Biomarkers of Inflammation (CRP, IL-6), coagulation (D-dimer), and tissue fibrosis (HA) measured pre-ART and at 1 month are associated with higher risk of AIDS events, IRIS, or death, warranting additional study as risk stratification strategies.

Purpose of review-HIV and pathogenic SIV infection are characterized by chronic immune activation. This review addresses the factors that influence immune activation and may thus determine the rate of disease progression during the asymptomatic period of HIV.Recent findings-Immune activation stems from foreign antigen stimulation including HIV, microbial products and co-infections, and compensatory homeostatic mechanisms. Continuous immune stimulation creates a permissive environment for further viral replication, while temporarily allowing successful replenishment of the T cell pool. Type I IFN, microbial translocation, activated (but ineffective) effector T cells, unruly regulatory T cells and inadequate Th17 cells all play important roles in the cycle of activation, functional exhaustion and T cell death that leads to immunodeficiency.Summary-The asymptomatic chronic phase of HIV infection is a dynamic balance between host and virus, the outcome of which determines an individual's course of disease. Evaluation of the factors that determine the immunologic threshold of disease progression could assist in designing therapeutic strategies including individualized timing of ART.

HIV infection alters the natural history of several cancers, in large part due to its effect on the immune system. Immune function in people living with HIV may vary from normal to highly dysfunctional and is largely dependent on the timing of initiation (and continuation) of effective antiretroviral therapy (ART). An individual's level of immune function in turn affects their cancer risk, management, and outcomes. HIV-associated lymphocytopenia and immune dysregulation permit immune evasion of oncogenic viruses and premalignant lesions and are associated with inferior outcomes in people with established cancers. Various types of immunotherapy, including monoclonal antibodies, interferon, cytokines, immunomodulatory drugs, allogeneic hematopoietic stem cell transplant, and most importantly ART have shown efficacy in HIV-related cancer. Emerging data suggest that checkpoint inhibitors targeting the PD-1/PD-L1 pathway can be safe and effective in people with HIV and cancer. Furthermore, some cancer immunotherapies may also affect HIV persistence by influencing HIV latency and HIV-specific immunity. Studying immunotherapy in people with HIV and cancer will advance clinical care of all people living with HIV and presents a unique opportunity to gain insight into mechanisms for HIV eradication.

These data suggest that diminished responsiveness to IL-7 in CD4 and CD8 T cells during ICL may be contributing to the dysregulation of T-cell homeostasis.