Quantifying the diversification of hepatitis C virus (HCV) during primary infection: estimates of the in vivo mutation rate.

Hepatitis C virus (HCV) is present in the host with multiple variants generated by its error prone RNA-dependent RNA polymerase. Little is known about the initial viral diversification and the viral life cycle processes that influence diversity. We studied the diversification of HCV during acute inf...

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Main Authors: Ruy M Ribeiro, Hui Li, Shuyi Wang, Mark B Stoddard, Gerald H Learn, Bette T Korber, Tanmoy Bhattacharya, Jeremie Guedj, Erica H Parrish, Beatrice H Hahn, George M Shaw, Alan S Perelson
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2012-01-01
Series:PLoS Pathogens
Online Access:https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1002881&type=printable
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author Ruy M Ribeiro
Hui Li
Shuyi Wang
Mark B Stoddard
Gerald H Learn
Bette T Korber
Tanmoy Bhattacharya
Jeremie Guedj
Erica H Parrish
Beatrice H Hahn
George M Shaw
Alan S Perelson
author_facet Ruy M Ribeiro
Hui Li
Shuyi Wang
Mark B Stoddard
Gerald H Learn
Bette T Korber
Tanmoy Bhattacharya
Jeremie Guedj
Erica H Parrish
Beatrice H Hahn
George M Shaw
Alan S Perelson
author_sort Ruy M Ribeiro
collection DOAJ
description Hepatitis C virus (HCV) is present in the host with multiple variants generated by its error prone RNA-dependent RNA polymerase. Little is known about the initial viral diversification and the viral life cycle processes that influence diversity. We studied the diversification of HCV during acute infection in 17 plasma donors, with frequent sampling early in infection. To analyze these data, we developed a new stochastic model of the HCV life cycle. We found that the accumulation of mutations is surprisingly slow: at 30 days, the viral population on average is still 46% identical to its transmitted viral genome. Fitting the model to the sequence data, we estimate the median in vivo viral mutation rate is 2.5×10⁻⁵ mutations per nucleotide per genome replication (range 1.6-6.2×10⁻⁵), about 5-fold lower than previous estimates. To confirm these results we analyzed the frequency of stop codons (N = 10) among all possible non-sense mutation targets (M = 898,335), and found a mutation rate of 2.8-3.2×10⁻⁵, consistent with the estimate from the dynamical model. The slow accumulation of mutations is consistent with slow turnover of infected cells and replication complexes within infected cells. This slow turnover is also inferred from the viral load kinetics. Our estimated mutation rate, which is similar to that of other RNA viruses (e.g., HIV and influenza), is also compatible with the accumulation of substitutions seen in HCV at the population level. Our model identifies the relevant processes (long-lived cells and slow turnover of replication complexes) and parameters involved in determining the rate of HCV diversification.
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spelling doaj-art-af358df6240443dc8307fd7f3fc760a72025-08-20T02:15:30ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742012-01-0188e100288110.1371/journal.ppat.1002881Quantifying the diversification of hepatitis C virus (HCV) during primary infection: estimates of the in vivo mutation rate.Ruy M RibeiroHui LiShuyi WangMark B StoddardGerald H LearnBette T KorberTanmoy BhattacharyaJeremie GuedjErica H ParrishBeatrice H HahnGeorge M ShawAlan S PerelsonHepatitis C virus (HCV) is present in the host with multiple variants generated by its error prone RNA-dependent RNA polymerase. Little is known about the initial viral diversification and the viral life cycle processes that influence diversity. We studied the diversification of HCV during acute infection in 17 plasma donors, with frequent sampling early in infection. To analyze these data, we developed a new stochastic model of the HCV life cycle. We found that the accumulation of mutations is surprisingly slow: at 30 days, the viral population on average is still 46% identical to its transmitted viral genome. Fitting the model to the sequence data, we estimate the median in vivo viral mutation rate is 2.5×10⁻⁵ mutations per nucleotide per genome replication (range 1.6-6.2×10⁻⁵), about 5-fold lower than previous estimates. To confirm these results we analyzed the frequency of stop codons (N = 10) among all possible non-sense mutation targets (M = 898,335), and found a mutation rate of 2.8-3.2×10⁻⁵, consistent with the estimate from the dynamical model. The slow accumulation of mutations is consistent with slow turnover of infected cells and replication complexes within infected cells. This slow turnover is also inferred from the viral load kinetics. Our estimated mutation rate, which is similar to that of other RNA viruses (e.g., HIV and influenza), is also compatible with the accumulation of substitutions seen in HCV at the population level. Our model identifies the relevant processes (long-lived cells and slow turnover of replication complexes) and parameters involved in determining the rate of HCV diversification.https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1002881&type=printable
spellingShingle Ruy M Ribeiro
Hui Li
Shuyi Wang
Mark B Stoddard
Gerald H Learn
Bette T Korber
Tanmoy Bhattacharya
Jeremie Guedj
Erica H Parrish
Beatrice H Hahn
George M Shaw
Alan S Perelson
Quantifying the diversification of hepatitis C virus (HCV) during primary infection: estimates of the in vivo mutation rate.
PLoS Pathogens
title Quantifying the diversification of hepatitis C virus (HCV) during primary infection: estimates of the in vivo mutation rate.
title_full Quantifying the diversification of hepatitis C virus (HCV) during primary infection: estimates of the in vivo mutation rate.
title_fullStr Quantifying the diversification of hepatitis C virus (HCV) during primary infection: estimates of the in vivo mutation rate.
title_full_unstemmed Quantifying the diversification of hepatitis C virus (HCV) during primary infection: estimates of the in vivo mutation rate.
title_short Quantifying the diversification of hepatitis C virus (HCV) during primary infection: estimates of the in vivo mutation rate.
title_sort quantifying the diversification of hepatitis c virus hcv during primary infection estimates of the in vivo mutation rate
url https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1002881&type=printable
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