"We observed a 1.4 log₁₀ decline in HIV among all the children with detectable viral loads, and no rebound of virus in children whose viral loads were suppressed to undetectable levels by antiretroviral therapy," said Theodore Ruel, MD, fellow in paediatric infectious diseases, University of California, San Francisco, California, United States.

"Our data, taking advantage of continuous monitoring of participants in the Children with HIV And Malaria Program (CHAMP) in Uganda, demonstrates the suppression of circulating HIV viral load by measles infection is universal and profound, but transient," Dr. Ruel said in his poster presentation on February 28^th.

His observations mirrored those reported earlier by William Moss (J Infect Dis. 2002;186(7):879-87).

In CHAMP, doctors are looking at various HIV parameters, including viral load, CD4-positive cell counts and other measures. During the course of the project 15 children have come down with measles. But instead of causing further deterioration in the children's immune systems, during the bouts of measles which lasted as long as 10 days, the viral loads decreased dramatically in patients on antiretroviral therapy and in those not on treatment.

For example, 1 child had an HIV viral load of 393,529 cells/mL before the child came down with the measles. During the measles infection period the HIV viral load was 5,029 cells/mL. After the child recovered from the measles, the HIV viral load rebounded to 300,489 cells/mL, Dr. Ruel said.

Another child -- who was receiving antiretroviral drugs -- had a viral load of 42,826 before getting measles; 612 cells/mL during the bout with measles and 445 cells/mL after the measles. This patient had begun antiretroviral treatment before getting measles.

Dr. Ruel said that measles apparently did not interfere with antiretroviral therapy.

He and other researchers are actively trying to understand the reasons why measles coinfection appears to stop or dramatically slow HIV replication. He said in vitro experiments show that measles coinfection stops HIV replication but does not kill the virus.

He suggested that scientific pursuit of the mechanism causing that change in replication could result in a future pharmaceutical in the fight against HIV/AIDS.


[Presentation title: Dramatic Reduction in HIV RNA Among HIV-Infected Children With Acute Measles in Uganda. Abstract 707]

Copyright © 2009 P\S\L Consulting Group Inc. All rights reserved. Republication or redistribution of P\S\L content is expressly prohibited without the prior written consent of P\S\L. P\S\L shall not be liable for any errors, omissions or delays in this content or any other content on its sites, newsletters or other publications, nor for any decisions or actions taken in reliance on such content.