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UCSF/Gladstone Finding May Explain HIV'S Ability To Infect Cells Lacking The Key Target Of HIV: The CD4 Receptor

ese cells, when infected, may be the underlying cause of some lethal HIV-associated diseases, including HIV-associated dementia and HIV-associated cardiomyopathy, or death of heart muscle.

Moreover, there is concern that reservoirs of latent or persistent virus may reside in cells that are protected from detection by the immune system, and that these hidden pools of virus may be less susceptible to the combinations of drugs currently used to combat HIV infection, known as highly active anti-retroviral therapy, or HAART.

CD4-negative cells, said Goldsmith, may be more apt to harbor sequestered HIV than CD4-positive cells, as the latter circulate in the blood and are fairly susceptible to HAART therapy.

To determine how HIV infects CD4-negative cells, the researchers developed a culture system in which various CD4-positive cells lacking the CCR5 receptor were mixed with CD4-negative cells expressing CCR5. Then, after verifying that neither cell type alone could be infected, the researchers exposed the cells to strains of HIV that are known to use CCR5 as a co-receptor.

The result, infection of both cell types, indicated that cooperative interaction between the co-mingled cell types could create an effective viral receptor complex.

"We observed that the CD4 receptor and a co-receptor do not need to be displayed together on target cell surfaces to be engaged by HIV, and that they can cooperate as an effective viral receptor complex," said Goldsmith. The team determined that successful infection depended on the presence of both CD4 and CCR5 (or CXCR4, another co-receptor that is sometimes used by HIV), and required physical proximity of the cells.

The researchers subsequently carried out tests aimed at documenting, and pinpointing, the underlying molecular interaction.

In doing so, they sought to determine whether the extra-cellular portion of CD4, in the form of soluble CD4, was itself sufficient to represent the CD4-positive cell in thes
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Contact: Jennifer O'Brien
jobrien@itsa.ucsf.edu
415-476-2557
University of California - San Francisco
5-Feb-1999


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