Hepatitis Cooperative Study Group. Gastroenterology 1994, 107:805–811.\nJaeckel E, Cornberg M, Wedemeyer H, et al.: Treatment of acute hepatitis C with interferon alfa-2b. N Engl J Med 2001, 345:1452–1457. Key reference for early therapy of acute hepatitis C with interferon alpha.\nManns MP, McHutchison JG, Gordon SC, et al.: Peginterferon alfa-2b plus ribavirin compared with interferon alfa-2b plus ribavirin for initial treatment of chronic hepatitis C: a randomised trial. Lancet 2001, 358:958–965.\nFried MW, Shiffman ML, Reddy KR, et al.: Peginterferon alfa-2a plus ribavirin for chronic hepatitis C virus infection. N Engl J Med 2002, 347:975–982.\nWiegand J, Boecher W, Buggisch P, et al.: 24 weeks of monotherapy with pegylated interferon alfa-2b in patients with acute hepatitis C [abstract]. Hepatology 2003, 38:277A.\nSantantonio T, Mazzola M, Guastadisegni A, et al.: A cohort study of acute hepatitis C virus (HCV) infection: natural course and outcome [abstract]. Hepatology 1999, 30:205A.\nWedemeyer H, Jackel E, Wiegand J, et al.: Whom? When? How? Another piece of evidence for early treatment of acute hepatitis C. Hepatology 2004, 39:1201–1203.\nHofer H, Watkins-Riedel T, Janata O, et al.: Spontaneous viral clearance in patients with acute hepatitis C can be predicted by repeated measurements of serum viral load. Hepatology 2003, 37:60–64.\nBerg T, Pascu M, Moller B: Prediction of spontaneous viral clearance in acute hepatitis C by viral load measurements. Hepatology 2003, 37:1495–1496.\nGerlach JT, Diepolder HM, Zachoval R, et al.: Acute hepatitis C: high rate of both spontaneous and treatment-induced viral clearance. Gastroenterology 2003, 125:80–88. Key reference for delayed therapy of acute hepatitis C with interferon alpha.\nKamal SM, Ismail A, Graham CS, et al.: Pegylated interferon alpha therapy in acute hepatitis C: relation to hepatitis C virus-specific T cell response kinetics. Hepatology 2004, 39:1721–1731.\nSantantonio T, Sinisi E, Signorile F, et al.: Successful treatment of acute hepatitis C with alpha 2b PEG-interferon monotherapy: an interim analysis [abstract]. Hepatology 2003, 38(suppl_1):642A.\nNomura H, Sou S, Tanimoto H, et al.: Short-term interferonalfa therapy for acute hepatitis C: a randomized controlled trial. Hepatology 2004, 39:1213–1219.\nDelwaide J, Bourgeois N, Gerard C, et al.: Treatment of acute hepatitis C with interferon alpha-2b: early initiation of treatment is the most effective predictive factor of sustained viral response. Aliment Pharmacol Ther 2004, 20:15–22.\nManns MP, Meyer S, Wedemeyer H: The German network of excellence for viral hepatitis (Hep-Net). Hepatology 2003, 38:543–544.\nLehmann M, Meyer MF, Monazahian M, et al.: High rate of spontaneous clearance of acute hepatitis C virus genotype 3 infection. J Med Virol 2004, 73:387–391.\nZeuzem S, Hultcrantz R, Bourliere M, et al.: Peginterferon alfa-2b plus ribavirin for treatment of chronic hepatitis C in previously untreated patients infected with HCV genotypes 2 or 3. J Hepatol 2004, 40:993–999.\nRahman F, Heller T, Sobao Y, et al.: Effects of antiviral therapy on the cellular immune response in acute hepatitis C. Hepatology 2004, 40:87–97. CD4+ and CD8+ T-cell immunity during interferon therapy of acute hepatitis C.\nLauer GM, Lucas M, Ouchi K, et al.: T-cell responses during early therapy for HCV infection [abstract]. Hepatology 2003, 38:354A.\nTester IA, Smyk-Pearson S, Dean S, Rosen HR: Acute hepatitis C infection following patellar tendon transplantation: immunologic correlates of recovery [abstract]. Hepatology 2003, 38:358A.\nThomson M, Nascimbeni M, Havert MB, et al.: The clearance of hepatitis C virus infection in chimpanzees may not necessarily correlate with the appearance of acquired immunity. J Virol 2003, 77:862–870.\nRosenberg ES, Billingsley JM, Caliendo AM, et al.: Vigorous HIV-1-specific CD4+ T cell responses associated with control of viremia. Science 1997, 278:1447–1450.\nRosenberg SA: Progress in human tumour immunology and immunotherapy. Nature 2001, 411:380–384.\nStevens AB, Coyle PV: Hepatitis C virus: an important occupational hazard? Occup Med (Lond) 2000, 50:377–382.\nThe German Consensus Conference on the treatment of viral hepatitis 2003. Accessible at http:\u002F\u002Fwww.kompetenznetz-hepatitis. de. Accessed March 2, 2004.\nJullien-Depradeux AM, Bloch J, Quellec-Nathan M, Abenhaim A: National campaign against hepatitis C in France (1999-2002). Acta Gastroenterol Belg 2002, 65:112–114.",{"EN":301},"Management of acute hepatitis C has been discussed controversially in recent years. Early administration of interferon alpha prevents chronicity in almost all cases. However, interferon treatment is associated with significant side effects and costs; thus, alternative treatment strategies were also investigated. These data also suggested that a delayed therapy may cure the infection in 80% to 90% of cases. A detailed understanding of the pathophysiologic mechanisms of acute hepatitis C virus infection may help to find the best way to treat our patients. It has been shown that antiviral humoral and cellular immune responses may influence the outcome of the disease. While a weak T-cell immunity is associated with chronicity, a strong and multispecific cellular immune response is observed in self-limited infection. This article summarizes very recent immunologic and clinical studies on acute hepatitis C and illustrates the knowledge transfer from bench to bedside.",{"EN":303},"Acute hepatitis C infection: Can immunology teach us the right way to treat?",{"VOID":305},"10.1007\u002Fs11901-004-0025-6","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs11901-004-0025-6",[308,325,332,339],{"id":309,"sortIndex":62,"researcher":20,"roles":310,"affiliations":311,"properties":322},"ef8ad9d0-8c73-4af5-b1ae-c06a23a5d57a",[107],[312],{"id":20,"sortIndex":21,"affiliation":313,"properties":20},{"id":314,"createTime":315,"updateTime":316,"relativeEntities":317,"slug":318,"properties":319,"entityType":126,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"3db17e2f-ec6f-46fb-94e6-7cb0811321e6","2023-12-18T05:33:41.895+00:00","2024-12-10T09:01:05.682+00:00",[],"Department-of-Gastroenterology-Hepatology-and-Endocrinology-Hannover-Medical-School-Hannover-Germany",{"title":320},{"VI":321},"Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany",{"title":323},{"VI":324},"Michael P. Manns",{"id":326,"sortIndex":21,"researcher":20,"roles":327,"affiliations":328,"properties":329},"0248e414-461e-42e9-864c-30f709cad481",[107],[],{"title":330},{"VI":331},"Johannes Wiegand",{"id":333,"sortIndex":48,"researcher":20,"roles":334,"affiliations":335,"properties":336},"4c9621ba-5f66-4448-aec1-9a4c870811d8",[107],[],{"title":337},{"VI":338},"Heiner Wedemeyer",{"id":340,"sortIndex":65,"researcher":20,"roles":341,"affiliations":342,"properties":343},"814b8254-4a3c-4a1f-84e4-3603afce4ea6",[107],[],{"title":344},{"VI":345},"Andrej 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D, Franco-Bronson K, Buchler N, et al.: Hepatitis C, interferon alfa, and depression. Hepatology 2000, 31:1207–1211.\nAlter MJ, Kruszon-Moran D, Nainan OV, et al.: The prevalence of hepatitis C virus infection in the United States, 1988 through 1994. N Engl J Med 1999, 341:556–562.\nRosenberg S, Goodman L, Osher FC, et al.: Prevalence of HIV, hepatitis B, and hepatitis C in people with severe mental illness. Am J Public Health 2001, 91:31–37.\nRoy K, Hay G, Andragetti R, et al.: Monitoring hepatitis C virus infection among injecting drug users in the European Union: a review of the literature. Epidemiol Infect 2002, 129:577–585.\nde Oliveira LC, Buso AG, de Oliveira AT, et al.: Prevalence of hepatitis B and hepatitis C markers in alcoholics with and without clinically evident hepatic cirrhosis. Rev Inst Med Trop Sao Paulo 1999, 41:69–73.\nel-Serag HB, Kunik M, Richardson P, et al.: Psychiatric disorders among veterans with hepatitis C infection. Gastroenterology 2002, 123:476–482. This study of HCV-infected patients highlights the high frequency of comorbid psychiatric illness among veterans.\nStraits-Tröster KA, Sloan KL, Dominitz JA, et al.: Hepatitis C virus (HCV) prevalence, access to care, and psychiatric co-morbidities in the Northwest Network. Paper presented at the Proceedings of the Veterans Affairs Health Services Research and Development 19th Annual Meeting. Washington, DC. February 2001.\nCawthorne CH, Rudat KR, Burton MS, et al.: Limited success of HCV antiviral therapy in United States veterans. Am J Gastroenterol 2002, 97:149–155.\nHo SB, Nguyen H, Tetrick LL, et al.: Influence of psychiatric diagnoses on interferon-alpha treatment for chronic hepatitis C in a veteran population. Am J Gastroenterol 2001, 96:157–164.\nVeterans Health Administration: Treatment Recommendations for Patients with Chronic Hepatitis C, Version 2.0; prepared by the San Francisco and Miami Centers of Excellence in Hepatitis C Research and Education and the Hepatitis C Technical Advisory Group, Department of Veterans Affairs. http:\u002F\u002Fwww.va.gov\u002F hepatitisC\u002Fpdf\u002FTrtmnt_Recmmndtns2002v2.pdf.