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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.

Original publication

DOI

10.1128/JVI.01743-09

Type

Journal article

Journal

J Virol

Publication Date

01/2010

Volume

84

Pages

492 - 502

Keywords

CD8-Positive T-Lymphocytes, Cohort Studies, Disease Progression, Gene Products, gag, HIV Infections, HIV-1, HLA-B Antigens, Host-Pathogen Interactions, Humans, Immune Evasion, Infant, Newborn, Infectious Disease Transmission, Vertical, Kinetics, Mutation, South Africa, Virus Replication