Parasitic worm may increase susceptibility to AIDS virus
People infected with schistosomes, and possibly other parasitic worm infections, may be more likely to become infected with HIV than persons without worm infections, according to a new study. Researchers at the U.S. Centers for Disease Control and Prevention and the Dana-Farber Cancer Institute and Harvard Medical School found that the infectious dose of an HIV-like virus necessary to infect rhesus macaques was 17-fold lower in animals with acute schistosomiasis than in controls. The study represents a novel in vivo demonstration that parasitic worms increase a host’s susceptibility to becoming infected with an AIDS-causing virus. The macaques co-infected with Schistosoma mansoni also demonstrated higher peak viral loads and higher memory cell concentrations of virus, both predictors of more rapid progression to AIDS. These findings are consistent with the hypothesis that persons living in areas highly endemic for parasitic worms may also have a higher risk of acquiring HIV/AIDS. Previous studies by this and other research groups have demonstrated that presence of schistosome infections increases viral replication in animal or human hosts with established immunodeficiency virus infections. The earlier findings, combined with the increased susceptibility to AIDS virus transmission shown in this study, may have profound public health implications for areas of the world where both parasitic worms and HIV-1 are endemic.
Acute Schistosoma mansoni Infection Increases Susceptibility to Systemic SHIV Clade C Infection in Rhesus Macaques after Mucosal Virus Exposure. PLoS Negl Trop Dis 2(7): e265
Individuals living in sub-Saharan Africa represent 10% of the world’s population but almost 2/3 of all HIV-1/ AIDS cases. The disproportionate HIV-1 infection rates in this region may be linked to helminthic parasite infections that affect many individuals in the developing world. However, the hypothesis that parasite infection increases an individual’s susceptibility to HIV-1 has never been prospectively tested in a relevant in vivo model. We measured whether pre-existing infection of rhesus monkeys with a parasitic worm would facilitate systemic infection after mucosal AIDS virus exposure. Two groups of animals, one consisting of normal monkeys and the other harboring Schistosoma mansoni, were challenged intrarectally with decreasing doses of R5-tropic clade C simian-human immunodeficiency virus (SHIV-C). Systemic infection occurred in parasitized monkeys at viral doses that remained sub-infectious in normal hosts. In fact, the 50% animal infectious (AID50) SHIV-C dose was 17-fold lower in parasitized animals compared to controls (P,0.001). Coinfected animals also had significantly higher peak viral RNA loads than controls (P,0.001), as well as increased viral replication in CD4+ central memory cells (P = 0.03). Our data provide the first direct evidence that acute schistosomiasis significantly increases the risk of de novo AIDS virus acquisition, and the magnitude of the effect suggests that control of helminth infections may be a useful public health intervention to help decrease the spread of HIV-1.
Related:
- Multiple parasite infections synergize to increase the risk of anemia
- HIV treatment in Africa as successful as in Europe, if started in time
- Immune exhaustion in HIV infection
Tags: Biology, Health, HIV/AIDS, Medicine, Microbiology, Parasitology, Virology
The mechanism that makes us vulnerable to HIV once we get prior parasitic exposure with schistosomes need to be worked out too. The fact that they sometimes cause bladder cancer may hint at weakening immunity (and possible angiogenesis).