Maudi Killian

TL;DR: It is revealed that persistence of a remarkably stable population of infected memory cells will be the primary barrier to a cure, and, with little evidence of viral replication, this population could be maintained by homeostatic cell proliferation or other processes.

TL;DR: HIV-infected subjects had thicker carotid IMT compared to controls, and while HIV patients also had higher T-cell activation, hs-CRP levels, and CMV-specific T- cell responses, onlyCMV- specific T-Cell responses were independently associated with IMT.

TL;DR: Low levels of HIV DNA and RNA were observed in non-CD4+ T leukocytes at low levels, particularly in gut tissues, and future studies should determine whether different mechanisms allow HIV to persist in these distinct reservoirs, and the degree to which different therapies can affect each reservoir.

TL;DR: Memory T cells maintained a relatively constant HIV-1 DNA integrant pool that was genetically stable during long-term effective ART, and these integrants appear to be maintained by cellular proliferation and longevity of infected cells, rather than by ongoing viral replication.

TL;DR: The results strongly suggest that Lin(-)/CD34(+) HPCs in bone marrow are not a source of persistent HIV-1 in patients on long-term suppressive therapy.