A weakened immune response resulting from HIV infection can lead to trouble when it comes to treating malaria, according to a new study appearing in the Oct. 1 issue of The Journal of Infectious Diseases, now available online.
"Our study demonstrates that HIV-1 infected patients with suppressed immunity represent, next to children and pregnant women, an additional vulnerable group for malaria," says Jean-Pierre Van geertruyden, MD, MSc, lead author of the article.
CD4 lymphocytes, white blood cells that serve a critical role in the immune response to malaria, are also the prime target for HIV. Low CD4 cell counts are a characteristic of HIV-induced immune suppression. In this study, Dr. Van geertruyden and colleagues from the Institute of Tropical Medicine in Belgium and the Tropical Disease Research Center in Zambia show that HIV-positive patients with low CD4 cell counts tended to have an increased risk of malaria treatment failure when compared to both HIV-negative patients and HIV-positive patients with higher CD4 cell counts.
Therefore, "HIV-1 associated immune suppression, rather than infection with HIV-1 per se, is the main determinant of malaria treatment outcome," says Dr. Van geertruyden.
This finding exposes a danger that implementing new malaria combination therapies to treat the disease in immune-suppressed patients could lead to the emergence and spread of antimalarial drug resistance. "This is a major concern, as antimalarial drug resistance is now generally acknowledged to be one of the greatest threats to our ability to roll back malaria," according to Dr. Van geertruyden.
The study suggests that malaria control and prevention, next to early diagnosis and a highly efficacious malaria treatment, are essential tools in areas where both diseases coexist. Furthermore, the interaction between antimalarial and antiretroviral therapies should continue to be examined in an effort to maximize the effects of
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Contact: Steve Baragona
sbaragona@idsociety.org
703-299-0412
Infectious Diseases Society of America
7-Sep-2006