Obesity and Fat Metabolism in HIV Infected Individuals

May 22 - 23, 2018

Background

Obesity is emerging as a critical factor in the pathogenesis of HIV and of its non-infectious co-morbidities. Conserved intracellular pathways link the biology of T cell metabolism, the immune response, and diabetes and a picture is beginning to emerge that suggests that obesity is both a consequence and a cause of immune activation. Increased immune activation is associated with the non-infectious comorbidities seen in individuals living with HIV. The origins of this chronic inflammatory condition are multifactorial, but one pathway relates to the loss of gut-associated lymphoid tissue, the disruption of the GI epithelial barrier and resultant microbial translocation. There is also a growing understanding that fat is an immunologically active tissue. HIV acts directly on adipose cells; specific HIV viral products affect adipocyte differentiation which may be independent of plasma viremia. These effects may pre-dispose individuals to the development of obesity and alter expression of pro-inflammatory cytokines. Altered expression of proinflammatory cytokines likely pre-disposes HIV-infected individuals to excess morbidity and mortality. For example, leptin, an adipokine produced by adipose tissue, has altered expression in people living with HIV and is a proinflammatory molecule with important immunological regulatory effects. Women with HIV may also be more adversely affected by these interactions than men. These discoveries have implications that stretch far beyond HIV.

Objectives

An Action Plan with specific recommendations for future obesity research in HIV
Identification of research gaps, needs, opportunities, and plans to facilitate progress and catalyze new research directions.
Knowledge exchange and the development of further collaborations and joint collaborations to advance the field.