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Detection and isolation of type C retrovirus particles from fresh and cultured lymphocytes of a patient with cutaneous T-cell lymphoma. Proc Natl Acad Sci U S A. 1980;77:7415–9.",{"doi":477},"10.1073\u002Fpnas.77.12.7415",{"id":18,"text":479,"url":18,"identifiers":480},"Yoshida M, Seiki M, Yamaguchi K, Takatsuki K. Monoclonal integration of human T-cell leukemia provirus in all primary tumors of adult T-cell leukemia suggests causative role of human T-cell leukemia virus in the disease. Proc Natl Acad Sci U S A. 1984;81:2534–7.",{"doi":481},"10.1073\u002Fpnas.81.8.2534",{"id":18,"text":483,"url":18,"identifiers":484},"Hinuma Y, Nagata K, Hanaoka M, Nakai M, Matsumoto T, Kinoshita KI, Shirakawa S, Miyoshi I. Adult T-cell leukemia: antigen in an ATL cell line and detection of antibodies to the antigen in human sera. 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Nat Genet. 2015;47:1304–15.",{"doi":684},"10.1038\u002Fng.3415",false,{"id":687,"createTime":688,"updateTime":689,"relativeEntities":690,"slug":691,"properties":692,"entityType":187,"verifyStatus":188,"verifyTime":701,"verifyNote":190,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":702,"fullTextUrl":18,"authors":703,"publicationType":414,"publisherRelationship":720,"citationCount":771,"citationInfo":772,"publishDate":788,"publishYear":773,"citationAnalyzeStatus":470,"lastCitationAnalyze":689,"indexDatabases":789,"openAccess":18,"references":790,"isForceReanalyzing":685},"05ff040e-e8a8-4516-803c-801e430315d4","2024-01-19T05:50:22.608+00:00","2026-08-17T06:21:11.384+00:00",[],"Revisiting-HIV-1-uncoating",{"abstract":693,"title":695,"gsPaper":697,"doi":699},{"EN":694},"HIV uncoating is defined as the loss of viral capsid that occurs within the cytoplasm of infected cells before entry of the viral genome into the nucleus. It is an obligatory step of HIV-1 early infection and accompanies the transition between reverse transcription complexes (RTCs), in which reverse transcription occurs, and pre-integration complexes (PICs), which are competent to integrate into the host genome. The study of the nature and timing of HIV-1 uncoating has been paved with difficulties, particularly as a result of the vulnerability of the capsid assembly to experimental manipulation. Nevertheless, recent studies of capsid structure, retroviral restriction and mechanisms of nuclear import, as well as the recent expansion of technical advances in genome-wide studies and cell imagery approaches, have substantially changed our understanding of HIV uncoating. Although early work suggested that uncoating occurs immediately following viral entry in the cell, thus attributing a trivial role for the capsid in infected cells, recent data suggest that uncoating occurs several hours later and that capsid has an all-important role in the cell that it infects: for transport towards the nucleus, reverse transcription and nuclear import. Knowing that uncoating occurs at a later stage suggests that the viral capsid interacts extensively with the cytoskeleton and other cytoplasmic components during its transport to the nucleus, which leads to a considerable reassessment of our efforts to identify potential therapeutic targets for HIV therapy. This review discusses our current understanding of HIV uncoating, the functional interplay between infectivity and timely uncoating, as well as exposing the appropriate methods to study uncoating and addressing the many questions that remain unanswered.",{"EN":696},"Revisiting HIV-1 uncoating",{"VOID":698},"[\"5069793568379385798\"]",{"VOID":700},"10.1186\u002F1742-4690-7-96","2024-05-01T13:36:52.118+00:00","https:\u002F\u002Fretrovirology.biomedcentral.com\u002Farticles\u002F10.1186\u002F1742-4690-7-96",[704],{"id":705,"sortIndex":19,"researcher":18,"roles":706,"affiliations":708,"properties":717,"displayName":719,"givenName":18,"familyName":18},"b10b65b0-3a5e-4988-8df8-037cae551c70",[707],"AUTHOR",[709],{"id":710,"sortIndex":19,"affiliation":711,"properties":18},"05c9789c-2520-48f7-80da-358eb95803c0",{"id":710,"createTime":18,"updateTime":18,"relativeEntities":712,"slug":18,"properties":713,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":716,"statistic":18},[],{"title":714},{"VI":715},"Department of Virology, URA3015, Institut Pasteur, Paris, France",[],{"title":718},{"VI":719},"Nathalie 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Virology. 