Are Monocytes the Canary in the Coal Mine for HIV-Related Atherosclerosis?

Abstract

In the era of well-controlled human immunodeficiency virus (HIV) infections with combination antiretroviral therapy (cART), serious non-AIDS events take center stage for people living with HIV infection. This has resulted in a greater focus on research to understand the pathogenesis of these conditions, to enable identification of those at most risk, and to investigate targeted interventions in order to successfully prevent them. Cardiovascular disease (CVD), which is one such non-AIDS event, is an increasing cause of morbidity and mortality in HIV-infected people, with a reported 2-fold heightened risk compared with the general community [1]. This increased risk is likely to result from interplays between the traditional cardiac risk factors, the effects of cART medications, and the pro-inflammatory actions of HIV. In this edition of the Journal of Infectious Diseases, Kelesidis et al [2 ]t ake us another step forward toward understanding the pathogenesis of CVD in HIV infection. In a prospective study of the progression of subclinical atherosclerosis, as measured by carotid intima media thickness (cIMT), the authors showed that baseline levels of lipopolysaccharide (LPS) and soluble CD14 (sCD14) predicted greater progression of cIMT in HIV-infected adults but not in the comparable HIV-uninfected group. This was despite the fact that neither HIV infection nor cART was associated with change in cIMT. Although immune activation and in