Rhesus monkeys are very interesting creatures. They achieved space exploration before we did, and it turns out they’ve also tackled the problem of how to block HIV much better than any scientist has been able to accomplish so far.
Nature has provided them with a very efficient way to defend against HIV infection, and understanding how this occurs could pave the way for designing better therapeutic interventions for humans. The key to this immunity is a protein found within the cells of these monkeys, called TRIM5α.
Strategically thinking, the best way to defend against an enemy is at the castle wall, not inside the king’s quarters. TRIM5α acts in this way, fighting HIV just after it enters the cell, before it has the chance to make its way to the inner sanctum of the cell—the nucleus—where the genetic material that codes for every component of the organism resides.
HIV’s “goal” is to insert a copy of its genetic material into the DNA of the monkey or human host that it is infecting. Once this viral DNA copy has been integrated with that of the host, every time the cell makes a copy of itself, the virus also makes many more copies of itself, which will go on to infect other cells within the body. However, HIV carries its genetic material in the form of RNA, which must first be copied into DNA in order to blend in with the cellular DNA of the organism it is infecting. TRIM5α stops the virus even before it makes this DNA copy, and this strategy works so well that rhesus monkeys cannot be infected with HIV.
What makes TRIM5α even more fascinating is that humans have a very similar version, but there are critical differences that make our version useless against HIV. Research investigating why the monkey version is so good at blocking HIV might one day allow us to fine-tune the human version to be more effective.
Through my research, I’m trying to gain a better understanding of the specific steps that happen when TRIM5α defends against HIV and what other cellular proteins are involved in helping TRIM5α carry out this job. While such basic research is not directly related to designing prevention or treatment strategies, the knowledge we obtain about how these biological processes work on the cellular and molecular level might one day provide the information necessary to turn something like TRIM5α into a therapeutic approach. So I’ll keep you posted.