Journal
JOURNAL OF VIROLOGY
Volume 84, Issue 1, Pages 492-502Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01743-09
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Funding
- Doris Duke Charitable foundation [2001 1031]
- Wellcome Trust
- Bristol Myers Squibb Secure the Future [RES 16/01]
- Marie Curie [41811 (IEF-FP6)]
- MRC [G0500384] Funding Source: UKRI
- Medical Research Council [G0500384] Funding Source: researchfish
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Human immunodeficiency virus (HIV)-infected infants in the developing world typically progress to AIDS or death within the first 2 years of life. However, a minority progress relatively slowly. This study addresses the potential contribution of viral factors to HIV disease progression in eight infants selected from a well-characterized cohort of C clade HIV-infected infants, monitored prospectively from birth in Durban, South Africa. Three infants were defined as progressors, and five were defined as slow progressors. We observed that slow-progressor infants carry HIV isolates with significantly lower replicative capacity compared to virus from progressors. Furthermore, our data suggest a link between the attenuated viral phenotype and HLA-B* 57/5801 epitope-specific Gag mutational patterns of the transmitted virus and not to coreceptor usage or to the presence of Nef deletions or insertions. These data underline the importance of virus-host interactions and highlight the contribution of viral attenuation through Gag-specific CD8(+) T-cell escape mutations, among other factors, in the control of pediatric HIV infection.
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