PMID- 21246583
OWN - NLM
STAT- MEDLINE
DCOM- 20110318
LR  - 20211020
IS  - 1527-3350 (Electronic)
IS  - 0270-9139 (Print)
IS  - 0270-9139 (Linking)
VI  - 53
IP  - 2
DP  - 2011 Feb
TI  - Effect of immune pressure on hepatitis C virus evolution: insights from a 
      single-source outbreak.
PG  - 396-405
LID - 10.1002/hep.24076 [doi]
AB  - The host's immune response to hepatitis C virus (HCV) can result in the selection 
      of characteristic mutations (adaptations) that enable the virus to escape this 
      response. The ability of the virus to mutate at these sites is dependent on the 
      incoming virus, the fitness cost incurred by the mutation, and the benefit to the 
      virus in escaping the response. Studies examining viral adaptation in chronic HCV 
      infection have shown that these characteristic immune escape mutations can be 
      observed at the population level as human leukocyte antigen (HLA)-specific viral 
      polymorphisms. We examined 63 individuals with chronic HCV infection who were 
      infected from a single HCV genotype 1b source. Our aim was to determine the 
      extent to which the host's immune pressure affects HCV diversity and the ways in 
      which the sequence of the incoming virus, including preexisting escape mutations, 
      can influence subsequent mutations in recipients and infection outcomes. 
      CONCLUSION: HCV sequences from these individuals revealed 29 significant 
      associations between specific HLA types within the new hosts and variations 
      within their viruses, which likely represent new viral adaptations. These 
      associations did not overlap with previously reported adaptations for genotypes 
      1a and 3a and possibly reflected a combination of constraint due to the incoming 
      virus and genetic distance between the strains. However, these sites accounted 
      for only a portion of the sites in which viral diversity was observed in the new 
      hosts. Furthermore, preexisting viral adaptations in the incoming (source) virus 
      likely influenced the outcomes in the new hosts.
CI  - Copyright (c) 2011 American Association for the Study of Liver Diseases.
FAU - Merani, Shahzma
AU  - Merani S
AD  - Centre for Forensic Science, University of Western Australia, Western Australia, 
      Australia.
FAU - Petrovic, Danijela
AU  - Petrovic D
FAU - James, Ian
AU  - James I
FAU - Chopra, Abha
AU  - Chopra A
FAU - Cooper, Don
AU  - Cooper D
FAU - Freitas, Elizabeth
AU  - Freitas E
FAU - Rauch, Andri
AU  - Rauch A
FAU - di Iulio, Julia
AU  - di Iulio J
FAU - John, Mina
AU  - John M
FAU - Lucas, Michaela
AU  - Lucas M
FAU - Fitzmaurice, Karen
AU  - Fitzmaurice K
FAU - McKiernan, Susan
AU  - McKiernan S
FAU - Norris, Suzanne
AU  - Norris S
FAU - Kelleher, Dermot
AU  - Kelleher D
FAU - Klenerman, Paul
AU  - Klenerman P
FAU - Gaudieri, Silvana
AU  - Gaudieri S
LA  - eng
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GR  - 091663/WT_/Wellcome Trust/United Kingdom
GR  - U19 AI082630/AI/NIAID NIH HHS/United States
GR  - 1U19AI082630-01/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20110118
PL  - United States
TA  - Hepatology
JT  - Hepatology (Baltimore, Md.)
JID - 8302946
RN  - 0 (Epitopes)
SB  - IM
MH  - Adaptation, Physiological/*genetics/*immunology/physiology
MH  - *Disease Outbreaks
MH  - Epitopes/genetics
MH  - Female
MH  - Hepacivirus/*genetics/*immunology/physiology
MH  - Hepatitis C, Chronic/*genetics/*immunology/physiopathology
MH  - Humans
MH  - Molecular Sequence Data
MH  - Mutation/genetics
MH  - Polymorphism, Single Nucleotide/genetics
MH  - Retrospective Studies
PMC - PMC3044208
MID - NIHMS251235
EDAT- 2011/01/20 06:00
MHDA- 2011/03/19 06:00
CRDT- 2011/01/20 06:00
PHST- 2010/04/25 00:00 [received]
PHST- 2010/11/05 00:00 [accepted]
PHST- 2011/01/20 06:00 [entrez]
PHST- 2011/01/20 06:00 [pubmed]
PHST- 2011/03/19 06:00 [medline]
AID - 10.1002/hep.24076 [doi]
PST - ppublish
SO  - Hepatology. 2011 Feb;53(2):396-405. doi: 10.1002/hep.24076. Epub 2011 Jan 18.