PMID- 14770175
OWN - NLM
STAT- MEDLINE
DCOM- 20040507
LR  - 20111117
IS  - 1078-8956 (Print)
IS  - 1078-8956 (Linking)
VI  - 10
IP  - 3
DP  - 2004 Mar
TI  - HIV evolution: CTL escape mutation and reversion after transmission.
PG  - 282-9
AB  - Within-patient HIV evolution reflects the strong selection pressure driving viral 
      escape from cytotoxic T-lymphocyte (CTL) recognition. Whether this intrapatient 
      accumulation of escape mutations translates into HIV evolution at the population 
      level has not been evaluated. We studied over 300 patients drawn from the B- and 
      C-clade epidemics, focusing on human leukocyte antigen (HLA) alleles HLA-B57 and 
      HLA-B5801, which are associated with long-term HIV control and are therefore 
      likely to exert strong selection pressure on the virus. The CTL response 
      dominating acute infection in HLA-B57/5801-positive subjects drove positive 
      selection of an escape mutation that reverted to wild-type after transmission to 
      HLA-B57/5801-negative individuals. A second escape mutation within the epitope, 
      by contrast, was maintained after transmission. These data show that the process 
      of accumulation of escape mutations within HIV is not inevitable. Complex 
      epitope- and residue-specific selection forces, including CTL-mediated positive 
      selection pressure and virus-mediated purifying selection, operate in tandem to 
      shape HIV evolution at the population level.
FAU - Leslie, A J
AU  - Leslie AJ
AD  - Department of Pediatrics, Fuffield Department of Medicine, Peter Medawar Building 
      for Pathogen Research, University of Oxford, Oxford OX1 3SY, UK.
FAU - Pfafferott, K J
AU  - Pfafferott KJ
FAU - Chetty, P
AU  - Chetty P
FAU - Draenert, R
AU  - Draenert R
FAU - Addo, M M
AU  - Addo MM
FAU - Feeney, M
AU  - Feeney M
FAU - Tang, Y
AU  - Tang Y
FAU - Holmes, E C
AU  - Holmes EC
FAU - Allen, T
AU  - Allen T
FAU - Prado, J G
AU  - Prado JG
FAU - Altfeld, M
AU  - Altfeld M
FAU - Brander, C
AU  - Brander C
FAU - Dixon, C
AU  - Dixon C
FAU - Ramduth, D
AU  - Ramduth D
FAU - Jeena, P
AU  - Jeena P
FAU - Thomas, S A
AU  - Thomas SA
FAU - St John, A
AU  - St John A
FAU - Roach, T A
AU  - Roach TA
FAU - Kupfer, B
AU  - Kupfer B
FAU - Luzzi, G
AU  - Luzzi G
FAU - Edwards, A
AU  - Edwards A
FAU - Taylor, G
AU  - Taylor G
FAU - Lyall, H
AU  - Lyall H
FAU - Tudor-Williams, G
AU  - Tudor-Williams G
FAU - Novelli, V
AU  - Novelli V
FAU - Martinez-Picado, J
AU  - Martinez-Picado J
FAU - Kiepiela, P
AU  - Kiepiela P
FAU - Walker, B D
AU  - Walker BD
FAU - Goulder, P J R
AU  - Goulder PJ
LA  - eng
GR  - AI46995-01A1/AI/NIAID NIH HHS/United States
GR  - N01-AI-15442/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20040208
PL  - United States
TA  - Nat Med
JT  - Nature medicine
JID - 9502015
RN  - 0 (Epitopes)
RN  - 0 (HLA-B Antigens)
RN  - 0 (HLA-B57 antigen)
SB  - IM
CIN - Nat Med. 2004 Mar;10(3):229-30. PMID: 14991039
MH  - Adult
MH  - Amino Acid Sequence
MH  - Child
MH  - Epitopes
MH  - *Evolution, Molecular
MH  - Female
MH  - Genetic Variation
MH  - HIV Infections/immunology/transmission/*virology
MH  - HIV-1/genetics/immunology/*physiology
MH  - HLA-B Antigens/genetics/immunology
MH  - Humans
MH  - Infectious Disease Transmission, Vertical
MH  - Likelihood Functions
MH  - *Mutation
MH  - Phylogeny
MH  - Selection, Genetic
MH  - T-Lymphocytes, Cytotoxic/*immunology/metabolism
MH  - Viral Load
EDAT- 2004/02/11 05:00
MHDA- 2004/05/08 05:00
CRDT- 2004/02/11 05:00
PHST- 2003/11/16 00:00 [received]
PHST- 2004/01/08 00:00 [accepted]
PHST- 2004/02/11 05:00 [pubmed]
PHST- 2004/05/08 05:00 [medline]
PHST- 2004/02/11 05:00 [entrez]
AID - nm992 [pii]
AID - 10.1038/nm992 [doi]
PST - ppublish
SO  - Nat Med. 2004 Mar;10(3):282-9. doi: 10.1038/nm992. Epub 2004 Feb 8.