2005, 337: 93-101. 10.1016\u002Fj.virol.2005.02.028.","https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.virol.2005.02.028",{"mag":1425,"openalex":1426,"pm":1427,"doi":1428},"2082465545","W2082465545","15882886","10.1016\u002Fj.virol.2005.02.028",{"id":1430,"createTime":1431,"updateTime":1432,"relativeEntities":1433,"slug":1434,"properties":1435,"entityType":187,"verifyStatus":188,"verifyTime":1446,"verifyNote":190,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1447,"fullTextUrl":18,"authors":1448,"publicationType":414,"publisherRelationship":1574,"citationCount":779,"citationInfo":1625,"publishDate":1628,"publishYear":1626,"citationAnalyzeStatus":1629,"lastCitationAnalyze":1630,"indexDatabases":1631,"openAccess":18,"references":18,"isForceReanalyzing":685},"6a84d15a-136e-4d85-80f9-5865af45fdda","2024-01-10T23:09:16.744+00:00","2026-07-26T10:04:28.419+00:00",[],"Characterization-of-HIV-1-envelopes-in-acutely-and-chronically-infected-injection-drug-users",{"abstract":1436,"title":1438,"gsPaper":1440,"references":1442,"doi":1444},{"EN":1437},"Mucosally acquired human immunodeficiency virus type 1 (HIV-1) infection results from a limited number of variants, and these infecting strains potentially have unique properties, such as increased susceptibility to entry blockers, relative interferon-alpha (IFN-α) resistance, and replication differences in some primary cells. There is no data about the phenotypic properties of HIV-1 envelope variants found early after acquisition among subjects infected through injection drug use (IDU). For the first time, we compared the characteristics of virus envelopes among injection drug users sampled prior to seroconversion (HIV RNA+\u002FAb-), within 1 year (early), and more than 2 years (chronic) after estimated acquisition. Virus envelopes from 7 HIV RNA+\u002FAb- subjects possessed lower genetic diversity and divergence compared to 7 unrelated individuals sampled during the chronic phase of disease. Replication competent recombinant viruses incorporating the HIV RNA+\u002FAb- as compared to the chronic phase envelopes were significantly more sensitive to a CCR5 receptor inhibitor and IFN-α and showed a statistical trend toward greater sensitivity to a fusion blocker. The early as compared to chronic infection envelopes also demonstrated a statistical trend or significantly greater sensitivity to CCR5 and fusion inhibitor and IFN- α. The HIV RNA+\u002FAb- as compared to chronic envelope viruses replicated to a lower extent in mature monocyte derived dendritic cells – CD4+ T cell co-cultures, but there were no significant replication differences in other primary cells among the viruses with envelopes from the 3 different stages of infection. Similar to mucosal acquisition, HIV-1 envelope quasispecies present in injection drug users prior to seroconversion have unique phenotypic properties compared to those circulating during the chronic phase of disease.",{"EN":1439},"Characterization of HIV-1 envelopes in acutely and chronically infected injection drug users",{"VOID":1441},"[\"8368414199044931667\"]",{"VOID":1443},"Sagar M, Kirkegaard E, Long EM, Celum C, Buchbinder S, Daar ES, Overbaugh J: Human immunodeficiency virus type 1 (HIV-1) diversity at time of infection is not restricted to certain risk groups or specific HIV-1 subtypes. J Virol. 2004, 78: 7279-7283. 10.1128\u002FJVI.78.13.7279-7283.2004.\nBar KJ, Li H, Chamberland A, Tremblay C, Routy JP, Grayson T, Sun C, Wang S, Learn GH, Morgan CJ, Schumacher JE, Haynes BF, Keele BF, Hahn BH, Shaw GM: Wide variation in the multiplicity of HIV-1 infection among injection drug users. 