HIV’s Jump From Apes to Humans May Have Been Aided by an Unfortunate Deficiency

How it all started.

Nobody really knows when it exactly happened. But at some point in the past past, a chimpanzee version of a pathogen that is commonly known as simian immunodeficiency virus has somehow started infecting humans.

It appears that mutations in simian Immunodeficiency virus have turn it into the (HIV-1) human immunodeficiency virus, which is responsible for the AIDS epidemic, speaking in global terms. There is a new research that is suggesting there should have been a group of proteins that would have protected us from this insidious infection, which is raising the question – how did it really happen?

An international crew that is led by scientists straight from the Heinrich-Heine-Universität Düsseldorf have recently made a research on how a specific group of proteins that is commonly known as cellular cytidine deaminases can offer humans some kind of protection from the virus that is attacking apes.

More specifically, the researched were focusing on some variants of a gene that is responsible for the cytidine deaminase and its role in terms of the replication and therefore – possible transmission of the chimpanzee-specific virus.

The first AIDS patient in the US were reported back in the early 1080s and since then, this epidemic is a huge problem.

Even if scientists are able to show a specific link with the simian version of the immunodefieciency virus, so far we can only speculate when and how exactly the virus managed to leap from apes to humans.

There is a chance that this transmission was passed through infected blood from meat, most likely captured for food. This happened a while back, since the virus had all this time to evolve into its current and very dangerous form.

What exactly happened at that first moment – mutations or just unfortunate series of events, is still, of course, just a mystery. Finally, now there is a study that may shed some light on this topic.

It is commonly known that a3H cytidine deaminase proteins have restricted the replication of the family of viruses of which both HIV and SIV belong to.

In general, these kinds of viruses are able to create a secret weapon of their own – a protective virulence factor that is commonly known as vif, but it doesn’t really work well against all the different version of these anti-viral proteins.

In order to determine the extent of the proteins potential virus-busting powers, the scientists had to infect human kidney cells with easily traced simian viruses from many various sources and later they also dosed these cells with genes in ordet to make human or chimpanzee anti-viral proteins.

One specific humanA3 protein (the a3H haplotype) appears to be different from the others because it was showed that it is particularly resistant to the virus’s vif.

Looking back in the data from the Great Ape Genome Project, it appears that chimpanzee version of A3H was much less diverse than the human one.

And even more, there were some experiments that have shown that vif from chimpanzee and gorilla SIV could still interfere with the chimpanzee A3H.

When we take all of this into consideration, it makes a compelling case for the hypothesis that humans somehow evolved a solid defence against SIV.

While humans evolved some remarkable versions of APOBEC that are offering protection from the SIVcpz, it is more likely that some individuals may lack that specific protection, or at least they are possessing a more weak or unstable version of it.

This piece of the puzzle will be added in the collection and definitely will be taken into consideration in the future research regarding the relationship between cytidine deaminase and HIV – which hopefully will led finally providing some answers on this topic.


Click to comment

You must be logged in to post a comment Login

Leave a Reply

To Top
%d bloggers like this: