Below the belt: new insights into potential complications of HIV-1/schistosome coinfections

Purpose of review Areas of the world with high endemnicity for helminth parasites overlap with those regions that have a seemingly disproportionate prevalence of HIV/AIDS. This has fueled speculation that potential pathological interactions between these infectious agents may accelerate disease progression. The proximity of many helminth infections to gastrointestinal mucosal sites combined with the recent discovery that acute HIV-1 infection causes early and massive depletion of CD4(+) T cells in the gut furthers the potential pathological significance of co-infection. In this review, the 'gut wrenching' consequences of schistosome infection on HIV disease progression that may ensue during coinfection are considered. Recent findings Massive depletion of CD4(+) T cells in the gut during acute HIV-1 infection suggests that in addition to the administration of highly active antiretroviral therapy, limiting viral infection of susceptible cells in the gut after initial exposure may offer the best opportunity for slowing disease progression. In addition to memory T cells, mast cells, which are present in the intestinal lamina propria and upregulated in the gut during schistosome infection, have been recently described as an inducible reservoir of persistent HIV-1 infection. Summary Schistosome infections create immune environments that may accelerate HIV disease progression. Their impact on highly active antiretroviral therapy should be considered.