\nSylvestre DL: Treating hepatitis C in methadone maintenance patients: an interim analysis. Drug Alcohol Depend 2002, 67:117–123. One of the only published reports describing HCV treatment and IFN outcomes in active drug users.\nDanta M, Dore GJ, Hennessy L, et al.: Factors associated with severity of hepatic fibrosis in people with chronic hepatitis C infection. Med J Aust 2002, 177:240–245.\nEdlin BR, Seal KH, Lorvick J, et al.: Is it justifiable to withhold treatment for hepatitis C from illicit-drug users? N Engl J Med 2001, 345:211–215. Addresses the need for further research to evaluate treatment models for HCV-positive patients with substance use disorders seeking IFN therapy.\nDavis GL, Rodrigue JR: Treatment of chronic hepatitis C in active drug users. N Engl J Med 2001, 345:215–217.\nLerner DM, Stoudemire A, Rosenstein DL: Neuropsychiatric toxicity associated with cytokine therapies. Psychosomatics 1999, 40:428–435.\nValentine AD, Meyers CA, Kling MA, et al.: Mood and cognitive side effects of interferon-alpha therapy. Semin Oncol 1998, 25:39–47.\nTrask P, Esper P, Riba M, et al.: Psychiatric side effects of interferon therapy: prevalence, proposed mechanisms, and future directions. J Clin Oncol 2000, 18:2316–2326.\nSchalm S, Hansen B, Chemello L, et al.: Ribavirin enhances the efficacy but not the adverse effects of interferon in chronic hepatitis C. J Hepatol 1997, 26:961–966.\nMaddrey W: Safety of combination interferon alfa-2b\u002Fribavirin therapy in chronic hepatitis C-relapsed and treatment-naive patients. Semin Liver Dis 1999, 19:67–75.\nMakino M, Kitano Y, Hirohashi M, et al.: Enhancement of immobility in mouse forced swimming test by treatment with human interferon. Eur J Pharmacol 1998, 356:1–7.\nSammut S, Bethus I, Goodall G, et al.: Antidepressant reversal of interferon-alpha-induced anhedonia. Physiol Behav 2002, 75:765–72.\nPollak Y, Yirmiya R: Cytokine-induced changes in mood and behaviour: implications for ‘depression due to a general medical condition,’ immunotherapy and antidepressive treatment. Int J Neuropsychopharmacol 2002, 5:389–399.\nReichlin S: Neuroendocrine-immune interactions. N Engl J Med 1993, 329:1246–1253.\nLeonard BE, Song C: Changes in the immune system in rodent models of depression. Int J Neuropsychopharmacol 2002, 5:345–356.\nTaylor MW, Feng GS: Relationship between interferongamma, indoleamine 2,3-dioxygenase, and tryptophan catabolism. FASEB J 1991, 5:2516–2522.\nBonaccorso S, Marino V, Puzella A, et al.: Increased depressive ratings in patients with hepatitis C receiving interferonalpha-based immunotherapy are related to interferon-alphainduced changes in the serotonergic system. J Clin Psychopharmacol 2002, 22:86–90.\nCapuron, L, Ravaud A, Neveu PJ, et al.: Association between decreased serum tryptophan concentrations and depressive symptoms in cancer patients undergoing cytokine therapy. Mol Psychiatry 2002, 7:468–473.\nBrown RR, Ozaki Y, Datta SP, et al.: Implications of interferoninduced tryptophan catabolism in cancer, auto-immune diseases and AIDS. Adv Exp Med Biol 1991, 294:425–435.\nDantzer R: Cytokine-induced sickness behavior: mechanisms and implications. Ann N Y Acad Sci 2001, 933:222–234.\nBonaccorso S, Puzella A, Marino V, et al.: Immunotherapy with interferon-alpha in patients affected by chronic hepatitis C induces an intercorrelated stimulation of the cytokine network and an increase in depressive and anxiety symptoms. Psychiatry Res 2001, 105:45–55.\nFoucart S, Abadie C: Interleukin-1 beta and tumor necrosis factor-alpha inhibit the release of [3H]-noradrenaline from mice isolated atria. Naunyn Schmiedebergs Arch Pharmacol 1996, 354:1–6.\nDunn AJ: Cytokine activation of the HPA axis. Ann N Y Acad Sci 2000, 917:608–617.\nBoyer P: Do anxiety and depression have a common pathophysiological mechanism? Acta Psychiatr Scand Suppl 2000, 406:24–29.\nParker KJ, Schatzberg AF, Lyons DM: Neuroendocrine aspects of hypercortisolism in major depression. Horm Behav 2003, 43:60–66.\nWichers M, Maes M: The psychoneuroimmuno-pathophysiology of cytokine-induced depression in humans. Int J Neuropsychopharmacol 2002, 5:375–388. Reviews immune, endocrine, and neurotransmitter interactions and suggests possible mechanisms for IFN-induced neuropsychiatric side effects.\nCarvajal GP, Garcia D, Sanchez SA, et al.: Hepatotoxicity associated with the new antidepressants. J Clin Psychiatry 2002, 63:135–137.\nGleason OC, Yates WR, Isbell MD, et al.: An open-label trial of citalopram for major depression in patients with hepatitis C. J Clin Psychiatry 2002, 63:194–198.\nHayasaka S, Nagaki Y, Matsumoto M, et al.: Interferon associated retinopathy. Br J Ophthalmol 1998, 82:323–325.\nHejny C, Sternberg P, Lawson DH, et al.: Retinopathy associated with high-dose interferon alfa-2b therapy. Am J Ophthalmol 2001, 131:782–787.\nMusselman D, Lawson D, Gumnick J, et al.: Paroxetine for the prevention of depression induced by high-dose interferon alfa. N Engl J Med 2001, 344:961–966.\nSkop BP, Brown TM: Potential vascular and bleeding complications of treatment with selective serotonin reuptake inhibitors. Psychosomatics 1996, 37:12–16.\nHergovich N, Aigner M, Eichler HG, et al.: Paroxetine decreases platelet serotonin storage and platelet function in human beings. Clin Pharmacol Ther 2000, 68:435–442.\nde Abajo, FJ, Rodriguez LA, Montero D: Association between selective serotonin reuptake inhibitors and upper gastrointestinal bleeding: population based case-control study. BMJ 1999, 319:1106–1109.\nvan Walraven C, Mamdani MM, Wells PS, et al.: Inhibition of serotonin reuptake by antidepressants and upper gastrointestinal bleeding in elderly patients: retrospective cohort study. BMJ 2001; 323:655–658.\nLevenson J, Fallon H: Fluoxetine treatment of depression caused by interferon-alpha. Am J Gastroenterol 1993, 88:760–761.\nGleason OC, Yates WR: Five cases of interferon-alpha-induced depression treated with antidepressant therapy. Psychosomatics 1999, 40:510–512.\nSchramm T, Lawford B, Macdonald GA, et al.: Sertraline treatment of interferon-alfa-induced depressive disorder. Med J Aust 2000, 173:359–361.\nHauser P, Khosla J, Aurora H, et al.: A prospective study of the incidence and open-label treatment of interferon-induced major depressive disorder in patients with hepatitis C. Mol Psychiatry 2002, 7:942–947.\nVan Thiel D, Friedlander L, Molloy PJ, et al.: Interferon-alpha can be used successfully in patients with hepatitis C viruspositive chronic hepatitis who have a psychiatric illness. Eur J Gastroenterol Hepatol 1995, 7:165–168.\nDieperink E, Ho SB, Thuras P, et al.: A prospective study of neuropsychiatric symptoms associated with interferonalpha-2b and ribavirin therapy for patients with chronic hepatitis C. Psychosomatics 2003, 44:104–112.\nBackmund M, Meyer K, Von Zielonka M, et al.: Treatment of hepatitis C infection in injection drug users. Hepatology 2001, 34:188–193.\nDalgard O, Bjoro K, Hellum K, et al.: Treatment of chronic hepatitis C in injecting drug users: 5 years’ follow-up. Eur Addict Res 2002, 8:45–49.\nDiClemente CC, Carbonari JP, Montgomery RP, et al.: The Alcohol Abstinence Self-Efficacy scale. J Stud Alcohol 1994, 55:141–148.\nBohn MJ, Babor TF, Kranzler HR: The Alcohol Use Disorders Identification Test (AUDIT): validation of a screening instrument for use in medical settings. J Stud Alcohol 1995, 56:423–432.\nMcLellan AT, Luborsky L, O’Brien CP, et al.: An improved diagnostic instrument for substance abuse patients: the Addiction Severity Index. J Nerv Ment Dis 1980, 168:26–33.\nBeck AT, Ward C, Mendelson M, et al.: An inventory for measuring depression. Arch Gen Psychiatry 1961, 4:561–571.\nBeck AT, Steer RA, Ball R, et al.: Comparison of Beck Depression Inventories-IA and -II in psychiatric outpatients. J Pers Assess 1996, 67:588–597.\nFlemenbaum A, Zimmermann RL: Inter- and intra-rater reliability of the Brief Psychiatric Rating Scale. Psychol Rep 1973, 32:783–792.\nSvanborg P, Asberg M: A comparison between the Beck Depression Inventory (BDI) and the self-rating version of the Montgomery Asberg Depression Rating Scale (MADRS). J Affect Disord 2001, 64:203–216.\nWeathers FW, Herman DS, Huska JA, Keane TM: The PTSD Checklist (PCL): reliability, validity, and diagnostic utility. Paper presented at the 9th Annual Conference of the International Society for Traumatic Stress Studies; 1993.\nYoung RC, Biggs JT, Ziegler VE, et al.: A rating scale for mania: reliability, validity and sensitivity. Br J Psychiatry 1978, 133:429–435.\nZung WW, Wonnacott TH: Treatment prediction in depression using a self-rating scale. Biol Psychiatry 1970, 2:321–329.\nWright IA: Monitoring depression in patients undergoing alpha-interferon and ribavirin therapy for hepatitis C. Gastroenterol Nurs 2000, 23:275–280.\nBush K, Kivlahan DR, McDonell MB, et al.: The AUDIT alcohol consumption questions (AUDIT-C): an effective brief screening test for problem drinking. Ambulatory Care Quality Improvement Project (ACQUIP). Alcohol Use Disorders Identification Test. Arch Intern Med 1998, 158:1789–1795.