Parasitic infections have no effect on HIV levels in adults in Malawi.

Parasitic infections, particularly infections with helminths, were more common in HIV-uninfected than in HIV-infected adult outpatients, and neither helminth infections nor antiparasitic treatment had an impact on HIV viral loads, Malawian and US researchers report in a recent edition of the Journal of Infectious Diseases.

Co-infection with parasites is common in African countries with high HIV prevalence and is a common cause of morbidity and mortality among the HIV infected. There has been a long-standing concern that helminth co-infections in people living with AIDS might drive the CD4 T-lymphocyte response from a Th1 to Th2 response and cause chronic immune activation. These effects might not only combine to exacerbate the virulence of both infections but might also increase the risk of HIV transmission to sexual partners or unborn babies.

Researchers looked at HIV-positive individuals in Lilongwe, Malawi. At enrolment, patients received HIV counselling and testing including viral load determinations, stool and urine samples were collected for parasitological examinations, and a demographic and clinical questionnaire was completed. One week after enrolment, all patients returned to receive treatment for the specific identified infections. HIV-infected patients and those with parasitic co-infections returned 4 weeks after treatment. Blood samples were taken again for HIV viral loads, as were stool and urine samples for parasitological examination to ascertain treatment success.

Out of 389 patients, 266 were HIV infected. At baseline, 43% of patients had evidence of at least one parasitic infection. Most had single infections; double and polyinfections were seen in 25% and 6% of patients, respectively. The commonest helminth infection was with hookworms. Overall, HIV-uninfected patients were significantly more likely to have at least one parasitic infection including a helminth, geohelminth, schistosomiasis, hookworm, or mixed infection compared with HIV-infected patients.

Lower CD4 counts were seen in patients who were not infected with parasites. There was also no significant change in HIV RNA type by type of parasitic infection, age, sex or CD4 baseline count.

The authors point out three major limitations of the study. First, worm burdens were not quantified and lighter worm burdens may not cause the immune activation or Th1 and Th2 response that is significant enough to affect HIV replication. Second, other co-endemic infections such as malaria and tuberculosis were not investigated and these are known to have an effect on HIV replication. Third, faecal stool samples may not have been enough to detect helminth infection. A more sensitive antigen detection technique would have been better. However, the study does suggest that treating parasitic infections will have no specific effect on HIV replication.

Hosseinipour M, et al. J Infect Dis 2007; 195: 1278-1282.