Immunotherapy of Chronic Hepatitis C Virus Infection with Antibodies against Programmed Cell Death-1 (PD-1) Blockade of PD-1 signaling improves in vitro proliferation of hepatitis C virus (HCV)-specific T lymphocytes, but whether antiviral function can be restored in infected individuals is unknown. To address this question, chimpanzees with persistent HCV infection were treated with anti-PD-1 antibodies. [Proc Natl Acad Sci USA] Abstract Parasite Infections in Multiple Sclerosis Modulate Immune Responses through a Retinoic Acid-Dependent Pathway Researchers evaluated the role of TLR2 and retinoic acid (RA) in parasite-driven protection in multiple sclerosis (MS) patients. RA serum levels were significantly higher in helminth-infected MS patients than in uninfected MS subjects or healthy controls. [J Immunol] Abstract Human Dendritic Cells Transfected with a Human Papilloma Virus-18 Construct Display Decreased Mobility and Upregulated Cytokine Production The authors examined the response of human dendritic cells transfected with a construct containing the human papilloma virus-18 genome and their subsequent expression of papilloma virus proteins. [Int J Oncol] Abstract HBcAg-Specific IL-21 Producing-CD4+T Cells Are Associated with Relative Viral Control in Patients with Chronic Hepatitis B Researchers investigated the role of interleukin (IL)-21-producing CD4+T cell response in viral control of hepatitis B virus infection. HBcAg -specific interleukin-21-producing CD4+T cells in blood were detected in patients with hepatitis B virus infection. [Scand J Immunol] Abstract HIV IL-7 Modulates In Vitro and In Vivo Human Memory T Regulatory Cell Functions through the CD39/ATP Axis The authors provide evidence that IL-7 exerts a synergistic effect through downmodulation of the ectoenzyme CD39, which converts ATP to ADP/AMP, and an increase in ATP receptor P2X7. Both effects lead to an increase in the ATP-mediated effect, tipping the balance to favor Th17 conversion. Using an IL-7 therapeutic study, they showed that IL-7 exerts the same effects in vitro and in vivo in HIV-infected individuals. [J Immunol] Abstract Gag-Dependent Enrichment of HIV-1 RNA near the Uropod Membrane of Polarized T Cells Using live-cell fluorescent microscopy, the authors demonstrated that full-length HIV-1 RNA is enriched at the uropod membrane; furthermore, the presence of HIV-1 Gag containing a functional nucleocapsid domain is necessary for this HIV-1 RNA enrichment. [J Virol] Abstract Effects of Cellular Activation on Anti-HIV-1 Restriction Factor Expression Profile in Primary Cells Scientists hypothesized that cellular activation modulates host restriction and susceptibility to HIV-1 infection. They measured the gene expression of 34 antiviral factors in healthy PBMC. [J Virol] Abstract Priming with Recombinant Auxotrophic BCG Expressing HIV-1 Gag, RT and Gp120 and Boosting with Recombinant MVA Induces a Robust T Cell Response in Mice The recombinant BCG vaccines tested in this study were able to prime the immune system for a boost with rMVA expressing matching antigens, inducing robust, HIV-specific T cell responses to both dominant and subdominant epitopes in the individual proteins when used as individual vaccines or in a mix. [PLoS One] Full Article Harnessing the CRISPR/Cas9 System to Disrupt Latent HIV-1 Provirus Researchers showed the potential of the CRISPR/Cas9 system to edit the HIV-1 genome and block its expression. When LTR-targeting CRISPR/Cas9 components were transfected into HIV-1 LTR expression-dormant and -inducible T cells, a significant loss of LTR-driven expression was observed after stimulation. [Sci Rep] Full Article The Majority of HIV-1 DNA in Circulating CD4+ T Lymphocytes Is Present in Non-Gut Homing Resting Memory CD4+ T Cells Memory CD4+ T lymphocytes in peripheral blood that express integrins α4ß7 preferentially recirculate through gut-associated lymphoid tissue (GALT), a proposed site of significant HIV-1 replication. Tregs and activated CD4+ T cells in GALT could also be particularly susceptible to infection. Scientists therefore hypothesized that infection of these subsets of memory CD4+ T cells may contribute disproportionately to the HIV-1 reservoir. [AIDS Res Hum Retroviruses] Abstract |