\nCoon GM, Pena D, Illich PA: Self-efficacy and substance abuse: assessment using a brief phone interview. J Subst Abuse Treat 1998, 15:385–391.\nNaranjo CA, Knoke DM: The role of selective serotonin reuptake inhibitors in reducing alcohol consumption. J Clin Psychiatry 2001, 62:18–25.\nSrisurapanont M, Kittiratanapaiboon P, Jarusuraisin N: Treatment for amphetamine psychosis. Cochrane Database Syst Rev 2001, 4:CD003026.",{"EN":423},"Increasingly, hepatologists and other health care providers have recognized the need for a systematic approach to hepatitis C that addresses the common comorbidities of psychiatric and substance use disorders, and one that demands active participation from mental health care providers. The majority of new and existing cases of hepatitis C are related to injection drug use, and in this population the prevalence of psychiatric comorbidity is high. Optimally, all hepatitis C-positive patients should be screened for psychiatric and substance use disorders prior to antiviral therapy. If a patient screens positive, he or she should be referred to a mental health care provider or addiction specialist, assessed for the presence of a psychiatric or substance use disorder, and appropriately treated prior to initiation of antiviral therapy. Although interferon therapy can lead to severe neuropsychiatric side effects, including suicidality, evidence suggests that many patients with comorbid psychiatric and substance use diagnoses can be treated safely and effectively using comanagement strategies.",{"EN":425},"Hepatitis C in patients with psychiatric disease and substance abuse: Screening strategies and comanagement models of care",{"VOID":427},"10.1007\u002Fs11901-003-0002-5","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11901-003-0002-5",[430,445],{"id":431,"sortIndex":65,"researcher":20,"roles":432,"affiliations":433,"properties":442},"e7b603b5-e017-4b52-bc65-8fe4e61b7795",[107],[434],{"id":20,"sortIndex":21,"affiliation":435,"properties":20},{"id":436,"createTime":437,"updateTime":437,"relativeEntities":438,"slug":20,"properties":439,"entityType":126,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"c08eede6-db7a-48bb-b7ab-fba12c3c55ee","2023-12-26T15:25:50.685+00:00",[],{"title":440},{"VI":441},"Portland VA Medical Center (P3MHAdm), Portland, USA",{"title":443},{"VI":444},"Peter Hauser",{"id":446,"sortIndex":21,"researcher":20,"roles":447,"affiliations":448,"properties":449},"d0d3d997-ae07-4459-81f5-ed0ab81437e9",[107],[],{"title":450},{"VI":451},"Jennifer M. 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Fusco DN, Chung RT. Novel Therapies for Hepatitis C: Insights from the structure of the virus. Annu Rev Med 2012;63:373–87. This is a comprehensive review of the activity of direct acting antiviral agents as well as host cofactor inhibitors. The review includes serine proteases, the NS5B RNA polymerases, as well as the NS5A and the NS4B. The host cofactor inhibitors include the cyclophilin inhibitors, miR122 antagonists, and the statins.",{"doi":560},"10.1146\u002Fannurev-med-042010-085715",{"id":20,"text":562,"url":20,"identifiers":563},"•• Gish R, Meanwell N. The NS5A replication complex inhibitors: difference makers? Clin Liver Dis 2011;15:627–639. This is a very comprehensive and excellent review that summarizes the development and discovery of the NS5A replication complex inhibitors.",{"doi":564},"10.1016\u002Fj.cld.2011.05.010",{"id":20,"text":566,"url":20,"identifiers":567},"Hwang J, Huang L, Cordek DG, et al. Hepatitis C virus nonstructural protein 5A: biochemical characterization of a novel structural class of RNA-binding proteins. J Virol. 2010;84:12480–91.",{"doi":568},"10.1128\u002FJVI.01319-10",{"id":20,"text":570,"url":20,"identifiers":571},"• Gao M, Nettles RE, Belema M, et al. Chemical genetics strategy identifies an HCV NS5a inhibitor with a potent clinical effect. Nature 2010;465:96–100. This is the description of the profile of BMS 790052 with the report of the EC 50. In addition, there is a review of the phase 1 clinical trial results as well as genotypic analysis for resistance testing.",{"doi":572},"10.1038\u002Fnature08960",{"id":20,"text":574,"url":20,"identifiers":575},"Schmitz U, Tan S. NS5A- from obscurity to new target for HCV therapy. Recent Patents Anti-Infect Drug Discover. 2008;3:77–92.",{"doi":576},"10.2174\u002F157489108784746597",{"id":20,"text":578,"url":20,"identifiers":579},"Tellinghuisen TL, Marcotrigiano J, Gorbalenya A, Rice CM. The NS5A protein of hepatitis C virus is a zinc metalloprotein. J Biol Chem. 2004;279:4856–8.",{"doi":580},"10.1074\u002Fjbc.M407787200",{"id":20,"text":582,"url":20,"identifiers":583},"Tellinghuisen TL, Marcotrigiano J, Rice CM. Function follows form: the structure of the N-terminal domain of HCV NS5A Structure of the zinc-binding domain of an essential component of the hepatitis C virus replicase. Nature. 2005;435:374–9.",{"doi":584},"10.1038\u002Fnature03580",{"id":20,"text":586,"url":20,"identifiers":587},"Flisiak R, Dumont JM, Crabbe R. Cyclophillin inhibitors in hepatitis C virus infections. Expert Opin Investig Drugs. 2007;16:1345–54.",{"doi":588},"10.1517\u002F13543784.16.9.1345",{"id":20,"text":590,"url":20,"identifiers":591},"Brass V, Bieck E, Montserret R, et al. An amino-terminal amphipathic alpha-helix mediates membrane association of the hepatitis C virus nonstructural protein 5A. J Biol Chem. 2002;277:8130–9.",{"doi":592},"10.1074\u002Fjbc.M111289200",{"id":20,"text":594,"url":20,"identifiers":595},"Dousson CB, La Colla M, Chapron C, et al. Idenix NS5A HCV replication inhibitors with low picomolar, pan-genotypicin vitro antiviral activity. Oral Presentation. EASL 46th Annual Meeting March 30th 2011 Berlin Germany.",{"doi":596},"10.1016\u002FS0168-8278(11)60817-9",{"id":20,"text":598,"url":20,"identifiers":599},"Soriano V, Vispo E, Poveda E, et al. Directly acting antivirals against hepatitis C virus. J Antimicro Chemother. 2011;66:1673–86.",{"doi":600},"10.1093\u002Fjac\u002Fdkr215",{"id":20,"text":602,"url":20,"identifiers":603},"• Asselah T. NS5A inhibitors: a new breakthrough for the treatment of chronic hepatitis C. J Hepatol 2011;54:1069–72. This is a short review of the NS5A inhibitors for the treatment of chronic hepatitis C.",{"doi":604},"10.1016\u002Fj.jhep.2010.11.033",{"id":20,"text":606,"url":20,"identifiers":607},"Fridell R, Qiu D, Valera L. Distinct functions of NS5A in hepatitis C virus RNA replication uncovered by studies with NS5A inhibitor BMS-790052. J Virology. 2011;85:7312.",{"doi":608},"10.1128\u002FJVI.00253-11",{"id":20,"text":610,"url":20,"identifiers":611},"MacDonald A, Harris M. Hepatitis C virus NS5A: tales of a promiscuous protein. J Gen Virology. 2004;85:2485–502.",{"doi":612},"10.1099\u002Fvir.0.80204-0",{"id":20,"text":614,"url":20,"identifiers":615},"Yupeng He, Kirk A, Staschke, Tan SL. HCV NS5A: A Multifunctional Regulator of Cellular Pathways and Virus Replication. Hepatitis C Viruses: Genomes and Molecular Biology. In: Tan SL, editor. Norfolk (UK): Horizon Bioscience; 2006.",{},{"id":20,"text":617,"url":20,"identifiers":618},"Vandermeeren AM, Gómez CE, Patiño C, et al. Subcellular forms and biochemical events triggered in human cells by HCV polyprotein expression from a viral vector. Virol J. 2008;5:102.",{"doi":619},"10.1186\u002F1743-422X-5-102",{"id":20,"text":621,"url":20,"identifiers":622},"Appel N, Schaller T, Penin F, et al. From structure to function: new insights into hepatitis C virus RNA replication. J Biol Chem. 2006;281:9833–6.",{"doi":623},"10.1074\u002Fjbc.R500026200",{"id":20,"text":625,"url":20,"identifiers":626},"Suzuki T. A hepatitis C virus-host interaction involved in viral replication: toward the identification of antiviral targets. J Infect Dis. 2010;63:307–11.",{},{"id":20,"text":628,"url":20,"identifiers":629},"Watashi K, Ishii N, Hijikata M, et al. Cyclophillin B is a functional regulator of hepatitis C virus RNA polymerase. Mol Cell. 2005;19:111–2.",{"doi":630},"10.1016\u002Fj.molcel.2005.05.014",{"id":20,"text":632,"url":20,"identifiers":633},"Lui Z, Yang F, Robotham JM, et al. Critical role of cyclophilin A and its prolyl-peptidyl isomerase activity in the structure and function of the hepatitis C virus replication complex. J Virol. 2009;83:6554–65.",{"doi":634},"10.1128\u002FJVI.02550-08",{"id":20,"text":636,"url":20,"identifiers":637},"Kaul A, Staffer S, Berger C, et al. Essential role of cyclophilin A for hepatitis C virus replication and virus production and possible link to polyprotein cleavage kinetics. PLoS Pathog. 2009;5:e1000546.",{"doi":638},"10.1371\u002Fjournal.ppat.1000546",{"id":20,"text":640,"url":20,"identifiers":641},"Hamamoto I, Nishimura Y, Okamoto, et al. Human VAP-B is involved in hepatitis C virus replication through interaction with NS5A and NS5B. J Zirol. 2005;79:13473–82.",{},{"id":20,"text":643,"url":20,"identifiers":644},"Tanji Y, Kaneko T, Satoh S, Shimotohno K. Phosphorylation of hepatitis C virus-encoded nonstructural protein NS5A. J Virol. 