Protein helps HIV avoid antiretrovirals
A protein expressed by HIV-1 has been shown to stimulate host cells in such a way that the virus is able to set up viral reservoirs and “hide” from antiretroviral therapy.
At one time it was thought that HIV-1 could attack only replicating CD4+T-cells,
but it is now known that the virus can infect T-cells even when they
are in their inactive state. HIV-1 in these cells is not destroyed by
current antiretrovirals, but forms persistent reservoirs in the body,
re-emerging when antiviral therapy stops.
Researchers from the University of Massachusetts medical school showed
that the viral protein HIV-1 Nef interacts with infected macrophages
leading to increased production of two soluble factors, sCD23 and sICAM-1.
In turn, these factors stimulate the production of surface molecules
on B-cells, which, upon contact with inactive T-cells, render the T-cells
vulnerable to HIV-1 infection. The researchers propose that it is the
activity of Nef that permits infection of resting cells by HIV-1. Interruption
of this process could inhibit the formation of cellular reservoirs of
HIV-1 cells (Nature 2003;424:213). |
