Hessell and ONPRC team discovers antibody treatment that halts SHIV infection in infant macaques

This post has been updated with proper author attribution.

OHSU researchers at the Oregon National Primate Research Center have shown that early short-term treatment with human anti-HIV1-1 monoclonal antibodies halts simian HIV infection, a chimeric virus that shares key properties with HIV,  in infant macaques. The study, published March 21 in Nature Medicine, shows that antibodies given to a baby macaque within 24 hours after being exposed to simian HIV can clear the virus completely, a discovery that paves the way for future therapies to prevent mother to child transmission of HIV.

(Left to Right) Don Siess, Michael Axthelm, Ann Hessell, Christoph Kahl, Alfred Legasse, Jeffrey Stanton, Byung Park, David Burke

(Left to Right) Don Siess, Michael Axthelm, Ann Hessell, Christoph Kahl, Alfred Legasse, Jeffrey Stanton, Byung Park, David Burke

Transmission of HIV from mother to child remains the most common way for children to become infected. Current therapeutic standards include treating HIV-positive pregnant women with antiretroviral therapy during pregnancy and birth while babies born to these women receive HIV medicine for 6 weeks after birth. These therapies carry health risks of their own and there are many women throughout the world who lack access to them.

In this study, Ann Hessell, Ph.D., Nancy Haigwood, Ph.D., and colleagues administered anti-HIV-1 human neutralizing monoclonal antibodies (NmAbs) subcutaneously on days 1, 4, 7 and 10 after the baby macaques were exposed to SHIV orally. The team quantified the systemic distribution of NmAb in multiple tissues within 24 hours following administration. Replicating virus was found in these tissues by day 1 in animals that did not receive antibody treatment while those treated with NmAb remained free of virus in both blood and tissue at 6-months after exposure.

Read the full media release.

The study was funded by U.S. Public Health Service grants from the National Institutes of Health and the Eunice Kennedy Shriver National Institute of Child Health and Human Development: R01-HD080459 (N.L.H) and P51-OD011092 (J. Robertson), P51-OD011092 pilot funding, (E.E.); the Elizabeth Glaser Pediatric AIDS Foundation (N.L.H.); and The Foundation for AIDS Research (amfAR) 108823-55-RGRL (N.L.H.).

This work also was funded, in part, by the intramural research program of the Vaccine Research Center, and of the Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Division of Health & Human Services, U.S. Public Health Service.

 

 

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About the Author

Julie Rogers is Research Development Associate in the Office of Research Funding & Development Services.

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