Reviews in Medical Virology

Vắc xin rotavirus an toàn và hiệu quả đang là nhu cầu cấp bách, đặc biệt là ở các nước đang phát triển. Cơ sở kiến thức quan trọng đối với phát triển và triển khai vắc xin là về dịch tễ học của các kiểu huyết thanh/kiểu gen G và P của rotavirus trên toàn thế giới. Phân bố theo thời gian và địa lý của các kiểu G và P rotavirus ở người được xem xét thông qua phân tích tổng cộng 45571 chủng được thu thập toàn cầu từ 124 nghiên cứu báo cáo từ 52 quốc gia trên năm châu lục, công bố trong giai đoạn 1989 đến 2004. Bốn kiểu G phổ biến (G1, G2, G3 và G4) kết hợp với P[8] hoặc P[4] chiếm hơn 88% tổng số chủng phân tích trên toàn thế giới. Ngoài ra, các virus kiểu huyết thanh G9 kết hợp với P[8] hoặc P[6] đã nổi lên là kiểu G quan trọng thứ tư trên toàn cầu với tần suất tương đối 4,1%. Khi phân phối toàn cầu các kiểu G và/hoặc P được chia thành năm lục địa/phân lục địa, nhiều đặc điểm đặc trưng đã nổi lên. Ví dụ, P[8]G1 chiếm hơn 70% các trường hợp nhiễm rotavirus ở Bắc Mỹ, Châu Âu và Úc, nhưng chỉ khoảng 30% các trường hợp nhiễm ở Nam Mỹ và Châu Á, cùng với 23% ở Châu Phi. Ngoài ra, ở Châu Phi (i) tần suất tương đối của G8 cao ngang với G3 hoặc G4 thường gặp trên toàn cầu, (ii) P[6] chiếm gần một phần ba tổng số các kiểu P xác định được và (iii) 27% các trường hợp nhiễm bệnh liên quan đến các chủng rotavirus mang các kết hợp không bình thường như P[6]G8 hoặc P[4]G8. Hơn nữa, ở Nam Mỹ, virus G5 ít phổ biến dường như tăng mức độ quan trọng dịch tễ học trong số các trẻ em bị tiêu chảy. Những phát hiện như vậy đã (i) khẳng định tầm quan trọng của việc giám sát liên tục các chủng rotavirus một cách chủ động trong nhiều bối cảnh địa lý khác nhau và (ii) cung cấp các cân nhắc quan trọng cho phát triển và triển khai một vắc xin rotavirus hiệu quả (ví dụ, điều chỉnh kiểu P-G theo địa lý trong việc bào chế vắc xin đa giá thế hệ tiếp theo). Bản quyền © 2004 John Wiley & Sons, Ltd.

Simian varicella virus (SVV) causes a natural varicella‐like disease in nonhuman primates. Epizootics of simian varicella occur sporadically in facilities housing Old World monkeys. SVV is antigenically and genetically related to varicella‐zoster virus (VZV), the etiologic agent of varicella (chickenpox) and herpes zoster (shingles) in humans. The SVV and VZV genomes are similar in size and structure, share 70%–75% DNA homology and are co‐linear with respect to gene organisation. Simian varicella is a highly contagious disease characterised by fever and vesicular skin rash and may progress to pneumonia and hepatitis. Infected monkeys may resolve the disease within 2 weeks although epizootics are sometimes associated with high morbidity and mortality. SVV, like VZV, establishes life‐long latent infection, as indicated by detection of viral DNA within neural ganglia. Subsequently, SVV may reactivate to cause secondary disease and spread of the virus to susceptible monkeys. The relatedness of VZV and SVV and the similarities in the clinical symptoms and pathogenesis of human and simian varicella make SVV infection of nonhuman primates an excellent animal model to investigate VZV pathogenesis and latency, and to evaluate potential antiviral strategies. Copyright © 2004 John Wiley & Sons, Ltd.