1995;69:3980–6.",{"doi":645},"10.1128\u002FJVI.69.7.3980-3986.1995",{"id":20,"text":647,"url":20,"identifiers":648},"McCormick CJ, Brown D, Griffin S, et al. A link between translation of the hepatitis C virus polyprotein and polymerase function; possible consequences for hyperphosphorylation of NS5A. J Gen Virol. 2006;87:93–102.",{"doi":649},"10.1099\u002Fvir.0.81180-0",{"id":20,"text":651,"url":20,"identifiers":652},"Buhler S, Bartenschlager R. New targets for antiviral therapy of chronic hepatitis C. Liver Int. 2011;32:9–16.",{"doi":653},"10.1111\u002Fj.1478-3231.2011.02701.x",{"id":20,"text":655,"url":20,"identifiers":656},"• Qiu D, Lemm J, O’Boyle D, et al. The effects of NS5A inhibitors on NS5A phosphorylation, polyprotein processing and localization. J Gen Virol 2011;92:2502–2511. This is a report of the activity of the various domains of the NS5A HCV nonstructural protein. In particular, the authors review the mechanism of the NS5A inhibitor compounds and their interaction with the various portions of the NS5A replication complex.",{"doi":657},"10.1099\u002Fvir.0.034801-0",{"id":20,"text":659,"url":20,"identifiers":660},"Lemm J, O’Boyle D, Liu M, et al. Identification of hepatitis C virus NS5A inhibitors. J Virol. 2010;84:482–91.",{"doi":661},"10.1128\u002FJVI.01360-09",{"id":20,"text":663,"url":20,"identifiers":664},"•• Halfon P, Sarrazin C. Future treatment of chronic hepatitis C with direct acting antivirals: is resistance important? Liver Int 2012;32:79–87. The authors examine the major resistant point mutations for the NS3 HCV protease region, as well as the NS5B polymerase, and most important to this paper, the NS5A region.",{"doi":665},"10.1111\u002Fj.1478-3231.2011.02716.x",{"id":20,"text":667,"url":20,"identifiers":668},"McPhee F, Hernandez D, Yu F, et al. Characterization of virologic escape in HCV genotype 1 null responders receiving a combination of the NS3 protease inhibitor BMS-650032 and NS5A inhibitor BMS-790052. J Hepatol. 2011;54:28–9.",{"doi":669},"10.1016\u002FS0168-8278(11)60065-2",{"id":20,"text":671,"url":20,"identifiers":672},"• Fridell RA, Qiu D, Wang C, Valera L, Gao M.: Resistance analysis of the hepatitis C virus NS5A inhibitor BMS-790052 in an in vitro replicon system. Antimicrob Agents Chemother 2010, 54:3641–3650. The authors perform resistance testing characterizing escape variants of the NS5A inhibitor BMS 790052 in a replicon system.",{"doi":673},"10.1128\u002FAAC.00556-10",{"id":20,"text":675,"url":20,"identifiers":676},"Pol S, Everson G, Ghalib R, et al. Once-daily NS5A inhibitor (BMS 790052) plus peginterfeon-alpha-2A and ribavirin produces high rates of extended rapid virological response in treatment-naïve HCV-genotype 1 subjects: phase 2A trial. J Hepatol. 2010;52:S462.",{"doi":677},"10.1016\u002FS0168-8278(10)61190-7",{"id":20,"text":679,"url":20,"identifiers":680},"Lok AS, Gardiner DF, Lawitz E, et al. Combination therapy with BMS-790052 and BMS-650032 alone or with pegIFN\u002FRBV results in undetectable HCV RNA through 12 weeks of therapy in HCV genotype null responders. Hepatology. 2010;52:877A.",{},{"id":20,"text":682,"url":20,"identifiers":683},"Ratziu V, Gadano A, Pol S, Hezode C, et al. Triple therapy with Daclatasvir (DCV; BMS-790052), peginterferon alfa-2a and ribavirin in HCV-infected prior null and partial responders: 12-week results of phase 2b COMMAND-2 Trial. Presented at 47th Annual Meeting of the European Association for the Study of the Liver. Barcelona, Spain; April 18–22, 2012.",{"doi":684},"10.1016\u002FS0168-8278(12)61219-7",{"id":20,"text":686,"url":20,"identifiers":687},"Olsen DB, Carroll SS, Handt L, et al. HCV antiviral activity and resistance analysis in chronically infected chimpanzees treated with NS3\u002F4A protease and NS513 polymerase inhibitors. J Hepatol. 2007;46:S298.",{"doi":688},"10.1016\u002FS0168-8278(07)62389-7",{"id":20,"text":690,"url":20,"identifiers":691},"•• Gane E, Roberts S, Stedman C, et al.: Interferon-free oral combination therapy with a nucleoside polymerase inhibitor (RG7128) and protease inhibitor (danoprevir\u002FRG7227) for the treatment of chronic hepatitis C genotype 1 infection: results of the INFORM-1 trial. Lancet 2010;376:1467–1475. A very important report of the first interferon-free oral combination therapy for treatment of chronic hepatitis C.",{"doi":692},"10.1016\u002FS0140-6736(10)61384-0",{"id":20,"text":694,"url":20,"identifiers":695},"•• Lok AS, Gardiner DF, Lawitz E, et al. Preliminary study of two antiviral agents for hepatitis C genotype 1. N Engl J Med 2012;366:216–224. Again, a very exciting study of the combination of two oral DAA’s against chronic hepatitis C. In particular, this was a protease inhibitor asunaprevir in combination with daclatasvir, a NS5A inhibitor. The two oral DAA’s were used together, as well in quadruple therapy with a pegylated interferon and ribavirin for the treatment of non-responders to prior interferon and ribavirin therapy.",{"doi":696},"10.1056\u002FNEJMoa1104430",{"id":20,"text":698,"url":20,"identifiers":699},"•• Chayama K, Takahashi S, Toyota J, et al. Dual therapy with the nonstructural protein 5A inhibitor, daclatasvir, and the nonstructural protein 3 protease inhibitor, asunaprevir, in hepatitis C virus genotype 1b–infected null responders. Hepatology 2012;3:742–748. This is a somewhat similar study to the above, however, in a Japanese population. Very impressive efficacy reported by the authors.",{"doi":700},"10.1002\u002Fhep.24724",{"id":20,"text":702,"url":20,"identifiers":703},"Sulkowski M, Gardiner D, Lawitz E, Hinestrosa F, et al. Potent viral suppression with the all-oral combination of Daclatasvir (NS5A inhibitor) and GS-7977 (nucleotide NS5B inhibitor), +\u002F- ribavirin, in treatment-naive patients with chronic HCV GT1, 2, or 3 (100 % SVR gt1, 91 % gt2). Presented at 47th Annual Meeting of the European Association for the Study of the Liver. Barcelona, Spain; April 18–22, 2012.",{"doi":704},"10.1016\u002FS0168-8278(12)61433-0",{"id":20,"text":706,"url":20,"identifiers":707},"Dumas E, Lawal A, Menon R.M, Podsadecki T, et al. Pharmacokinetics, safety and tolerability of the HCV NS5A inhibitor ABT-267 following single and multiple doses in healthy adult volunteers. Presented at 46th Annual Meeting of the European Association for the Study of the Liver. Berlin, Germany; March 30-April 3rd 2011.",{"doi":708},"10.1016\u002FS0168-8278(11)61206-3",{"id":20,"text":710,"url":20,"identifiers":711},"Clinical Trials Gov. Study of ABT-267 in Treatment Naïve Hepatitis C Virus (HCV) Genotype 1 Infected Subjects. Available at http:\u002F\u002Fclinicaltrials.gov\u002Fct2\u002Fshow\u002FNCT01314261 . Accessed February 2012.",{},{"id":20,"text":713,"url":20,"identifiers":714},"Sullivan JG, Rodriguez-Torres M, Lawitz E, Poordad F, et al. ABT-267 combined with pegylated interferon alpha-2a\u002Fribavirin in genotype 1 (GT1) HCV-infected treatment-naïve subjects: 12-week antiviral and safety analysis. Presented at 47th Annual Meeting of the European Association for the Study of the Liver. Barcelona, Spain; April 18–22, 2012.",{"doi":715},"10.1016\u002FS0168-8278(12)61222-7",{"id":20,"text":717,"url":20,"identifiers":718},"National Aids Treatment Advocacy Project. A study to evaluate the efficacy, safety, and pharmacokinetics of ABT-450 with ritonavir (ABT-450\u002Fr) when given together with ABT-333 and Ribavirin (RBV) in treatment-naïve and non-responder subjects with genotype 1 chronic hepatitis C virus (HCV) infection. Available at http:\u002F\u002Fclinicaltrials.gov\u002Fct2\u002Fshow\u002FNCT01306617?cond=%22Hepatitis+C%22&rank=2 . Accessed March 2012.",{},{"id":20,"text":720,"url":20,"identifiers":721},"Achillion Announces Preliminary Phase 1b Proof-of-Concept Data with ACH-2928 NS5A Inhibitor for the Treatment of Hepatitis C. Available at http:\u002F\u002Fir.achillion.com\u002Freleasedetail.cfm?ReleaseID=629849 . Accessed March 2012.",{},{"id":20,"text":723,"url":20,"identifiers":724},"National Aids Treatment Advocacy Project. Achillion Announces Nomination of Second Generation NS5A Inhibitor for the Treatment of Hepatitis C. Available at http:\u002F\u002Fwww.natap.org\u002F2011\u002FHCV\u002F101311_01.htm . Accessed February 2012.",{},{"id":20,"text":726,"url":20,"identifiers":727},"National Aids Treatment Advocacy Project. Enanta’s Lead NS5A Inhibitor Candidate for HCV, EDP-239, Selected as One of Windhover’s Top 10 Infectious Disease Projects to Watch. Available at www.natap.org\u002F2010\u002FHCV\u002F030410_02.htm . Accessed March 2012.",{},{"id":20,"text":729,"url":20,"identifiers":730},"Lawitz E, Gruener D, Hill J, et al. A phase 1, randomized, placebo-controlled, three-day, dose-ranging study of GS-5885, an NS5A inhibitor, in patients with genotype 1 hepatitis C. J Hepatol 2012; [Epub ahead of print]",{"doi":731},"10.1016\u002Fj.jhep.2011.12.029",{"id":20,"text":733,"url":20,"identifiers":734},"Clinical Trials Gov. GS 5885 Administered Concomitantly With GS-9451, Tegobuvir and Ribavirin (RBV) in Chronic Genotype 