Even after intense anti-viral treatment, HIV-1 can still lurk in inactive cells in the human body, only to reappear at a later date. New research in this week's Nature (Vol. 424, No. 6945, dated 10 July 2003, pp. 213-219) shows how viruses can create these reservoirs and infect inactive T cells.
Three cell types are involved in the process, according to Mario Stevenson and colleagues. First of all, HIV-1 infects a macrophage, causing it to produce a key viral protein, called Nef. The macrophage then releases at least two soluble factors, which stimulate another component of the immune system - nearby B cells. When these cells come into contact with non-cell-cycling T cells, the T cells become susceptible to HIV-1 infection.
"Nef is a key viral protein in disease induction in vivo by both HIV-1 and SIV, acting in the pathway that induces changes in the activation of an infected cell," says Roger J. Pomerantz in an accompanying News and Views article. "So Nef seems to engage in molecular piracy, taking over an existing cellular pathway and allowing HIV-1 to replicate in T cells in diverse activation states," he adds.
(University of Massachusetts Medical School, Worcester, MA, USA)
Tel: +1 508 856 4582
Roger J. Pomerantz
(Thomas Jefferson University, Philadelphia, PA, USA)
Tel: +1 215 503 8575
(C) Nature press release.
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