  
Acute malaria infection may activate latent HIV
Last Updated: 2001-04-19 14:45:20 EDT (Reuters Health)
WESTPORT, CT (Reuters Health) - Malaria infection may act as a cofactor for latent HIV reactivation, according to animal study data published in the April 15th issue of The Journal of Infectious Diseases.
Dr. Alan Sher, from the National Institutes of Health in Bethesda, Maryland, and colleagues examined changes in HIV viral mRNA and p24 protein expression after infecting HIV transgenic mice with a malaria parasite, Plasmodium chabaudi.
Spleen cells and plasma showed dramatic increases in p24 levels and HIV RNA expression 8 and 10 days after infection with P. chabaudi, the report indicates. Levels returned to near baseline values by day 15 after infection.
During recrudescence or after secondary P. chabaudi infection, however, HIV expression was not restimulated, the authors report.
Although malaria infection seemed to induce HIV activation by way of antigen-presenting cell activation rather than by T-cell activation, the researchers note, CD4+ T lymphocytes were nevertheless required for the malaria-induced HIV expression.
"Malaria is a possible cofactor in AIDS progression that warrants further analysis," Dr. Sher told Reuters Health. He suggested that research in children might prove fruitful. "The pediatric AIDS setting is most relevant," he said. "[We] would look for elevated virus in HIV-positive kids acutely infected with malaria. We would like to plan such a study with colleagues working in Gabon."
"Elucidation of the costimulatory mechanism involved is of obvious importance," the researchers say in the journal, "because it may be relevant to the pathway responsible for viral activation from latent non-CD4 reservoirs in HIV-infected persons."
J Infect Dis 2001;183:1260-1268.
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