Just when you think it couldn’t get any worse, well, it does. A new variant of HIV spotted in Cuba, which is more aggressive that the former versions of the deadly virus, has recently been documented by researchers in a paper published in the journal EBioMedicine.
Generally, HIV spreads around the body gradually, until the person suffers from AIDS years later. This implies that, generally, he leads a normal life for some years after infection. But, the new variant progresses to AIDS so fast that symptoms begin to appear 3 years after being infected.
How does such an aggressive variant come into existence?
A person might become infected with several strains of the virus. This can happen as a result of promiscuity, gaining different strains from different people. When this happens, the strains recombine in the body of the host to form a new HIV variant, recombinant HIV. This is how the new Cuban variant of HIV has been formed.
How does the recombinant HIV work?
For the virus to infect the cells, it has to attach itself to proteins called co-receptors found on the cell surface membranes. During the first stages of infection, the HIV anchors onto the protein known as CCR5 – at this point, the infected individual is able to lead a relatively normal life. It only begins to stick to another co-receptor called CXCR4 years later, and this triggers a faster progression to AIDS.
The new variant diverts from the usual development of events and shifts to CXCR4 soon after infection. This causes the progression to AIDS to be initiated earlier than normal. The health condition of the infected person thus greatly deteriorates a little while after infection.
The transition from CCR5 to CXCR4
The blood of patients who went through the normal stages of HIV infection and of those who were infected with the recombinant virus were compared to find out the discrepancies between the two groups.
It was found that those with the new Cuban variant had abnormal levels of the virus in their blood. Furthermore, they also had high concentrations of defensive molecules known as RANTES which bind to CCR5 as an immune response. The researchers interpreted this as possibly meaning that the RANTES molecules anchored onto the CCR5 such that the HIV could not compete with their great number. As a consequence, the HIV shifted to the CXCR4 when not being able to anchor onto the CCR5.
Another of the findings of the researchers entailed an enzyme known as protease. This was suggested to ease the transition to the CXCR4 as the protease cleaves proteins in viruses allowing them to replicate more and more.