Brett Baker

TL;DR: Differences in binding to viral peptide antigens by HLA may be the major factors underlying genetic differences between HIV controllers and progressors, and genome-wide association results implicate the nature of the HLA–viral peptide interaction as the major factor modulating durable control of HIV infection.

TL;DR: Even low-level viremia among HIV controllers was associated with measurable T cell dysfunction, which has implications for current prophylactic vaccine strategies.

TL;DR: It is reported that the inhibitory immunoregulatory receptor CTLA-4 was selectively upregulated in human immunodeficiency virus–specific CD4+ T cells but not CD8- T cells in all categories of HIV-infected subjects evaluated, with the exception of rare people able to control viremia in the absence of antiretroviral therapy.

TL;DR: A dual mechanism for durable control of HIV replication is suggested, consisting of viral fitness loss resulting from CTL escape mutations together with strong CD8 T-cell immune responses to the arising variant epitopes.

TL;DR: Low-level viremia is present in the majority of elite controllers and is associated with higher HIV-1-specific antibody responses, and absolute CD4(+) T cell loss is more common among viremic individuals, suggesting that even very low-levelviremia has negative consequences over time.