1 Hepatitis C Virus (HCV) Infection. Available at http:\u002F\u002Fclinicaltrials.gov\u002Fct2\u002Fshow\u002FNCT01353248 . Accessed March 2012.",{},{"id":20,"text":736,"url":20,"identifiers":737},"Sulkowski M, Rodriguez-Torres M, Lawitz E, Shiffman M, et al. Gilead: Interim sustained virologic response rates in treatment-naïve HCV genotype 1a and 1b patients treated for 12 or 24 weeks with an interferon-free all-oral quad regimen. Presented at 47th Annual Meeting of the European Association for the Study of the Liver. Barcelona, Spain; April 18–22, 2012.",{"doi":738},"10.1016\u002FS0168-8278(12)61432-9",{"id":20,"text":740,"url":20,"identifiers":741},"National Aids Treatment Advocacy Project. Nomination of Second Generation NS5A Inhibitor for the Treatment of Hepatitis C. Available at http:\u002F\u002Fwww.natap.org\u002F2011\u002FHCV\u002F101311_01.htm . Accessed March 2012.",{},{"id":20,"text":743,"url":20,"identifiers":744},"National Aids Treatment Advocacy Project. Idenix Update Slides—IDX184 Nucleotide, new IDX719 NS5A (slides attached from investor call this morning), 2 new nucleotides in development. Available at http:\u002F\u002Fwww.natap.org\u002F2012\u002FHCV\u002F010912_03.htm . Accessed March 2012",{},{"id":20,"text":746,"url":20,"identifiers":747},"Idenix Pharmaceuticals. Idenix Announces Positive Clinical Data for HCV Drug Candidates IDX184 and IDX719. Available at http:\u002F\u002Fir.idenix.com\u002Freleasedetail.cfm?ReleaseID=684347 Accessed June 2012",{},{"id":20,"text":749,"url":20,"identifiers":750},"Nicholas JB, Buckman B, Serebryany V, et al. Characterization of novel, highly potent NS5A inhibitors with qd dosing potential and robust activity in an HCV chimeric animal model. J Hepatol. 2011;54:S485–5.",{"doi":751},"10.1016\u002FS0168-8278(11)61230-0",{"id":20,"text":753,"url":20,"identifiers":754},"National Aids Treatment Advocacy Project. Dose-Ranging Trial of PPI-461, a Potent New Pan-Genotypic HCV NS5A Inhibitor, in Patients with HCV Genotype-1 Infection. Available at http:\u002F\u002Fwww.natap.org\u002F2011\u002FAASLD\u002FAASLD_10.htm Accessed March 2012",{},{"id":20,"text":756,"url":20,"identifiers":757},"Presido Pharmaceuticals Inc. Clinical Proof-of-Concept Data for its First HCV NS5A Inhibitor, PPI-461, and Initiation of Clinical Testing for its Second-Generation NS5A Inhibitor, PPI-668. Available at http:\u002F\u002Fwww.presidiopharma.com\u002Fdocs\u002FPresidio%20Pharmaceuticals%20Announces%20Clinical%20POC%20Data-PPI-461%20%20Initiation%20of%20Clinical%20Studies%20of%20PPI-668%20Press%20Release%20November%204%202011.pdf Accessed March 2012.",{},{"id":759,"createTime":760,"updateTime":761,"relativeEntities":762,"slug":763,"properties":764,"entityType":100,"verifyStatus":182,"verifyTime":761,"verifyNote":183,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":773,"fullTextUrl":20,"authors":774,"publicationType":137,"publisherRelationship":802,"citationCount":20,"citationInfo":20,"publishDate":828,"publishYear":829,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":20,"openAccess":20,"references":20,"isForceReanalyzing":166},"1aebbc9a-5f49-4d58-b53f-f66c3c72fc9c","2023-12-06T14:29:15.272+00:00","2025-02-26T23:10:53.807+00:00",[],"Liver-transplantation-for-HBV-and-management-of-reinfection",{"references":765,"abstract":767,"title":769,"doi":771},{"VOID":766},"Torisu M, Yokoyama T, Amemiya H, et al.: Immunosuppression, liver injury, and hepatitis in renal, hepatic, and cardiac homograft recipients: with particular reference to the Australia antigen. Ann Surg 1971, 174:621–639.\nDavies SE, Portmann BC, O’Grady JG, et al.: Hepatic histological findings after transplantation for chronic hepatitis B virus infection, including a unique pattern of fibrosing cholestatic hepatitis. Hepatology 1991, 13:150–157.\nTodo S, Demetris AJ, Van Thiel D, et al.: Orthotopic liver transplantation for patients with hepatitis B virus related liver disease. Hepatology 1991, 13:619–626.\nO’Grady JG, Smith HM, Davies SE, et al.: Hepatitis B virus reinfection after orthotopic liver transplantation. Serological and clinical implications. J Hepatol 1992, 14:104–111.\nLau JY, Bain VG, Davies SE, et al.: High-level expression of hepatitis B viral antigens in fibrosing cholestatic hepatitis. Gastroenterology 1992, 102:956–962.\nStarzl TE, Demetris AJ, Van Thiel D: Liver transplantation (2). N Engl J Med 1989, 321:1092–1099.\nSteinmuller T, Seehofer D, Rayes N, et al.: Increasing applicability of liver transplantation for patients with hepatitis B-related liver disease. Hepatology 2002, 35:1528–1535.\nKim WR, Poterucha JJ, Kremers WK, et al.: Outcome of liver transplantation for hepatitis B in the United States. Liver Transpl 2004, 10:968–974.\nSamuel D, Muller R, Alexander G, et al.: Liver transplantation in European patients with the hepatitis B surface antigen. N Engl J Med 1993, 329:1842–1847.\nMcMillan JS, Shaw T, Angus PW, et al.: Effect of immunosuppressive and antiviral agents on hepatitis B virus replication in vitro. Hepatology 1995, 22:36–43.\nTur-Kaspa R, Shaul Y, Moore DD, et al.: The glucocorticoid receptor recognizes a specific nucleotide sequence in hepatitis B virus DNA causing increased activity of the HBV enhancer. Virology 1988, 167:630–633.\nTrautwein C, Shrem H, Tillmann HL, et al.: Hepatitis B virus mutations in the pre S genome before and after liver transplantation. Hepatology 1996, 24:482–488.\nTerrault NA, Zhiou S, McCory RW, et al.: Incidence and clinical consequences of surface and polymerase gene mutations in liver transplant recipients on hepatitis B immunoglobulin. Hepatology 1998, 28:555–561.\nGrellier L, Mutimer D, Ahmed M, et al.: Lamivudine prophylaxis against reinfection in liver transplantation for hepatitis B cirrhosis. Lancet 1996, 348:1212–1215.\nPerrillo RP, Wright T, Rakela J, et al.: Multicenter United States-Canadian trial to assess lamivudine monotherapy before and after liver transplantation for chronic hepatitis B. Hepatology 2001, 33:424–432. A large multicenter study that confirmed the lack of complete efficacy of lamivudine monotherapy as prophylaxis for viral recurrence following transplantation.\nPerrillo R, Rakela J, Dienstag J, et al.: Multicenter study of lamivudine therapy for hepatitis B after liver transplantation. Hepatology 1999, 29:1581–1586.\nMcGory RW, Ishitani MB, Oliveira WM, et al.: Improved outcome of orthotopic liver transplantation for chronic hepatitis B cirrhosis with aggressive passive immunization. Transplantation 1996, 61:1358–1364.\nBrind A, Jiang JJ, Samuel D, et al.: Evidence for selection of hepatitis B mutants after liver transplantation through peripheral blood mononuclear cell infection. J Hepatol 1997, 26:228–235.\nGish RG, Keeffe EB, Lim J, et al.: Survival after liver transplantation for chronic hepatitis B using reduced immunosuppression. Hepatology 1995, 22:257–262.\nSamuel D, Kimmoun E: Immunosuppression in hepatitis B virus and hepatitis C virus transplants: special considerations. Clin Liver Dis 2003, 7:667–681.\nTerrault N, Holland C, Ferrell L, et al.: Interferon alfa for recurrent hepatitis B infection after liver transplantation. Liver Transpl Surg 1996, 2:132–138.\nAndreone P, Caraceni P, Grazi GL, et al.: Lamivudine treatment for acute hepatitis B after liver transplantation. J Hepatol 1998, 29:985–989.\nNery JR, Weppler D, Rodriguez M, et al.: Efficacy of lamivudine in controlling hepatitis B virus recurrence after liver transplantation. Transplantation 1998, 65:1615–1621.\nRoche B, Samuel D, Roque AM, et al.: Lamivudine therapy for HBV infection after liver transplantation. J Hepatol 1999, 30(suppl_1):78.\nBalan V, Dodson FS, Vargas HE, et al.: Long-term follow up of lamivudine therapy for hepatitis B before and after liver transplantation; clinical implication of development of the YMDD mutant. Hepatology 1999, 30:346A.\nMalkan G, Cattral MS, Humar A, et al.: Lamivudine for hepatitis B in liver transplantation: a single-center experience. Transplantation 2000, 69:1403–1407.\nSeehofer D, Rayes N, Berg T, et al.: Lamivudine as first- and second-line treatment of hepatitis B infection after liver transplantation. Transpl Int 2000, 13:290–296.\nFontana RJ, Hann HW, Wright T, et al.: A multicenter study of lamivudine treatment in 33 patients with hepatitis B after liver transplantation. Liver Transpl 2001, 7:504–510.\nBen-Ari Z, Mor E, Shapira Z, Tur-Kaspa R: Long-term experience with lamivudine therapy for hepatitis B virus infection after liver transplantation. Liver Transpl 2001, 7:113–117.\nPapatheodoridis GV, Sevastianos V, Burroughs AK: Prevention of and treatment for hepatitis B virus infection after liver transplantation in the nucleoside analogues era. Am J Transplant 2003, 3:250–258.\nFontana RJ, Keeffe EB, Carey W, et al.: Effect of lamivudine treatment on survival of 309 North American patients awaiting liver transplantation for chronic hepatitis B. Liver Transpl 2002, 8:433–439. This report clarified the role of lamivudine in patients with HBV and decompensated cirrhosis.