The mechanisms by which HIV binds to and fuses with host cells are well documented, but the pathway mediating the intermediate steps between binding and fusion is murky. Now, researchers in France and Italy have teased out a signaling cascade modulated by purines that leads to fusion following HIV-1 binding.1
The findings open up a suite of new therapeutic target candidates, as inhibiting any member of the purinergic pathway impaired the replication of both standard and drug-resistant strains of the virus.
Originally, the researchers were studying whether HIV-induced alterations of a host cell's plasma membrane facilitated the process of infection.
"Recent studies had revealed that membrane stress induced by infection or other stressors stimulates ATP release. We decided to determine whether ATP was released during HIV-1 infection and what could be its precise contribution to the early steps of infection," said Jean-Luc Perfettini, a senior scientist and group leader of the apoptosis, cancer and immunity research unit at the