Interleukin‐10 Promoter Polymorphisms Influence HIV‐1 Susceptibility and Primary HIV‐1 Pathogenesis
Author(s) -
Dshanta Dyanedi. Naicker,
Lise Werner,
E Kormúth,
JoAnn Passmore,
Koleka Mlisana,
Salim S. Abdool Karim,
Thumbi Ndung’u
Publication year - 2009
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/600072
Subject(s) - pathogenesis , virology , genotype , immunology , viral load , biology , lentivirus , immune system , viral disease , viral replication , virus , single nucleotide polymorphism , effector , human immunodeficiency virus (hiv) , gene , genetics
Interleukin (IL)-10 directly inhibits human immunodeficiency virus type 1 (HIV-1) replication, but it may also promote viral persistence by inactivation of effector immune mechanisms. Here, we show in an African cohort that individuals with genotypes associated with high IL-10 production at 2 promoter single-nucleotide polymorphisms (-1082 and -592) were less likely to become HIV-1 infected but had significantly higher median plasma viral loads during the acute phase (<or=3 months after infection). However, as the infection progressed, the association between genotype and median viral load was reversed. Thus, IL-10 may influence HIV-1 susceptibility and pathogenesis, but effects on the latter may differ according to the infection phase.
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