\nSchiff ER, Lai CL, Hadziyannis S, et al.: Adefovir dipivoxil therapy for lamivudine-resistant hepatitis B in pre- and post-liver transplantation patients. Hepatology 2003, 38:1419–1427. This large multicenter study clearly established the role of adefovir as salvage therapy for YMDD mutants in the transplant setting.\nKruger M, Tillmann HL, Trautwein C, et al.: Famciclovir treatment of hepatitis B virus recurrence after liver transplantation: a pilot study. Liver Transpl Surg 1996, 2:253–262.\nSeehofer D, Rayes N, Bechstein WO, et al.: Therapy of recurrent hepatitis B infection after liver transplantation. A retrospective analysis of 200 liver transplantations based on hepatitis B associated liver diseases. Z Gastroenterol 2000, 38:773–783.\nRayes N, Seehofer D, Hopf U, et al.: Comparison of famciclovir and lamivudine in the long-term treatment of hepatitis B infection after liver transplantation. Transplantation 2001, 71:96–101.\nTillmann HL, Trautwein C, Bock T, et al.: Mutational pattern of hepatitis B virus on sequential therapy with famciclovir and lamivudine in patients with hepatitis B virus reinfection occurring under HBIg immunoglobulin after liver transplantation. Hepatology 1999, 30:244–256.\nPichoud C, Seigneres B, Wang Z, et al.: Transient selection of a hepatitis B virus polymerase gene mutant associated with a decreased replication capacity and famciclovir resistance. Hepatology 1999, 29:230–237.\nGish R, Lau J, Brooks L, et al.: Ganciclovir treatment of hepatitis B virus infection in liver transplant recipients. Hepatology 1996, 23:1–7.\nBochet M, Tubiana R, Benhamou Y, et al.: Tenofovir disoproxil fumarate suppresses lamivudine-resistant HBV replication in patients coinfected with HIV\u002FHBV. Paper presented at the 9th Conference on Retroviruses and Opportunistic Infections. Seattle, WA; February 22–28, 2002.\nRayes N, Seehofer D, Hopf U, et al.: Comparison of famciclovir and lamivudine in the long-term treatment of hepatitis B infection after liver transplantation. Transplantation 2001, 71:96–101.\nSeigneres B, Pichoud C, Ahmed SS, et al.: Evolution of hepatitis B virus polymerase gene sequence during famciclovir therapy for chronic hepatitis B. J Infect Dis 2000, 181:1221–1233.\nMutimer D, Pillay D, Cook P, et al.: Selection of multiresistant hepatitis B virus during sequential nucleoside-analogue therapy. J Infect Dis 2000, 181:713–716.\nSeehofer D, Rayes N, Neuhaus R, et al.: Antiviral combination therapy for lamivudine resistant hepatitis B reinfection after liver transplantation. Transpl Int 2000, 13(suppl):S359-S362.\nZoulim F: Treatment of pre- and post-liver transplantation HBV infection: should we aim at combination therapy? Hepatology 2003, 38:1353–1355.\nRoche B, Samuel D, Feray C, et al.: Retransplantation of the liver for recurrent hepatitis B virus infection: the Paul Brousse experience. Liver Transpl Surg 1999, 5:166–174.\nLo CM, Cheung ST, Ng IO, et al.: Fibrosing cholestatic hepatitis secondary to precore\u002Fcore promoter hepatitis B variant with lamivudine resistance: successful retransplantation with combination adefovir dipivoxil and hepatitis B immunoglobulin. Liver Transpl 2004, 10:557–563.\nChen CH, Chen PJ, Chu JS, et al.: Fibrosing cholestatic hepatitis in a hepatitis B surface antigen carrier after renal transplantation. Gastroenterology 1994, 107:1514–1518.\nMcIvor C, Morton J, Bryant A, et al.: Fatal reactivation of precore mutant hepatitis B virus associated with fibrosing cholestatic hepatitis after bone marrow transplantation. Ann Intern Med 1994, 121:274–275.\nFang JW, Wright TL, Lau JY: Fibrosing cholestatic hepatitis in patient with HIV and hepatitis B. Lancet 1993, 342:1175.\nChan TM, Wu PC, Li FK, et al.: Treatment of fibrosing cholestatic hepatitis with lamivudine. Gastroenterology 1998, 115:177–181.\nJamal H, Regenstein F, Farr G, et al.: Prolonged survival in fibrosing cholestatic hepatitis with long-term ganciclovir therapy. Am J Gastroenterol 1996, 91:1027–1030.",{"EN":768},"Despite the application of vaccination and the growing list of agents effective in chronic hepatitis B, this disease remains an important indication for transplantation. Early experience was marked by viral recurrence and dismal outcomes; current protocols using hepatitis B immunoglobulin and nucleoside analogues now make recurrence uncommon and outcomes excellent. 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Antiviral drug resistance testing in patients with chronic hepatitis B. Dig Dis Sci. 2011;57:221–31. This study showed approximately two thirds of patients undergoing genotypic resistance testing had antiviral drug associated resistance and subsequent management was altered in more than 50 % of cases based on the genotypic resistance profile knowledge.\nChainuvati S, Cheng J, Hou JL, et al. Patterns of managing chronic hepatitis B treatment-related rug resistance: a survey of physicians in Mainland China, South Korea, Taiwan and Thailand. Hepatol Int. 2009;3:453–60.\nLocarnini S, Bowden S. Drug resistance in antiviral therapy. Clin Liver Dis. 2010;14:439–59.\nLee Y-S, Suh DJ, Lim Y-S, et al. Increased risk of adefovir resistance in patients with lamivudine-resistant chronic hepatitis B after 48 weeks of adefovir dipivoxil monotherapy. Hepatology. 2006;43:1385–91.\nWarner N, Locarnini S. The antiviral drug selected hepatitis B virus rtA181T\u002FsW172• mutant has a dominant negative secretion defect and alters the typical profile of viral rebound. Hepatology. 2008;48:88–98.\nWarner N, Locarnini S, Kuiper M, Bartholomeusz A, Ayres A, Yuen L, et al. The L80I substitution in the reverse transcriptase domain of the hepatitis B virus polymerase is associated with lamivudine resistance and enhanced viral replication in vitro. Antimicrob Agents Chemother. 2007;51:2285–92.\nLocarnini S. Molecular virology and the development of resistant mutants: implications for therapy. Semin Liver Dis. 2005;25 Suppl 1:9–19.\nChisari F, Ferrari C. Hepatitis B virus immunopathogenesis. Annu Rev Immunol. 1995;13:29–60.\nIloeje U, Yang H, Su J, Jen C, You S, Chen C. Predicting cirrhosis risk based on the level of circulating hepatitis B viral load. Gastroenterology. 2006;130:678–86.\nShaw T, Bartholomeusz A, Locarnini S. HBV drug resistance: mechanisms, detection and intepretation. J Hepatol. 2006;44:593–606.\nDomingo E. Quasispecies and the development of new antiviral strategies. Progr Drug Res. 2003;60:133–58.\nClavel F, Hance A. HIV drug resistance. N Engl J Med. 2004;350:1023–35.\nDienstag JL, Perrillo R, Schiff E, et al. A preliminary trial of lamivudine for chronic hepatitis B infection. N Engl J Med. 1995;333:1657–61.\nDienstag JL, Schiff E, Wright T, et al. Lamivudine as initial treatment for chronic hepatitis B in the United States. N Engl J Med. 1999;341:1256–63.\nLai CL, Chien RN, Leung NW. A one-year trial of lamivudine for chronic hepatitis B. Asia Hepatitis Lamivudine Study Group. N Engl J Med. 1998;339:241–4.\nLai CL, Dienstag JL, Schiff E. Prevalence and clinical correlates of YMDD variants during lamivudine therapy for patients with chronic hepatitis B. Clin Infect Dis. 2003;36:687–96.\n•• Papatheodoris G, Lampertico P, Manolakopolous S, Lok A. Incidence of heptocellular carcinoma in chronic hepatitis B patients receiving nucleos(t)ide therapy: a systematic review. J Hepatol. 2010;53:348–56. This meta-analysis showed an increased risk of HCC in patients who failed to maintain virological remission. Furthermore, comparing antiviral naive patients to those with LMV resistance, whether or not cirrhosis was present, the rate of HCC was higher if there was LMV resistance as well.\nLiaw YF, Sung JJ, Chow WC, Farrell G, Lee CZ, Yuen H, et al. Lamivudine for patients with chronic hepatitis B and advanced liver disease. N Engl J Med. 2004;351:1521–31.\nThompson AJ, Ayres A, Yuen L, Bartholomeusz A, Bowden DS, Iser DM, et al. Lamivudine resistance in patients with chronic hepatitis B: role of clinical and virological factors. J Gastroenterol Hepatol. 2007;22:1078–85.\nDelaney WET, Locarnini S, Shaw T. Resistance of hepatitis B virus to antiviral drugs: current aspects and directions for future investigation. Antivir Chem Chemother. 2001;12:1–35.\nZoulim F, Locarnini S. Hepatitis B virus resistance to nucleos(t)ide analogues. Gastroenterology. 2009;137:1593–608.\nOgata N, Fujii K, Takigawa S. Novel patterns of amino acid mutations in the hepatitis B virus polymerase in association with resistance to lamivudine therapy in Japanese patients with chronic hepatitis B. J Med Virol. 1999;59:270–6.\nDelaney W, Yang H, Westland CE, Das K, et al. The hepatitis B virus polymerase mutation rtV173L is selected during lamivudine therapy and enhances viral replication in vitro. J Virol. 2003;77:11833–43.\nAngus PW, Locarnini SA, McCaughan GW, Jones RM, McMillan JS, Bowden DS. Hepatitis B virus precore mutant infection is associated with severe recurrent disease after liver transplantation. Hepatology. 1995;21:14–8.