Format

Send to

Choose Destination
See comment in PubMed Commons below
J Acquir Immune Defic Syndr. 2014 Jan 1;65(1):1-9. doi: 10.1097/QAI.0b013e3182a1bc81.

Susceptibility to CD8 T-cell-mediated killing influences the reservoir of latently HIV-1-infected CD4 T cells.

Author information

1
*Infectious Disease Division, Massachusetts General Hospital, Boston, MA; †Ragon Institute of MGH, MIT, and Harvard, Boston, MA; ‡Laboratory of AIDS Immunology, The First Affiliated Hospital of China Medical University, Shenyang, People's Republic of China; and §Infectious Disease Division, Brigham and Women's Hospital, Boston, MA.

Abstract

BACKGROUND:

HIV-1 establishes a lifelong infection in the human body, but host factors that influence viral persistence remain poorly understood. Cell-intrinsic characteristics of CD4 T cells, the main target cells for HIV-1, may affect the composition of the latent viral reservoir by altering the susceptibility to CD8 T-cell-mediated killing.

RESULTS:

We observed that susceptibilities of CD4 T cells to CD8 T-cell-mediated killing, as determined in direct ex vivo assays, were significantly higher in persons with natural control of HIV-1 (elite controllers) than in individuals effectively treated with antiretroviral therapy. These differences were most pronounced in naive and in terminally differentiated CD4 T cells and corresponded to a reduced viral reservoir size in elite controllers. Interestingly, the highest susceptibility to CD8 T-cell-mediated killing and lowest reservoirs of cell-associated HIV-1 DNA was consistently observed in elite controllers expressing the protective HLA class I allele B57.

CONCLUSIONS:

These data suggest that the functional responsiveness of host CD4 T cells to cytotoxic effects of HIV-1-specific CD8 T cells can contribute to shaping the structure and composition of the latently infected CD4 T-cell pool.

PMID:
23846565
PMCID:
PMC3874432
DOI:
10.1097/QAI.0b013e3182a1bc81
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wolters Kluwer Icon for PubMed Central
    Loading ...
    Support Center