In:
Journal of Virology, American Society for Microbiology, Vol. 79, No. 8 ( 2005-04-15), p. 4580-4588
Kurzfassung:
The expression of particular major histocompatibility complex (MHC) class I alleles can influence the rate of disease progression following lentiviral infections. This effect is a presumed consequence of potent cytotoxic T-lymphocyte (CTL) responses that are restricted by these MHC class I molecules. The present studies have examined the impact of the MHC class I allele Mamu-A*01 on simian/human immunodeficiency virus 89.6P (SHIV-89.6P) infection in unvaccinated and vaccinated rhesus monkeys by exploring the contribution of dominant-epitope specific CTL in this setting. Expression of Mamu-A*01 in immunologically naive monkeys was not associated with improved control of viral replication, CD4 + T-lymphocyte loss, or survival. In contrast, Mamu-A*01 + monkeys that had received heterologous prime/boost immunizations prior to challenge maintained higher CD4 + T-lymphocyte levels and better control of SHIV-89.6P replication than Mamu-A*01 − monkeys. This protection was associated with the evolution of high-frequency anamnestic CTL responses specific for a dominant Mamu-A*01-restricted Gag epitope following infection. These data indicate that specific MHC class I alleles can confer protection in the setting of a pathogenic SHIV infection by their ability to elicit memory CTL following vaccination.
Materialart:
Online-Ressource
ISSN:
0022-538X
,
1098-5514
DOI:
10.1128/JVI.79.8.4580-4588.2005
Sprache:
Englisch
Verlag:
American Society for Microbiology
Publikationsdatum:
2005
ZDB Id:
1495529-5