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HIV-infected people, resting CD4+ T cells are the main reservoir of latent virus and the reason for the failure of drug therapy to cure HIV infection. Still, we do not have a complete understanding of the factors regulating HIV replication in these cells. A recent paper in Cell describes a new trick that the virus uses to infect resting T cells. Interaction between the viral gp120 and cellular HIV co-receptor, CXCR4, during viral entry initiates signaling that activates cofilin, the main regulator of actin polymerization. As a result of this activation, actin is depolymerized, thus destroying the natural barrier to HIV replication. I discuss implications of this study for our understanding of HIV biology and development of novel anti-HIV therapeutic approaches.",{"EN":1803},"How to engage Cofilin",{"VOID":1805},"[\"14456264738610610986\"]",{"VOID":1807},"Berger EA, Murphy PM, Farber JM: Chemokine receptors as HIV-1 coreceptors: roles in viral entry, tropism, and disease. Annu Rev Immunol. 1999, 17: 657-700. 10.1146\u002Fannurev.immunol.17.1.657.\nPopik W, Hesselgesser JE, Pitha PM: Binding of human immunodeficiency virus type 1 to CD4 and CXCR4 receptors differentially regulates expression of inflammatory genes and activates the MEK\u002FERK signaling pathway. J Virol. 1998, 72: 6406-6413.\nDavis CB, Dikic I, Unutmaz D, Hill CM, Arthos J, Siani MA, Thompson DA, Schlessinger J, Littman DR: Signal transduction due to HIV-1 envelope interactions with chemokine receptors CXCR4 or CCR5. J Exp Med. 1997, 86: 1793-1798. 10.1084\u002Fjem.186.10.1793.\nWeissman D, Rabin RL, Arthos J, Rubbert A, Dybul M, Swofford R, Venkatesan S, Farber JM, Fauci AS: Macrophage-tropic HIV and SIV envelope proteins induce a signal through the CCR5 chemokine receptor. Nature. 1997, 389: 981-985. 10.1038\u002F40173.\nGosling J, Monteclaro FS, Atchison RE, Arai H, Tsou CL, Goldsmith MA, Charo IF: Molecular uncoupling of C-C chemokine receptor 5-induced chemotaxis and signal transduction from HIV-1 coreceptor activity. Proc Natl Acad Sci USA. 1997, 94: 5061-5066. 10.1073\u002Fpnas.94.10.5061.\nFarzan M, Choe H, Martin KA, Sun Y, Sidelko M, Mackay CR, Gerard NP, Sodroski J, Gerard C: HIV-1 entry and macrophage inflammatory protein-1beta-mediated signaling are independent functions of the chemokine receptor CCR5. J Biol Chem. 1997, 272: 6854-6857. 10.1074\u002Fjbc.272.11.6854.\nLu Z, Berson JF, Chen Y, Turner JD, Zhang T, Sharron M, Jenks MH, Wang Z, Kim J, Rucker J, Hoxie JA, Peiper SC, Doms RW: Evolution of HIV-1 coreceptor usage through interactions with distinct CCR5 and CXCR4 domains. Proc Natl Acad Sci USA. 1997, 94: 6426-6431. 10.1073\u002Fpnas.94.12.6426.\nIyengar S, Hildreth JE, Schwartz DH: Actin-dependent receptor colocalization required for human immunodeficiency virus entry into host cells. J Virol. 1998, 72: 5251-5255.\nKinter A, Catanzaro A, Monaco J, Ruiz M, Justement J, Moir S, Arthos J, Oliva A, Ehler L, Mizell S, Jackson R, Ostrowski M, Hoxie J, Offord R, Fauci AS: CC-chemokines enhance the replication of T-tropic strains of HIV-1 in CD4(+) T cells: role of signal transduction. Proc Natl Acad Sci USA. 1998, 95: 11880-11885. 10.1073\u002Fpnas.95.20.11880.\nAlfano M, Schmidtmayerova H, Amella CA, Pushkarsky T, Bukrinsky M: The B-Oligomer of Pertussis Toxin Deactivates CC Chemokine Receptor 5 and Blocks Entry of M-tropic HIV-1 Strains. J Exp Med. 1999, 190: 597-606. 10.1084\u002Fjem.190.5.597.\nYoder A, Yu D, Dong L, Iyer SR, Xu X, Kelly J, Liu J, Wang W, Vorster PJ, Agulto L, Stephany DA, Cooper JN, Marsh JW, Wu Y: HIV Envelope-CXCR4 Signaling Activates Cofilin to Overcome Cortical Actin Restriction in Resting CD4 T Cells. Cell. 2008, 134: 782-792. 10.1016\u002Fj.cell.2008.06.036.\nFinzi D, Blankson J, Siliciano JD, Margolick JB, Chadwick K, Pierson T, Smith K, Lisziewicz J, Lori F, Flexner C, Quinn TC, Chaisson RE, Rosenberg E, Walker B, Gange S, Gallant J, Siliciano RF: Latent infection of CD4+ T cells provides a mechanism for lifelong persistence of HIV-1, even in patients on effective combination therapy. Nat Med. 1999, 5: 512-517. 10.1038\u002F8394.\nZack JA, Arrigo SJ, Weitsman SR, Go AS, Haislip A, Chen IS: HIV-1 entry into quiescent primary lymphocytes: molecular analysis reveals a labile, latent viral structure. Cell. 1990, 61: 213-222. 10.1016\u002F0092-8674(90)90802-L.\nBukrinsky MI, Stanwick TL, Dempsey MP, Stevenson M: Quiescent T lymphocytes as an inducible virus reservoir in HIV-1 infection. Science. 1991, 254: 423-427. 