Researchers find cell protein that nips HIV in the bud

By Enrique Rivero

UCLA researchers have found that a key protein in the body's dendritic cells can stop the virus that causes AIDS from "budding" — part of the virus' life cycle that is crucial to its ability to replicate and infect other cells.

The study, scheduled for publication in the April issue of the Federation of American Societies for Experimental Biology's FASEB Journal, is currently available here.

"If we can block virus generation, then we can control the disease," said lead author Shen Pang, associate professor in the division of oral biology and medicine at the UCLA School of Dentistry and a member of the UCLA AIDS Institute.

Dendritic cells are specialized white blood cells in the skin, mucosa and lymph nodes that kick-start a primary immune response to foreign invaders by activating lymphocytes, including the T cells that HIV targets. Though dendritic cells can be infected with HIV — and indeed play a crucial role in transmitting the virus to T cells — studies have shown that viral generation from these cells is nearly a hundred times lower than from infected T cells, indicating that the cells may possess some inhibiting property.

Pang hypothesized that DC-SIGN, a protein expressed in dendritic cells, may be responsible for such inhibition. He and his colleagues found that DC-SIGN and a related protein, DC-SIGNR, both demonstrated 95 percent to 99.5 percent inhibition of viral production from host cells.

"The strong inhibition of viral production by DC-SIGN suggests the possibility of using this protein for treatment of HIV-infected patients," the researchers write. "Expression of this protein in various CD4-positive cells should inhibit viral production from infected cells. Because it can also enhance the immune response, DC-SIGN is expected to be useful for in vivo studies for developing an HIV vaccine."

This study was supported by the UCLA AIDS Institute, the UCLA School of Dentistry and a grant from the National Institutes of Health.