scholarly journals Hepatitis C Virus: Viral Quasispecies and Genotypes

2017 ◽  
Vol 19 (1) ◽  
pp. 23 ◽  
Author(s):  
Kyoko Tsukiyama-Kohara ◽  
Michinori Kohara
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Viral Quasispecies

scholarly journals Hepatitis C viral quasispecies in hepatitis C virus carriers with normal liver enzymes and patients with type C chronic liver disease

Hepatology ◽  
1995 ◽  
Vol 22 (2) ◽  
pp. 407-412 ◽  
Author(s):  
Masafumi Naito ◽  
Norio Hayashi ◽  
Toyoki Moribe ◽  
Hideki Hagiwara ◽  
Eiji Mita ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Liver Disease ◽  
Hepatitis C ◽  
Chronic Liver Disease ◽  
Liver Enzymes ◽  
Normal Liver ◽  
Chronic Liver ◽  
Viral Quasispecies ◽  
Type C

Evolution of viral quasispecies in interferon-treated patients with chronic hepatitis C virus infection

1999 ◽  
Vol 31 (4) ◽  
pp. 618-627 ◽  
Author(s):  
Howayda M Hassoba ◽  
Natalie Bzowej ◽  
Marina Berenguer ◽  
Michael Kim ◽  
Shuan Zhou ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Infection ◽  
Chronic Hepatitis C ◽  
Viral Quasispecies ◽  
Hepatitis C Virus Infection ◽  
Chronic Hepatitis C Virus

scholarly journals Deep Sequencing and Phylogenetic Analysis of Variants Resistant to Interferon-Based Protease Inhibitor Therapy in Chronic Hepatitis Induced by Genotype 1b Hepatitis C Virus

2015 ◽  
Vol 89 (11) ◽  
pp. 6105-6116 ◽  
Author(s):  
Mitsuaki Sato ◽  
Shinya Maekawa ◽  
Nobutoshi Komatsu ◽  
Akihisa Tatsumi ◽  
Mika Miura ◽  
...  
Keyword(s):  
Phylogenetic Analysis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Protease Inhibitor ◽  
Deep Sequencing ◽  
Pegylated Interferon ◽  
Inhibitor Therapy ◽  
Protease Inhibitor Therapy ◽  
Viral Quasispecies ◽  
Deep Sequencing Technology

ABSTRACTBecause of recent advances in deep sequencing technology, detailed analysis of hepatitis C virus (HCV) quasispecies and their dynamic changes in response to direct antiviral agents (DAAs) became possible, although the role of quasispecies is not fully understood. In this study, to clarify the evolution of viral quasispecies and the origin of drug-resistant mutations induced by interferon (IFN)-based protease inhibitor therapy, the nonstructural-3 (NS3) region of genotype 1b HCV in 34 chronic hepatitis patients treated with telaprevir (TVR)/pegylated interferon (PEG-IFN)/ribavirin (RBV) was subjected to a deep sequencing study coupled with phylogenetic analysis. Twenty-six patients (76.5%) achieved a sustained viral response (SVR), while 8 patients did not (non-SVR; 23.5%). When the complexity of the quasispecies was expressed as the mutation frequency or Shannon entropy value, a significant decrease in theIFNL3(rs8099917) TT group and a marginal decrease in the SVR group were found soon (12 h) after the introduction of treatment, whereas there was no decrease in the non-SVR group and no significant decrease in mutation frequency in theIFNL3TG/GG group. In the analysis of viral quasispecies composition in non-SVR patients, major populations greatly changed, accompanied by the appearance of resistance, and the compositions were unlikely to return to the pretreatment composition even after the end of therapy. Clinically TVR-resistant variants were observed in 5 non-SVR patients (5/8, 62.5%), all of which were suspected to have acquired resistance by mutations through phylogenetic analysis. In conclusion, results of the study have important implications for treatment response and outcome in interferon-based protease inhibitor therapy.IMPORTANCEIn the host, hepatitis C virus (HCV) consists of a variety of populations (quasispecies), and it is supposed that dynamic changes in quasispecies are closely related to pathogenesis, although this is poorly understood. In this study, recently developed deep sequencing technology was introduced, and changes in quasispecies associated with telaprevir (TVR)/pegylated interferon (PEG-IFN)/ribavirin (RBV) triple therapy and their clinical significance were investigated extensively by phylogenetic tree analysis. Through this study, the associations among treatment response, changes in viral quasispecies complexity in the early stage of treatment, changes in the quasispecies composition, and origin of TVR-resistant variant HCV were elucidated.

scholarly journals Replication of Hepatitis C Virus in Ascitic Mononuclear Cells with Development of Distinct Viral Quasispecies

1999 ◽  
Vol 180 (4) ◽  
pp. 992-1000 ◽  
Author(s):  
Chao‐Wei Hsu ◽  
Chau‐Ting Yeh ◽  
Peggy Guey‐Chi Chen ◽  
Yun‐Fan Liaw
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Mononuclear Cells ◽  
Viral Quasispecies

Dynamics of viral quasispecies in hepatitis C virus infection

1997 ◽  
Vol 148 (2) ◽  
pp. 171-176
Author(s):  
A. Manzin ◽  
L. Solforosi ◽  
M. Clementi
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Infection ◽  
Viral Quasispecies ◽  
Hepatitis C Virus Infection

scholarly journals Evolutionary Rate and Genetic Drift of Hepatitis C Virus Are Not Correlated with the Host Immune Response: Studies of Infected Donor-Recipient Clusters

2000 ◽  
Vol 74 (6) ◽  
pp. 2541-2549 ◽  
Author(s):  
Jean-Pierre Allain ◽  
Yan Dong ◽  
Anne-Mieke Vandamme ◽  
Vincent Moulton ◽  
Marco Salemi
Keyword(s):  
Immune Response ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Genetic Drift ◽  
Evolutionary Rate ◽  
Phylogenetic Analyses ◽  
Hypervariable Region ◽  
Viral Quasispecies ◽  
Evolutionary Patterns ◽  
Immune Pressure

ABSTRACT Six donor-recipient clusters of hepatitis C virus (HCV)-infected individuals were studied. For five clusters the period of infection of the donor could be estimated, and for all six clusters the time of infection of the recipients from the donor via blood transfusion was also precisely known. Detailed phylogenetic analyses were carried out to investigate the genomic evolution of the viral quasispecies within infected individuals in each cluster. The molecular clock analysis showed that HCV quasispecies within a patient are evolving at the same rate and that donors that have been infected for longer time tend to have a lower evolutionary rate. Phylogenetic analysis based on the split decomposition method revealed different evolutionary patterns in different donor-recipient clusters. Reactivity of antibody against the first hypervariable region (HVR1) of HCV in donor and recipient sera was evaluated and correlated to the calculated evolutionary rate. Results indicate that anti-HVR1 reactivity was related more to the overall level of humoral immune response of the host than to the HVR1 sequence itself, suggesting that the particular sequence of the HVR1 peptides is not the determinant of reactivity. Moreover, no correlation was found between the evolutionary rate or the heterogeneity of the viral quasispecies in the patients and the strength of the immune response to HVR1 epitopes. Rather, the results seem to imply that genetic drift is less dependent on immune pressure than on the rate of evolution and that the genetic drift of HCV is independent of the host immune pressure.

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