\nTorresi J, Earnest-Silveira L, Civitico G, Walters TE, Lewin SR, Fyfe J, et al. Restoration of replication phenotype of lamivudine-resistant hepatitis B virus mutants by compensatory changes in the \"fingers\" subdomain of the viral polymerase selected as a consequence of mutations in the overlapping S gene. Virology. 2002;299:88–99.\nKamili Samili SV, Thompson G, Campbell K, Walker CM, Locarnini S, Krawczynski K. Efficacy of hepatitis B vaccine against antiviral drug-resistant hepatitis B virus mutants in the chimpanzee model. Hepatology. 2009;49:1483–92.\nYang H, Qi X, Sabogal A, et al. Cross-resistance testing of next-generation nucleoside and nucleotide analogues against lamivudine- resistant HBV. Antivir Ther. 2005;10:625–33.\nLai C-L, Gane E, Liaw YF, et al. Telbivudine versus lamivudine in patients with chronic hepatitis B. N Engl J Med. 2007;357:2576–88.\nLiaw YF, Gane E, Leung N, et al. 2-year globe trial results: telbivudine is superior to lamivudine in patients with chronic hepatitis B. Gastroenterology. 2009;136:486–95.\nDando T, Plosker G. Adefovir dipivoxil. A review of its use in chronic HBVAdis drug evaluation. Drugs. 2003;63:2215–34.\nHadziyannis S, Tassopoulos N, Heathcote J, et al. Long-term therapy with adefovir dipivoxil for HBeAg-negative chronic hepatitis B for up to 5 years. Gastroenterology. 2006;131:1743–51.\nAngus P, Vaughan R, Xiong S, Yang H, Delaney W, Gibbs C, et al. Resistance to adefovir dipivoxil therapy associated with the selection of a novel mutation in the HBV polymerase. Gastroenterology. 2003;125:292–7.\n•• Patterson SJ, George J, Strasser SI, Lee AU, Sievert W, Nicoll AJ, et al. Tenofovir disoproxil fumarate rescue therapy following failure of both lamivudine and adefovir dipivoxil in chronic hepatitis B. Gut. 2011;60:247–54. This study showed TFV would be an appropriate antiviral agent in patients who had prior exposure to LMV and ADV with high rate of genotypic resistance, but if the patient was infected with HBV that had both rtA181T\u002FV and rtN236T, then the virological response to TFV was sub-optimal, demonstrating the value of genotypic resistance testing.\nSnow-Lampert A, Chappell B, Curtis M. No resistance to tenofovir disoproxil fumarate detected after up to 144 weeks of therapy in patients monoinfected with chronic hepatitis B virus. Hepatology. 2011;53:763–73.\nLin P-F, Nowicka-Sans B, Terry B, et al. Entecavir exhibits inhibitory activity against human immunodeficiency virus under conditions of reduced viral challenge. Antimicrob Agents Chemother. 2008;52:1759–67.\nMcMahon M, Benjamin B, et al. The HBV drug entecavir—effects on HIV-1 replication and resistance. N Engl J Med. 2007;356:2614–21.\nLevine S, Hernandez D, Yamanak G, Zhang S, Rose RE, et al. Efficacies of entecavir against lamivudine-resistant hepatitis b virus replication and recombinant polymerases in vitro. Antimicrob Agents Chemother. 2002;46:2525–32.\nWoo G, Tomlinson G, Nishikawa Y, Kowgier M, Morris S, Wong D, et al. Tenofovir and entecavir are the most effective antiviral agents for chronic hepatitis B: a systematic review and bayesian meta-analyses. Gastroenterology. 2010;139:1218–29.\nTenney D, Rose R, Baldick C, Pokornowski K, Eggers B, Fang J, et al. Long-term monitoring shows hepatitis B virus resistance to entecavir in nucleoside-naive patients is rare through 5 years of therapy. Hepatology. 2009;49:1503–14.\nTenney DJ, Levine SM, Rose RE, Walsh AW, Weinheimer SP, Discotto L, et al. Clinical emergence of entecavir-resistant hepatitis B virus requires additional substitutions in virus already resistant to lamivudine. Antimicrob Agents Chemother. 2004;48:3498–507.\nVillet S, Ollivet A, Pichoud C, Barraud L, Villeneuve J, Trepo C, et al. Stepwise process for the development of entecavir resistance in a chronic hepatitis B virus infected patient. 2007;46:531–8.\nLiu Y, Wang C, Zhong Y, Chen L, Li X, Ji D, et al. Evolution and suppression of HBV strains with multidrug resistance to lamivudine, adefovir dipivoxil and entecavir in a patient with chronic hepatitis B. Antivir Ther. 2010;15:1185–90.\nBrunelle M, Jacquard A, Pichoud C, Durantel D, Carrouee-Durantel S, Villeneuve J, et al. Susceptibility to antivirals of a human HBV strain with mutations conferring resistance to both lamivudine and adefovir. Hepatology. 2005;41:1391–8.\nChang T, Lai CNEJM. Hepatitis B virus with primary resistance to adefovir. N Engl J Med. 2006;355:322–3.\nKim H, Han K, Ahn S, Kim E, Chang H, et al. Evaluation of methods for monitoring drug resistance in chronic hepatitis B patients during lamivudine therapy based on mass spectrometry and reverse hybridization. Antivir Ther. 2005;10:441–9.\nHussain M, Fung S, Libbrecht E, Sablon E, Cursaro C, Andreone P, et al. Sensitive line probe assay that simultaneously detects mutations conveying resistance to lamivudine and adefovir. J Clin Microbiol. 2006;44:1094–7.\nJang H, Cho M, Heo J, Kim H, Jun H, Shin W, et al. Oligonucleotide chip for detection of lamivudine-resistant hepatitis B virus. J Clin Microbiol. 2004;42:4181–8.\nMarrgeridon-Thermet S, Shulman NS, Ahmed A, et al. Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)–treated patients and NRTI-naive patients. J Infect Dis. 2009;199:1275–85.\nSolmone M, Vincenti D, Prosperi M, Bruselles A, et al. Use of massively parallel ultradeep pyrosequencing to characterize the genetic diversity of hepatitis B virus in drug-resistant and drug-naive patients and to detect minor variants in reverse transcriptase and hepatitis B S antigen. 2009;83:1718–26.\nZoulim F. In- vitro models for studying hepatitis B virus drug resistance. Liver Dis. 2006;26:171–80.\nSeigneres B, Pichoud C, Martin P, Furman P, Trepo C, Zoulim F. Inhibitory activity of dioxolane purine analogs on wild-type and lamivudine-resistant mutants of hepadnaviruses. Hepatology. 2002;36:710–22.\nDurantel D, Carrouee-Durantel S, Werle-Lapostolle B, Brunelle M, Pichoud C, Trepo C, et al. A new strategy for studying in vitro the drug susceptibility of clinical isolates of human hepatitis B virus. Hepatology. 2004;40:855–64.\nLok AS, Zoulim F, Locarnini S, Mangia A, Niro G, Decraemer H, et al. Monitoring drug resistance in chronic hepatitis B virus (HBV)-infected patients during lamivudine therapy: evaluation of performance of INNO-LiPA HBV DR assay. J Clin Microbiol. 2002;40:3729–34.\nYuen LK, Ayres A, Littlejohn M, Colledge D, Edgely A, Maskill WJ, et al. SeqHepB: a sequence analysis program and relational database system for chronic hepatitis B. Antivir Res. 2007;75:64–74.\nLok AS, Zoulim F, Locarnini S, Bartholomeusz A, Ghany MG, Pawlotsky JM, et al. Antiviral drug-resistant HBV: standardization of nomenclature and assays and recommendations for management. Hepatology. 2007;46:254–65.\nLocarnini S, Hatzakis A, Heathcote J, Keeffe EB, Liang TJ, Mutimer D, et al. Management of antiviral resistance in patients with chronic hepatitis B. Antivir Ther. 2004;9:679–93.\nCarrouee-Durantel S, Durantel D, Werle-Lapostolle B, Pichoud C, Naesens L, Neyts J, et al. Suboptimal response to adefovir dipivoxil therapy for chronic hepatitis B in nucleoside-naive patients is not due to pre-existing drug-resistant mutants. Antivir Ther. 2008;13:381–8.\nThibault V, Aubron-Olivier C, Agut H, Katlama C. Primary infection with a lamivudine-resistant hepatitis B virus. AIDS. 2002;16:131–3.\nBesisik F, Karaca C, Akyuz F, et al. Occult HBV infection and YMDD variants in hemodialysis patients with chronic HCV infection. Hepatology. 2003;38:506.\nHayashi K, Katano Y, Ishigami M, Itoh A, Hirooka Y, Nakano I, et al. Prevalence and clinical characterization of patients with acute hepatitis B induced by lamivudine-resistant strains. J Gastroenterol Hepatol. 2010;25:745–9.\nAlvarado-Esquivel C, Carrera-Gracia MA, Conde-González CJ, et al. Genotypic resistance to lamivudine among hepatitis B virus isolates in Mexico. J Antimicrob Chemother. 2006;57:221–3.\nPol S, Sogni P. Treatment of chronic hepatitis B: adherence and safety. Gastroenterol Clin Biol. 2010;34(Supple 2):S142–8.\nChotiyaputta W, Peterson C, Ditah F, Goodwin D, Lok A. Persistence and adherence to nucleos(t)ide analogue treatment for chronic hepatitis B. J Hepatol. 2010;54:12–8.\nLok A, McMahon B. Chronic hepatitis B: update 2009. AASLD Practice Guidelines. Hepatology. 2009:1–36.\nFung S, Chae HB, Fontana R. Virologic response and resistance to adefovir in patients with chronic hepatitis B. J Hepatol. 2006;43:283–90.\nFlorian B, Mahnaz A, Francesco N. The new EASL guidelines for the management of chronic hepatitis B infection adapted for Swiss physicians. Swiss Med Wkly. 2010;140:154–9.\nHui CK, Zhang HY, Bowden S, Locarnini S, Luk JM, Leung KW, et al. 96 weeks combination of adefovir dipivoxil plus emtricitabine vs. adefovir dipivoxil monotherapy in the treatment of chronic hepatitis B. J Hepatol. 