Virus fighter uses malaria strain to conquer HIV in monkeys
Adding tropical disease to treatment cocktail wipes out infection in animals, scientist finds
The effects were quite obvious and impressive. We introduced the plasmodium [single-cell malarial parasite] to six monkeys, and the viral reservoir of their immunodeficiency virus was completely eliminated in three of them, while the levels in the others were reduced to the point where they could be barely detected with sensitive equipment. The monkeys also received antiretroviral "cocktails" that reduced the presence of the virus to very low levels, but could not eliminate the viral reservoir. Our study showed that adding malaria to the traditional cocktail could wipe out the immunodeficiency virus completely. In order to obtain high-quality data, we used a dozen Chinese rhesus macaques, which are genetically more similar to humans than the common Indian rhesus macaques. We infected them only with malaria. If the process is repeated, the results could be even better. We cannot say yet how effective the method will be on humans because our study was only limited to animals, however the future looks promising.
According to our analysis, the malaria parasite does not launch a direct assault on the immunodeficiency virus. A very smart and effective strategy was adapted instead. The reason why HIV can stay in humans so long and is so tremendously difficult to remove is that it hides well. The virus genome can take a long "sleep" in human cells without any remarkable traits being identified by the immune system for clean-up action. The malaria infection, however, interrupts this slumber and lures the virus out of its hiding place. We have seen an impressive slaughter of the virus by the monkey's immune system after the malaria did its magic.
This was a challenging issue, but we found the answer. The malaria parasite can release a special chemical to activate an important signal pathway in the virus, like a wake-up call. Then the parasite changed certain protein structures of the virus to allow it to move freely, like untying ropes on its hands and feet. Once the immunodeficiency virus stuck its head out, the immune system would jump and kill it.
That would be complicated. There are many types of malaria parasites and the one we used in the lab was a relatively mild species. The most deadly malaria types could kill a HIV patient before any positive effects occurred. But in Africa, some patients have already suffered both infections. Doctors could refer to our study when treating these patients. It's possible that repeated infection with mild malaria might have some positive effects in seeking a cure for Aids.
Our lab has done some work towards developing HIV vaccines. For instance, we cloned some genes of HIV into the malaria parasite with the hope of developing a new vaccine. That would be hitting two birds with one stone.