Allergy Medicine

Scientists at National Institute of Allergy and Infectious Diseases detail research in allergies

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"To address the pathogenic significance of RP-specific variants, we generated infectious molecular clones from the terminal-phase plasma of an RP macaque. Inoculation of macaques with a representative clone, SIVsmH635FC, resulted in a persistent viremia, comparable to that produced by pathogenic SIVsmE543-3, and a chronic disease with progressive loss of CD4(+) T cells. However, SIVsmH635FC did not reproduce the rapid-disease phenomenon. Molecular analyses of viruses from these macaques revealed rapid reversion to the wild-type SIVsmE543-3 sequence at two RP-specific sites and slower reversion at another three sites. SIVsmH635FC infection was not sufficient to cause rapid progression even following coinoculation with SIVsmE543-3, despite acute depletion of memory CD4(+) T cells. SIVsmH635FC competed efficiently during primary infection in the coinoculated macaques, but SIVsmE543-3 predominated after the development of SIV-specific immune responses. These data suggest that the replication fitness of the R-P variant was similar to that of SIVsmE543-3 in a naive host; however, SIVsmH635FC was at a disadvantage following the development of SIV-specific immune responses. Consistent with these findings, neutralization assays revealed that SIVsmH635FC was highly sensitive to neutralization but that the parental SIVsmE543-3 strain was highly resistant," wrote T. Kuwata and colleagues, National Institute of Allergy and Infectious Diseases.

The researchers concluded: "This study suggests that the evolution of RP-specific variants is the result of replication in a severely immunocompromised host, rather than the direct cause of rapid progression."

Kuwata and colleagues published their study in the Journal of Virology (Rapid progressor-specific variant clone of simian immunodeficiency virus replicates efficiently in vivo only in the absence of immune reponses. Journal of Virology, 2007;81(17):8891-8904).

For additional information, contact V.M. Hirsch, NIAID, Molecular Microbiology Laboratory, National Institute Health, Bldg 4, Rm B1-33, 4Center Dr., Bethesda, MD 20892, USA.

The publisher of the Journal of Virology can be contacted at: American Society Microbiology, 1752 N St. NW, Washington, DC 20036-2904, USA.

Keywords: United States, Bethesda, Allergies, Allergy Medicine, National Institute of Allergy and Infectious Diseases.

This article was prepared by Immunotherapy Weekly editors from staff and other reports. Copyright 2007, Immunotherapy Weekly via NewsRx.com.