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SIV replication in the infected rhesus macaque is limited by the size of the preexisting TH17 cell compartment.

Abstract：

:The mechanisms by which some HIV-infected subjects resist disease progression, whereas others progress rapidly, are incompletely understood. Viral and host genetic factors, such as nef deletions and major histocompatibility complex alleles, explain a portion of the observed variability. However, it has been difficult to identify host immune functions that may be present before infection and that allow resistance to lentiviral disease progression. Here, we show that simian immunodeficiency virus replication in the infected rhesus macaque is limited by the size of the preexisting T helper 17 (T(H)17) cell compartment: Animals with a high representation of such cells in blood and intestinal tissue before infection experienced peak and set-point viral loads about one log unit lower than those with a lower representation of T(H)17 cells. Reciprocally, treatment of macaques with interleukin-2 and granulocyte colony-stimulating factor before infection led to depletion of T(H)17 cells, reduction of the ratio between T(H)17 cells and CD3(+)CD4(+)CD25(+)CD127(low) regulatory T cells, and higher viral loads for 6 months after infection. These results demonstrate that the composition of the host immune system before infection has an influence on the course of disease after infection. Furthermore, to the extent that this influence shapes and interacts with T cell-mediated responses to virus, our findings provide a new framework for understanding interindividual variation in responses to therapies and vaccines against HIV.

journal_name

Sci Transl Med

journal_title

Science translational medicine

authors

Hartigan-O'Connor DJ,Abel K,Van Rompay KK,Kanwar B,McCune JM

doi

10.1126/scitranslmed.3003941

subject

Has Abstract

pub_date

2012-05-30 00:00:00

pages

136ra69

issue

136

eissn

1946-6234

issn

1946-6242

pii

4/136/136ra69

journal_volume

4

pub_type

杂志文章

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