Routine and mass administration of oral polio vaccine (OPV) since 1961 has prevented many millions of cases of paralytic poliomyelitis. The public health value of this inexpensive and easily administered product has been extraordinary. Progress of the Global Polio Eradication Initiative has further defined the value of OPV as well as its risk through vaccine‐associated paralytic poliomyelitis (VAPP) and vaccine‐derived polioviruses (VDPV). Although both are rare, once wild poliovirus transmission has been interrupted by OPV, the only poliomyelitis due to poliovirus will be caused by OPV. Poliovirus will be eradicated only when OPV use is discontinued. This paradox provides a major incentive for eventually stopping polio immunization or replacing OPV, but it also introduces complexity into the process of identifying safe and scientifically sound strategies for doing so. The core post eradication immunization issues include the risk/benefits of continued OPV use, the extent of OPV replacement with IPV, possible strategies for discontinuing OPV, and the potential for development and licensure of a safe and effective replacement for OPV. Formulation of an informed post eradication immunization policy requires careful evaluation of polio epidemiology, surveillance capability, vaccine availability, laboratory containment, and the risks posed by the very tool responsible for successful interruption of wild poliovirus transmission. Copyright © 2003 John Wiley & Sons, Ltd.

Influenza viruses attach to susceptible cells via multivalent interactions of their haemagglutinins with sialyloligosaccharide moieties of cellular glycoconjugates. Soluble macromolecules containing sialic acid from animal sera and mucosal fluids can act as decoy receptors and competitively inhibit virus‐mediated haemagglutination and infection. Although a role for these natural inhibitors in the innate anti‐influenza immunity is still not clear, studies are in progress on the design of synthetic sialic acid‐containing inhibitors of receptor binding which could be used as anti‐influenza drugs. Copyright © 2003 John Wiley & Sons, Ltd.

Cytomegalovirus (CMV) infection does not usually produce symptoms when it causes primary infection, reinfection, or reactivation because these three types of infection are all controlled by the normal immune system. However, CMV becomes an important pathogen in individuals whose immune system is immature or compromised, such as the unborn child. Several vaccines against CMV are currently in clinical trials that aim to induce immunity in seronegative individuals and/or to boost the immunity of those with prior natural infection (seropositives). To facilitate estimation of the burden of disease and the need for vaccines that induce de novo immune responses or that boost pre‐existing immunity to CMV, we conducted a systematic survey of the published literature to describe the global seroprevalence of CMV IgG antibodies. We estimated a global CMV seroprevalence of 83% (95%UI: 78‐88) in the general population, 86% (95%UI: 83‐89) in women of childbearing age, and 86% (95%UI: 82‐89) in donors of blood or organs. For each of these three groups, the highest seroprevalence was seen in the World Health Organisation (WHO) Eastern Mediterranean region 90% (95%UI: 85‐94) and the lowest in WHO European region 66% (95%UI: 56‐74). These estimates of the worldwide CMV distribution will help develop national and regional burden of disease models and inform future vaccine development efforts.

Nucleotide sequences from a total of 421 HEV isolates were retrieved from Genbank and analysed. Phylogenetically, HEV was classified into four major genotypes. Genotype 1 was more conserved and classified into five subtypes. The number of genotype 2 sequences was limited but can be classified into two subtypes. Genotypes 3 and 4 were extremely diverse and can be subdivided into ten and seven subtypes. Geographically, genotype 1 was isolated from tropical and several subtropical countries in Asia and Africa, and genotype 2 was from Mexico, Nigeria, and Chad; whereas genotype 3 was identified almost worldwide including Asia, Europe, Oceania, North and South America. In contrast, genotype 4 was found exclusively in Asia. It is speculated that genotype 3 originated in the western hemisphere and was imported to several Asian countries such as Japan, Korea and Taiwan, while genotype 4 has been indigenous and likely restricted to Asia. Genotypes 3 and 4 were not only identified in swine but also in wild animals such as boar and a deer. Furthermore, in most areas where genotypes 3 and 4 were characterised, sequences from both humans and animals were highly conserved, indicating they originated from the same infectious sources. Based upon nucleotide differences from five phylogenies, it is proposed that five, two, ten and seven subtypes for HEV genotypes 1, 2, 3 and 4 be designated alphabetised subtypes. Accordingly, a total of 24 subtypes (1a, 1b, 1c, 1d, 1e, 2a, 2b, 3a, 3b, 3c, 3d, 3e, 3f, 3g, 3h, 3i, 3j, 4a, 4b, 4c, 4d, 4e, 4f and 4g) were given. Copyright © 2005 John Wiley & Sons, Ltd.