10.1126\u002Fscience.1925601.\nFassati A: HIV infection of non-dividing cells: a divisive problem. Retrovirology. 2006, 3: 74-10.1186\u002F1742-4690-3-74.\nWu Y, Marsh JW: Selective transcription and modulation of resting T cell activity by preintegrated HIV DNA. Science. 2001, 293: 1503-1506. 10.1126\u002Fscience.1061548.\nBukrinsky MI, Sharova N, Dempsey MP, Stanwick TL, Bukrinskaya AG, Haggerty S, Stevenson M: Active nuclear import of human immunodeficiency virus type 1 preintegration complexes. Proc Natl Acad Sci USA. 1992, 89: 6580-6584. 10.1073\u002Fpnas.89.14.6580.\nHoward TH, Meyer WH: Chemotactic peptide modulation of actin assembly and locomotion in neutrophils. J Cell Biol. 1984, 98: 1265-1271. 10.1083\u002Fjcb.98.4.1265.\nSotsios Y, Whittaker GC, Westwick J, Ward SG: The CXC Chemokine Stromal Cell-Derived Factor Activates a Gi-Coupled Phosphoinositide 3-Kinase in T Lymphocytes. J Immunol. 1999, 163: 5954-5963.\nBalabanian K, Harriague J, Decrion C, Lagane B, Shorte S, Baleux F, Virelizier JL, Renzana-Seisdedos F, Chakrabarti LA: CXCR4-tropic HIV-1 envelope glycoprotein functions as a viral chemokine in unstimulated primary CD4+ T lymphocytes. J Immunol. 2004, 173: 7150-7160.\nBukrinskaya A, Brichacek B, Mann A, Stevenson M: Establishment of a functional human immunodeficiency virus type 1 (HIV-1) reverse transcription complex involves the cytoskeleton. J Exp Med. 1998, 188: 2113-2125. 10.1084\u002Fjem.188.11.2113.\nCampbell EM, Nunez R, Hope TJ: Disruption of the actin cytoskeleton can complement the ability of Nef to enhance human immunodeficiency virus type 1 infectivity. J Virol. 2004, 78: 5745-5755. 10.1128\u002FJVI.78.11.5745-5755.2004.\nLu TC, He JC, Wang ZH, Feng X, Fukumi-Tominaga T, Chen N, Xu J, Iyengar R, Klotman PE: HIV-1 Nef disrupts the podocyte actin cytoskeleton by interacting with diaphanous interacting protein. J Biol Chem. 2008, 283: 8173-8182. 10.1074\u002Fjbc.M708920200.\nMcDonald D, Vodicka MA, Lucero G, Svitkina TM, Borisy GG, Emerman M, Hope TJ: Visualization of the intracellular behavior of HIV in living cells. J Cell Biol. 2002, 159: 441-452. 10.1083\u002Fjcb.200203150.\nBamburg JR, Wiggan OP: ADF\u002Fcofilin and actin dynamics in disease. Trends Cell Biol. 2002, 12: 598-605. 10.1016\u002FS0962-8924(02)02404-2.\nLappalainen P, Drubin DG: Cofilin promotes rapid actin filament turnover in vivo. Nature. 1997, 388: 78-82. 10.1038\u002F40418.\nArber S, Barbayannis FA, Hanser H, Schneider C, Stanyon CA, Bernard O, Caroni P: Regulation of actin dynamics through phosphorylation of cofilin by LIM-kinase. Nature. 1998, 393: 805-809. 10.1038\u002F31729.\nAmbach A, Saunus J, Konstandin M, Wesselborg S, Meuer SC, Samstag Y: The serine phosphatases PP1 and PP2A associate with and activate the actin-binding protein cofilin in human T lymphocytes. Eur J Immunol. 2000, 30: 3422-3431. 10.1002\u002F1521-4141(2000012)30:12\u003C3422::AID-IMMU3422>3.0.CO;2-J.\nIordanskiy S, Berro R, Altieri M, Kashanchi F, Bukrinsky M: Intracytoplasmic maturation of the human immunodeficiency virus type 1 reverse transcription complexes determines their capacity to integrate into chromatin. Retrovirology. 2006, 3: 4-10.1186\u002F1742-4690-3-4.\nMcKinstry KK, Strutt TM, Swain SL: The effector to memory transition of CD4 T cells. 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J Immunol Methods. 1990, 135: 59-69.",{"doi":861},{"id":857,"text":2578,"url":859,"identifiers":2579},"Naif HM, Li S, Alali M, Sloane A, Wu L, Kelly M, Lynch G, Lloyd A, Cunningham AL: CCR5 expression correlates with susceptibility of maturing monocytes to human immunodeficiency virus type 1 infection. J Virol. 1998, 72: 830-836.",{"doi":861},{"id":857,"text":2581,"url":859,"identifiers":2582},"Arfi V, Riviere L, Jarrosson-Wuilleme L, Goujon C, Rigal D, Darlix JL, Cimarelli A: Characterization of the early steps of infection of primary blood monocytes by human immunodeficiency virus type 1. J Virol. 2008, 82: 6557-6565.",{"doi":861},{"id":857,"text":2584,"url":859,"identifiers":2585},"Triques K, Stevenson M: Characterization of restrictions to human immunodeficiency virus type 1 infection of monocytes. 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