HIV 'Cloaking Device' Hinders Its Ability to Replicate

The Human Immunodeficiency Virus (HIV) is one of the most dangerous and widespread in the world today, and its basic survival tactic is to “cloak” itself from the immune system, so as not to get detected. It does that by mutating extensively and over short periods of time and first attacking the fighter-cells in the blood. After it “hijacks” them, it's free to mutate again and take over even more of the body. Still, a new research, published in the April 13th issue of the Journal of Experimental Medicine, shows that extensive mutations are detrimental to the virus itself, as it loses its ability to replicate properly.

The research paper, which was first published online on March 23rd, shows that the differences that exist between people's individual immune systems are a very important factor in determining how HIV acts in the long run. Basically, the first line of defense against the pathogen is a complex of human immune proteins called HLA (human leukocyte antigen). They scrap off little pieces of the virus and then “show” them to killer T cells, which subsequently do what they do best.

But, in individuals with certain variations of the HLA complex, especially in those with HLA-B*5703, killer T cells act several times faster than in others. This means that the virus has to mutate very fast in order to avoid being destroyed. It does that by changing three of its internal amino-acids, whose succession helps the immune system cells realize which cell is infected and which is not. After the process is complete, the virus is again free of its followers and ready to replicate.

However, the problem is that it can no longer do it at very high speeds. The mutation, coupled with the fact that HIV now lives in an HLA-B*5703-filled environment, causes it to replicate up to 20 times slower than in ideal conditions, in the laboratory. In charge of the study that has revealed this amazing trait of the virus has been a team of researchers from the University of Oxford, led by renown expert Hayley Crawford.

While studying the effects of the HLA complex on the virus, Crawford noticed that, if the virus was transmitted from an HLA-B*5703 person to another one with some other HLA configuration, then it would backtrack its own steps, renouncing the three mutated amino-acids and reverting to its original form. This was the virus' way of letting the researchers know that it no longer feared the new host's immune system.