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 online at www.fasebj.org/cgi/rapidpdf/fj.07-9443comv3.pdf.
"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.
Very few cells are infected when HIV first enters the human body, but the virus rapidly creates new copies of itself, which in turn infect more cells. To achieve this, the virus, after infecting a cell, sends envelopes of protein to the cell's membrane. The viral genomes then combine with viral structural proteins and move into these envelopes. The envelopes bubble, or bud, outward, releasing viral particles that will infect more cells and start new viral life cycles.