HIV: ART and Immune Activation

Dear Colleagues,

Antiretroviral therapy (ART) has greatly reduced HIV infection-associated morbidity and mortality. ART improved the lifespan of persons living with HIV infection by reducing viral replication, restoring CD4+ T cells and preventing the progression of HIV infection to acquired immunodeficiency syndrome (AIDS). However, despite long-term ART, low level of viral replication persists in HIV reservoirs residing in resting CD4+ T cells in the blood, central nervous system (CNS), gut-associated lymphoid tissue, bone marrow, and genital tract. Persisting low level viral replication in the ART controlled patients can contribute to sustained systemic immune activation and inflammation. ART reduces systemic inflammation and immune activation dramatically, but not to levels synchronous with HIV-uninfected populations. HIV proteins such as gp120 and Tat, secreted from HIV reservoirs, are capable of inducing generation of reactive oxygen species (ROS) which in turn can initiate immune activation/inflammation via production of cytokines and chemokines. Chronic inflammation has the potential to attenuate the efficacy of ART as well as promote pathological conditions and end-organ disease in HIV patients. Indeed in HIV patients on long-term ART, inflammation has been linked to cardiovascular disease (CVD), neurocognitive dysfunction, osteoporosis, cancer, muscle wasting, premature aging and frailty among others. 

In this special issue we will focus on molecular mechanisms underlying persisting immune activation and inflammation in ART suppressed HIV infected patients, and also that are affecting various end-organ functions. Such comprehensive issue will deliver an overall understanding on the effect of inflammation on HIV and ART related diseases, and provide prospect for the development of therapeutics.   

Assoc. Prof. Santhi Gorantla
Prof. Larisa Poluektova
Guest Editors

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