AIDSWEEKLY Plus; Monday, December 7, 1998
Daniel J. DeNoon, Senior Editor
The virus infecting the animals could be passaged in vivo. However, it established only low-level, nonpathogenic infections. But the findings provide hope for an inexpensive new animal model for AIDS.
To this end the researchers are hoping to develop lines of transgenic cotton rats.
"Transgenic mice expressing human CD4, CXCR4, and CCR5 are made more permissible for HIV-1 entry and genomic incorporation of the provirus," wrote Raymond J. Langley of Virion Systems Inc., Rockville, Maryland, and colleagues. "Similar approaches in expressing the necessary coreceptors on the surface of cotton rat cells could lead to an improvement of the model and provide a platform with which to establish a reliable, reproducible, inexpensive, and accessible inbred rodent laboratory host to study aspects of HIV infection conveniently in vivo."
They reported their findings in the Proceedings of the National Academy of Sciences ("HIV Type 1 Infection of the Cotton Rat (Sigmodon fulviventer and S. hispidus," PNAS, 1998;95:14355-60).
The cotton rat can be infected with a wide range of human pathogens and has been a valuable animal model in the study of poliovirus, respiratory syncytial virus (RSV), influenza A and B viruses, parainfluenza virus, adenovirus, typhus, and filariasis.
Langley and colleagues found that among cotton rat species, Sigmodon fulviventer was more susceptible to HIV-1 than S. hispidus.
Up to three serial passages from animal to animal was possible. After infection the virus could be detected only as provirus and viral burden never exceeded the relatively low level of one provirus per 1.8x105 cotton-rat peripheral blood mononuclear cells (PBMC).
Animals responded to infection with an anti-HIV antibody response that in some cases involved neutralizing antibodies. Humoral responses recognized all major HIV-1 antigens and were still present 52 weeks after infection.
This work was supported by the National Institutes of Health.
The corresponding author for this study is Harold S. Ginsberg, Laboratory of Infectious Diseases, Immunodeficiency Viruses Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Twinbrook II, 12441 Parklawn Drive, Rockville, Maryland 20852. Email: <hginsberg@atlas.niaid.nih.gov>.
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