Parasitic worm increases HIV infection risk

Monkeys infected with schistosomes (parasitic worms common in Africa) were substantially more susceptible to infection with a simian equivalent of HIV than those without the worm, researchers have found. They say their findings suggest that control of helminth infections may be a useful public health intervention to help decrease the spread of HIV.

Schistosomiasis and other parasite, or helminth, infections have been shown to shift the immune response to HIV in ways that encourage HIV replication in people already infected, but studies have shown mixed results concerning the effect of treating helminth infections on HIV levels in the blood (see 2008 and 2005 reports).

The effect of a helminth infection on susceptibility to HIV infection has not been previously studied, but there are good reasons to believe that such infections may make individuals more vulnerable, by persistently activating the immune system and expanding the pool of cells vulnerable to HIV infection. This effect is distinct from the vulnerability to HIV infection due to genital lesions caused by schistosomiasis reported in a 2006 study carried out in Zimbabwe.

This study, carried out by the US Centers for Disease Control, Harvard Medical School and the Dana-Farber Cancer Institute, used rhesus macaques infected with Schistosoma mansoni to test the infectivity of different doses of SHIV, a form of HIV adapted to infect monkeys. The particular variant used, from HIV-1 subtype C, was engineered to enhance replication. These macaques were compared with macaques uninfected with Schistosoma.

The macaques were rectally challenged with SHIV doses that ranged from a dilution of 1 part in 1000 through to neat virus, and viral load was then measured during 20 weeks of follow-up.

The researchers found that the average infectious dose of SHIV for animals infected with schistosoma was 17-fold lower, and the mean peak viral load was 1 log₁₀ copies/ml higher (despite a significantly lower viral inoculum leading to systemic infection) (p

The authors say that their findings confirm that it is the host, and not the amount of virus that causes infection, that determines the severity of primary HIV infection.

A limitation of the study, they say, is that it only models the effect of acute schistosomiasis infection on SHIV susceptibility (the macaques were infected seven weeks prior to SHIV exposure) and does not reflect what might happen in the later, chronic phase of infection when the immune system is less profoundly activated.

The authors say that their findings “strengthen the hypothesis that helminth infection may be a risk factor for increased susceptibility to HIV infection, and support control of schistosomiasis and perhaps other helminths in persons living in areas endemic for these parasites…as a public health intervention for individuals at risk for acquiring HIV-1.”

Professor Ruth Ruprecht of Harvard Medical School told aidsmap.com by e-mail that studies to prove the HIV prevention benefit might be difficult to design however. It would not be possible, for instance, to carry out a randomised study in which some communities received delayed treatment for helminth infections.

"Because of ethical considerations, helminth infections in people need to be treated upon diagnosis," she noted. "Therefore, their impact on HIV transmission would be difficult to assess. Furthermore, people living in areas where parasite infections are endemic are exposed to other potential pathogens associated with lack of adequate infrastructure and poverty, which could render the interpretation of clinical studies a challenge. In our view, primate model studies can fill an important gap and provide answers that are hard to obtain through clinical studies."