Persistently raised genital inflammation increases HIV risk

31 May 2015

Research conducted by the mucosal immunology team at CAPRISA indicates that  the risk of HIV acquisition in a cohort of South African women was significantly higher in those with persistently raised genital inflammatory cytokine concentrations (including HIV target cell-recruiting chemokines MIP-1α, MIP-1β and IP-10).

This study, which was led by Dr Lindi Masson, aimed to  investigated whether genital inflammation influenced HIV acquisition.

Twelve selected cytokines, including 9 inflammatory cytokines and chemokines (IL-1α, IL-1β, IL-6, TNF-α, IL-8, IP-10, MCP-1, MIP-1α, MIP-1β), hematopoeitic IL-7 and GM-CSF, and regulatory IL-10 were measured prior to HIV infection in cervicovaginal lavages from 58 HIV seroconvertors and 58 matched uninfected controls and plasma from a subset of 107 of these women from the CAPRISA 004 tenofovir gel trial.

HIV seroconversion was associated with raised genital inflammatory cytokines (including chemokines MIP-1α, MIP-1β and IP-10). The risk of HIV acquisition was significantly higher in women with evidence of genital inflammation, defined by at least 5 of 9 inflammatory cytokines being raised [OR 3.2; 95% confidence interval 1.3-7.9; p=0.014] (Figure). Genital cytokine concentrations were persistently raised (for about one year before infection), with no readily identifiable cause despite extensive investigation of several potential factors, including sexually transmitted infections (STIs) and systemic cytokines.

While a fraction of the genital inflammation may be attributed to asymptomatic STIs, the dominant cause of genital inflammation remains to be elucidated. Treatment of asymptomatic STIs and
topical agents to modulate inflammation are potentially important mechanisms for reducing susceptibility to HIV infection,
especially in young women, where the epidemic is most severe in Africa.

For further reading see:
Masson L, et al. Genital inflammation and the risk of HIV acquisition in women. Clinical Infectious Diseases 2015 ; DOI: 10.1093/cid/civ298