@Sellah
All the HAART drugs target a protein of the virus. Proteins are expressed on active cells. Resting cells are the fraction that harbours the intergrated provirus, in their inactive site they are "out of the radar". Currently i am working on cloning the cytoplasmic domain of the envelope that is responsible for retrograde transport from the cell surface to the trans golgi network that making the HIV - virus a master of disguise......... hiding itself from the immune surveillance of the body.

@ Intelligentsia…. Viruses including HIV survive in hosts, some hosts are compatible while others are not. In that case mosquitoes are not compatible hosts for HIV... period. But a point of information which may be useful. Worldwide infection rate with HIV-1 is estimated at 14,000 per day but millions are exposed to the virus and this may be explained by thousands of discordant couples where the virus has a chance to infect but it does not. Transmission probability per exposure event explains why HIV is transmitted with moderate efficiency (1 in 200-1 in 2000) by heterosexual sex and apparently greater efficiency through the intestinal tract @ 1 in 20-1 in 300 via semen and upto 95 in 100 in drug users via contaminated sharps.

For a HIV infection to be productive and systemic three factors are very critical (i) Viral load of the donor, in this case millions of sperms implies greater genetic diversity hence increased chances (fitness) because out of the millions very few perhaps only one seed the infection. (ii) Availability of target cells at the site of infection. (iii) Cellular phenotype (Naïve or memory) with HIV preferring memory in most mucosal sites (vagina and rectum).

@ mburuke: Immunosuppressants + HAART combinations has been proposed to decrease the activation of CD4+ T cells and reduce their susceptibility to viral infection and replication with a cyclosporine A producing interesting results in a controlled clinical trial. However, drug withdrawal causes viral load to return to basal levels. But my position is that general use of immunosuppressants is not justified because of their toxicity.

On the same note, In the laboratory (in vitro) we can design miRNAs which could be involved in maintaining HIV latency or in controlling low ongoing viral replication. However, the dynamics in human body are completely different. HIV dominates the proceedings through strategies that overcome the cellular miRNA restriction machinery or enhance the expression of certain favourable miRNAs to achieve its replication.

By the way, as at dec 2009 we had 25 different active compounds belonging to 6 different drug families that have been developed and approved. However, regardless of the use of all these, a cure is NOT YET ACHIEVABLE.