AIDSWEEKLY Plus, Monday, 21 April 1997
Daniel J. DeNoon, Senior Editor
A pathogenic simian immunodeficiency virus (SIV) infects cells via the same coreceptor as macrophage-tropic strains of HIV-1.
The finding suggests that HIV infectivity may depend on an extraordinarily well-conserved region of HIV. If so, the virus would likely be very limited in its ability to develop resistance to future drugs or vaccines exploiting this region.
"Human and simian CCR5 molecules are very closely related, with only four amino-acid differences in the extracellular sequences of these proteins," reported Harvard researcher Luisa Marcon and colleagues. "Both can serve as entry cofactors for HIV-1 and SIV."
Marcon et al. published their findings in the Journal of Virology ("Utilization of C-C Chemokine Receptor 5 by the Envelope Glycoproteins of a Pathogenic Simian Immunodeficiency Virus, SIVmac239," J Virol, 1997;71(3):2522-7).
When either human or simian CCR5 was expressed by CD4(+) cells, the cells were susceptible to virus entry and syncytium formation mediated by SIVmac239. SIVmac239 causes AIDS-like illness in Old World monkeys.
If there is indeed a well-conserved structure in the binding portion of the HIV envelope, it must be well hidden: genetic analysis show this to be one of the most variable parts of the virus. Indeed, this region is known as the V3 loop, with the "V" standing for "variable."
"Conserved structures in the V3 loop that are not apparent from direct examination of the primary amino acid sequence might interact with CCR5," Marcon et al. suggested. "It is also theoretically possible that completely different HIV-1 and SIVmac envelope glycoprotein regions mediate the interaction with CCR5.
This work was supported by grants AI 24755, HL51366, and AI 36162 from the National Institutes of Health; by a Center for AIDS Research grant; by a Cancer Center grant from the NIH; by an NCI National Research Science Award Training Grant (CA 09382); by an award from Istituto Superiore di Sanita and by the University of Padua; by the Rubenstein/Cable Fund at the Perlmutter Laboratory; and by gifts from the late William McCarty-Cooper, from the G. Harold and Leila Y. Mathers Charitable Foundation, and from the Friends 10.
The corresponding author for this study is Joseph Sodroski, Division of Human Retrovirology, Dana-Farber Cancer Institute, 44 Binney St., JFB 824, Boston, Massachusetts. Phone: (617) 632-3371. Fax: (617) 632-4338. Email: Joseph_Sodroski@dfci.harvard.edu.
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