Highly active antiretroviral therapy (HAART) to immobilize key HIV enzymes such as reverse transcriptase and protease has improved the condition of many HIV infected. However, with the advent of drug resistant HIV variants, it has become imperative to identify alternate targets.
New research1 seeking to unravel the mechanism by which the envelope protein of HIV-1 assembles into infectious virus particles, has provided some answers. Researchers say the 'Gag' protein of HIV-1 by acting as cargo transport intermediate, carries the envelope protein and assembles them into budding virions that act as the infectious agents.
The Gag protein takes the trans-golgi route sorting into domains of lipid rafts enabling the assembly of the virions in primary CD4+ T cells. Lipid rafts are small groups of lipids and cholesterol on the cell surface of the infected primary CD4+ T cells that are natural targets of HIV-1 in vivo.
"We envisage that compounds that would interfere in the gag-envelope interaction will lead to the abolition of HIV-1 envelope assembly into budding virus particles. This will lead to production of defective infectious virus particles and limit virus entry," says lead researcher Jayanta Bhattacharya.