2008;48:714–20.",{"EN":1254},"Hepatitis B virus (HBV) DNA replication is an error prone mechanism and coupled with selection pressure from antiviral agents, emergence of resistance can be frequent. Antiviral drug resistance has been associated with treatment failure, and the widespread use of readily available antiviral agents with limited potency and low genetic barrier, the risk of emergence of multidrug resistant HBV makes the management of chronic hepatitis B (CHB) challenging. Studies have shown that timely recognition of resistance and the introduction of appropriate antiviral therapy is associated with better clinical outcome. Genotypic resistance profiling is able to identify the cause of treatment failure and provide essential information on management options. It also enables clinicians to determine cross resistance and so implement therapy with the most favorable outcome. Currently genotypic resistance testing is not widely available and is costly. However, long-term benefits of resistance testing both in terms of clinical outcome and cost-effectiveness, are well recognized in other fields of medicine, and should be more readily available for patients with chronic hepatitis B",{"EN":1256},"Role of Resistance Testing During Oral Antiviral Therapy of Chronic Hepatitis B",{"VOID":1258},"10.1007\u002Fs11901-012-0132-8","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11901-012-0132-8",[1261,1277],{"id":1262,"sortIndex":65,"researcher":20,"roles":1263,"affiliations":1264,"properties":1274},"d765ee24-1f2a-4578-8258-d4ac3a96df16",[107],[1265],{"id":20,"sortIndex":21,"affiliation":1266,"properties":20},{"id":1267,"createTime":1268,"updateTime":1268,"relativeEntities":1269,"slug":1270,"properties":1271,"entityType":126,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"d50da2a8-7297-410e-8f63-c70f5a6253bc","2024-04-15T05:51:22.650+00:00",[],"Victorian-Infectious-Diseases-Reference-Laboratory-North-Melbourne-Australia",{"title":1272},{"EN":1273},"Victorian Infectious Diseases Reference Laboratory, North Melbourne, Australia",{"title":1275},{"VI":1276},"Stephen Locarnini",{"id":1278,"sortIndex":21,"researcher":20,"roles":1279,"affiliations":1280,"properties":1296},"7385867a-80ed-447e-836e-a0eb021fe51a",[107],[1281,1286],{"id":20,"sortIndex":21,"affiliation":1282,"properties":20},{"id":1267,"createTime":1268,"updateTime":1268,"relativeEntities":1283,"slug":1270,"properties":1284,"entityType":126,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},[],{"title":1285},{"EN":1273},{"id":1287,"sortIndex":65,"affiliation":1288,"properties":1295},"06648742-3767-4ccd-ad6a-7c6c354c4ca2",{"id":1289,"createTime":1290,"updateTime":1290,"relativeEntities":1291,"slug":20,"properties":1292,"entityType":126,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"5bd44583-c8b0-46c2-969c-3e7b0175968f","2024-01-18T14:45:27.190+00:00",[],{"title":1293},{"VI":1294},"Infectious Diseases Unit, Eastern Health, Ringwood East, Australia",{},{"title":1297},{"VI":1298},"Uma Devi",{"url":1259,"publisher":1300,"properties":1320},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1301,"slug":10,"properties":1302,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":1306,"manageAffiliations":1307,"indexDatabases":1308,"url":42,"thumbnailPath":20,"statistic":1315,"gsStatistic":20,"type":80,"analyzePriority":20},[],{"issn":1303,"eissn":1304,"title":1305},{"VOID":13},{"VOID":15},{"EN":17},[],[],[1309],{"id":26,"indexDatabase":1310,"url":39,"indexYears":40,"academicFieldIds":20,"indexDatabaseRanking":41},{"id":28,"createTime":29,"updateTime":30,"relativeEntities":1311,"label":1312,"description":1313,"key":36,"publicationTags":1314,"standard":20},[],{"EN":33,"VI":33},{"EN":33,"VI":35},[38],{"impactFactor":21,"impactFactorByYear":1316,"i10Index":48,"i10IndexLast5Year":21,"totalPublication":49,"totalPublicationByYear":1317,"totalCitation":60,"totalCitationByYear":1318,"totalCitationPerPublication":68,"totalCitationPerPublicationByYear":1319,"hindexLast5Year":55,"hindex":55},{"2012":45,"2013":46,"2014":47},{"2002":51,"2003":52,"2004":53,"2005":54,"2006":54,"2007":55,"2008":54,"2009":56,"2010":57,"2011":58,"2012":57,"2013":59},{"2003":62,"2004":62,"2005":48,"2006":63,"2007":64,"2008":54,"2009":65,"2010":66,"2011":62,"2012":67,"2013":65},{"2003":70,"2004":71,"2005":72,"2006":73,"2007":74,"2008":65,"2009":75,"2010":76,"2011":77,"2012":78,"2013":79},{"volume":1321,"pages":1322},{"VOID":924},{"VOID":1323},"55-64","2012-04-26",{"id":1326,"createTime":1327,"updateTime":1328,"relativeEntities":1329,"slug":1330,"properties":1331,"entityType":100,"verifyStatus":19,"verifyTime":1328,"verifyNote":101,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1340,"fullTextUrl":20,"authors":1341,"publicationType":137,"publisherRelationship":1364,"citationCount":20,"citationInfo":20,"publishDate":1390,"publishYear":1391,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":20,"openAccess":20,"references":20,"isForceReanalyzing":166},"ae597d5f-4b2d-4ef1-9ad8-7471f613b4a6","2024-01-25T11:34:26.815+00:00","2025-01-13T22:35:48.049+00:00",[],"Treatment-of-chronic-hepatitis-B-virus-infection-in-children",{"references":1332,"abstract":1334,"title":1336,"doi":1338},{"VOID":1333},"Lavanchy D: Hepatitis B virus epidemiology, disease burden, treatment, and current and emerging prevention and control measures. 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J Clin Gastroenterol 2005, 39:68–70.\nSarin SK, Sood A, Kumar M, et al.: Effect of lowering HBV DNA levels by initial antiviral therapy before adding immunomodulator on treatment of chronic hepatitis B. Am J Gastroenterol 2007, 102:96–104.\nD’Antiga L, Aw M, Atkins M, et al.: Combined lamivudine\u002Finterferon-alpha treatment in “immunotolerant” children perinatally infected with hepatitis B: a pilot study. J Pediatr 2006, 148:228–233.",{"EN":1335},"Hepatitis B virus (HBV) remains an important global pathogen. In countries of high endemicity, virus is typically acquired either vertically or during the preschool years, contributing to a large burden of pediatric infection. Seroconversion and progression to the inactive carrier phase of infection is associated with improved outcome and decreased rates of cirrhosis and hepatocellular carcinoma. Success in treating chronic HBV disease in children, as defined by hepatitis B e antigen (HBeAg) seroconversion, approaches only 25% to 30% with interferon-α, the most efficacious agent. Lamivudine and other nucleoside analogues achieve HBeAg seroconversion at slightly lower rates and are better tolerated. However, this class of medications is limited by the frequency of development of mutations in the YMDD locus of the reverse transcriptase gene. Interest is growing in treatment of children in the immune-tolerant stage of infection, thereby holding promise for the largest number of children with HBV infection.",{"EN":1337},"Treatment of chronic hepatitis B virus infection in children",{"VOID":1339},"10.1007\u002Fs11901-009-0014-x","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11901-009-0014-x",[1342,1349],{"id":1343,"sortIndex":21,"researcher":20,"roles":1344,"affiliations":1345,"properties":1346},"7c92908e-f924-48cd-967f-adbcc3d3fed8",[107],[],{"title":1347},{"VI":1348},"David E. Brumbaugh",{"id":1350,"sortIndex":65,"researcher":20,"roles":1351,"affiliations":1352,"properties":1361},"1dc72ebb-ca85-4d90-b1c7-cfe2add81f19",[107],[1353],{"id":20,"sortIndex":21,"affiliation":1354,"properties":20},{"id":1355,"createTime":1356,"updateTime":1356,"relativeEntities":1357,"slug":20,"properties":1358,"entityType":126,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"7fee14d6-75b7-4b93-9694-ac4656e24f15","2024-01-25T11:34:26.833+00:00",[],{"title":1359},{"VI":1360},"Section of Pediatric Gastroenterology, Hepatology, and Nutrition, The Children’s Hospital and the University of Colorado Denver, Aurora, USA",{"title":1362},{"VI":1363},"Ronald J. Sokol",{"url":1340,"publisher":1365,"properties":1385},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1366,"slug":10,"properties":1367,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":1371,"manageAffiliations":1372,"indexDatabases":1373,"url":42,"thumbnailPath":20,"statistic":1380,"gsStatistic":20,"type":80,"analyzePriority":20},[],{"issn":1368,"eissn":1369,"title":1370},{"VOID":13},{"VOID":15},{"EN":17},[],[],[1374],{"id":26,"indexDatabase":1375,"url":39,"indexYears":40,"academicFieldIds":20,"indexDatabaseRanking":41},{"id":28,"createTime":29,"updateTime":30,"relativeEntities":1376,"label":1377,"description":1378,"key":36,"publicationTags":1379,"standard":20},[],{"EN":33,"VI":33},{"EN":33,"VI":35},[38],{"impactFactor":21,"impactFactorByYear":1381,"i10Index":48,"i10IndexLast5Year":21,"totalPublication":49,"totalPublicationByYear":1382,"totalCitation":60,"totalCitationByYear":1383,"totalCitationPerPublication":68,"totalCitationPerPublicationByYear":1384,"hindexLast5Year":55,"hindex":55},{"2012":45,"2013":46,"2014":47},{"2002":51,"2003":52,"2004":53,"2005":54,"2006":54,"2007":55,"2008":54,"2009":56,"2010":57,"2011":58,"2012":57,"2013":59},{"2003":62,"2004":62,"2005":48,"2006":63,"2007":64,"2008":54,"2009":65,"2010":66,"2011":62,"2012":67,"2013":65},{"2003":70,"2004":71,"2005":72,"2006":73,"2007":74,"2008":65,"2009":75,"2010":76,"2011":77,"2012":78,"2013":79},{"volume":1386,"pages":1388},{"VOID":1387},"8",{"VOID":1389},"96-102","2009-07-24",2009]