Optimal Maturation of the SIV-Specific CD8 T Cell Response after Primary Infection Is Associated with Natural Control of SIV: ANRS SIC Study.

Highly efficient CD8 T cells are associated with natural HIV control, but it has remained unclear how these cells are generated and maintained. We have used a macaque model of spontaneous SIVmac251 control to monitor the development of efficient CD8 T cell responses. Our results show that SIV-specific CD8 T cells emerge during primary infection in all animals.

Metabolic plasticity of HIV-specific CD8 T cells is associated with enhanced antiviral potential and natural control of HIV-1 infection.

Spontaneous control of human immunodeficiency virus (HIV) is generally associated with an enhanced capacity of CD8 T cells to eliminate infected CD4 T cells, but the molecular characteristics of these highly functional CD8 T cells are largely unknown. In the present study, using single-cell analysis, it was shown that HIV-specific, central memory CD8 T cells from spontaneous HIV controllers (HICs) and antiretrovirally treated non-controllers have opposing transcriptomic profiles. Genes linked to effector functions and survival are upregulated in cells from HICs.

SUGT1 controls susceptibility to HIV-1 infection by stabilizing microtubule plus-ends.

Understanding the viral-host cell interface during HIV-1 infection is a prerequisite for the development of innovative antiviral therapies. Here we show that the suppressor of G2 allele of skp1 (SUGT1) is a permissive factor for human immunodeficiency virus (HIV)-1 infection. Expression of SUGT1 increases in infected cells on human brain sections and in permissive host cells.

HIV-1 Envelope Overcomes NLRP3-Mediated Inhibition of F-Actin Polymerization for Viral Entry.

Purinergic receptors and nucleotide-binding domain leucine-rich repeat containing (NLR) proteins have been shown to control viral infection. Here, we show that the NLR family member NLRP3 and the purinergic receptor P2Y2 constitutively interact and regulate susceptibility to HIV-1 infection. We found that NLRP3 acts as an inhibitory factor of viral entry that represses F-actin remodeling.

p21 Restricts HIV-1 in Monocyte-Derived Dendritic Cells through the Reduction of Deoxynucleoside Triphosphate Biosynthesis and Regulation of SAMHD1 Antiviral Activity.

HIV-1 infection of noncycling cells, such as dendritic cells (DCs), is impaired due to limited availability of deoxynucleoside triphosphates (dNTPs), which are needed for HIV-1 reverse transcription. The levels of dNTPs are tightly regulated during the cell cycle and depend on the balance between dNTP biosynthesis and degradation. SAMHD1 potently blocks HIV-1 replication in DCs, although the underlying mechanism is still unclear.