Transmission and long-term stability of compensated CD8 escape mutations.
Human immunodeficiency virus effectively evades CD8(+) T-cell responses through the development of CD8 escape mutations. Recent reports documenting reversion of transmitted mutations and the impact of specific escape mutations upon viral replication suggest that complex forces limit the accumulation of CD8 escape mutations at the population level. However, the presence of compensatory mutations capable of alleviating the impact of CD8 escape mutations on replication capacity may enable their persistence in an HLA-mismatched host. Herein, we illustrate the long-term stability of stereotypic escape mutations in the immunodominant HLA-B27-restricted epitope KK10 in p24/Gag following transmission when accompanied by a specific compensatory mutation.
Schneidewind
Arne
A
Partners AIDS Research Center, Massachusetts General Hospital, Boston, MA, USA.
Brumme
Zabrina L
ZL
Brumme
Chanson J
CJ
Power
Karen A
KA
Reyor
Laura L
LL
O'Sullivan
Kristin
K
Gladden
Adrianne
A
Hempel
Ursula
U
Kuntzen
Thomas
T
Wang
Yaoyu E
YE
Oniangue-Ndza
Cesar
C
Jessen
Heiko
H
Markowitz
Martin
M
Rosenberg
Eric S
ES
Sékaly
Rafick-Pierre
RP
Kelleher
Anthony D
AD
Walker
Bruce D
BD
Allen
Todd M
TM
D000595:Amino Acid Sequence; D000818:Animals; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D018984:Epitopes, T-Lymphocyte / Q000235:genetics* / Q000276:immunology*; D006678:HIV / Q000235:genetics / Q000254:growth & development* / Q000276:immunology*; D016655:HIV Core Protein p24 / Q000235:genetics; D006801:Humans; D008969:Molecular Sequence Data; D020125:Mutation, Missense / Q000276:immunology*; D014779:Virus Replication
D018984:Epitopes, T-Lymphocyte; D016655:HIV Core Protein p24