Occult HBV infection is a well‐recognised clinical entity characterised by the detection of HBV‐DNA in serum and/or in liver in the absence of detectable hepatitis B surface antigen (HBsAg). Occult HBV infection has been described not only in patients who have resolved an acute or chronic HBV infection but also in patients without any serological markers of a past HBV infection. Occult HBV infection in patients with chronic HCV infection may induce more severe liver disease and lower response rate to interferon treatment. The existence of occult HCV infections has been also reported more recently. Occult HCV infection is characterised by the presence of HCV‐RNA in liver and peripheral blood mononuclear cells in the absence of detectable serum HCV‐RNA. Occult HCV infection may occur under two different clinical situations: in hepatitis C antibody‐(anti‐HCV) negative and serum HCV‐RNA‐negative patients with abnormal liver function tests and in anti‐HCV‐positive patients who have no detectable serum HCV‐RNA and who have normal liver enzymes. The clinical relevance of occult HCV infections is still under investigation. Copyright © 2008 John Wiley & Sons, Ltd.

In this review, we systematically searched and summarized the evidence on the immune response and reinfection rate following SARS‐CoV‐2 infection. We also retrieved studies on SARS‐CoV and MERS‐CoV to assess the long‐term duration of antibody responses. A protocol based on Cochrane rapid review methodology was adhered to and databases were searched from 1/1/2000 until 26/5/2020.

Of 4744 citations retrieved, 102 studies met our inclusion criteria. Seventy‐four studies were retrieved on SARS‐CoV‐2. While the rate and timing of IgM and IgG seroconversion were inconsistent across studies, most seroconverted for IgG within 2 weeks and 100% (N = 62) within 4 weeks. IgG was still detected at the end of follow‐up (49‐65 days) in all patients (N = 24). Neutralizing antibodies were detected in 92%‐100% of patients (up to 53 days). It is not clear if reinfection with SARS‐CoV‐2 is possible, with studies more suggestive of intermittent detection of residual RNA.

Twenty‐five studies were retrieved on SARS‐CoV. In general, SARS‐CoV‐specific IgG was maintained for 1‐2 years post‐infection and declined thereafter, although one study detected IgG up to 12 years post‐infection. Neutralizing antibodies were detected up to 17 years in another study. Three studies on MERS‐CoV reported that IgG may be detected up to 2 years.

In conclusion, limited early data suggest that most patients seroconvert for SARS‐CoV‐2‐specific IgG within 2 weeks. While the long‐term duration of antibody responses is unknown, evidence from SARS‐CoV studies suggest SARS‐CoV‐specific IgG is sustained for 1‐2 years and declines thereafter.

Emerging and reemerging infectious diseases have a strong negative impact on public health. However, because many of these pathogens must be handled in biosafety level, 3 or 4 containment laboratories, research and development of antivirals or vaccines against these diseases are often impeded. Alternative approaches to address this issue have been vigorously pursued, particularly the use of pseudoviruses in place of wild‐type viruses. As pseudoviruses have been deprived of certain gene sequences of the virulent virus, they can be handled in biosafety level 2 laboratories. Importantly, the envelopes of these viral particles may have similar conformational structures to those of the wild‐type viruses, making it feasible to conduct mechanistic investigation on viral entry and to evaluate potential neutralizing antibodies. However, a variety of challenging issues remain, including the production of a sufficient pseudovirus yield and the inability to produce an appropriate pseudotype of certain viruses. This review discusses current progress in the development of pseudoviruses and dissects the factors that contribute to low viral yields.

Upon HIV attachment, fusion and entry into the host cell cytoplasm, the viral core undergoes rearrangement to become the mature reverse transcription complex (RTC). Reduced infectivity of viral deletion mutants of the core proteins, capsid and negative factor (Nef), can be complemented by vesicular stomatitis virus (VSV) pseudotyping suggesting a role for these viral proteins in a common event immediately post‐entry. This event may be necessary for correct trafficking of the early complex. Enzymatic activation of the complex occurs either before or during RTC maturation, and may be dependent on the presence of deoxynucleotides in the host cell. The RTC initially becomes enlarged immediately after entry, which is followed by a decrease in its sedimentation rate consistent with core uncoating. Several HIV proteins associated with the RTC and recently identified host‐cell proteins are important for reverse transcription while genome‐wide siRNA knockdown studies have identified additional host cell factors that may be required for reverse transcription. Determining precisely how these proteins assist the RTC function needs to be addressed. Copyright © 2009 John Wiley & Sons, Ltd.