It is a common assumption that the fittest creature among a population will survive. In a culture of bacteria treated with antibiotics, for instance, the surviving bacteria will most likely be the bacteria that acquired resistance to the antibiotics. The same assumption can be made when considering viruses. After the virus penetrates a cell it starts to kill it, while using the cell’s systems to multiply. The fittest virus is the virus that keeps the host cell alive long enough to produce many copies of itself, making it easier for the virus to spread and survive.
However, as Dominik Wodarz of the University of California in Irvine and his colleague David N. Levy at New York University assume, this fit virus won’t be able to kill enough T-cells and thus is not virulent enough to cause AIDS. Apparently, there is a trade-off between the fitness of the virus and its virulence, a trade-off that is not necessary when two strains of viruses- a fast killing one and an easily spreading one- act together.
The HIV recognizes T-cells by a unique protein located on the T-cells’ outer membrane, called CD4. After the virus penetrated the cell it shuts off the production of new CD4 proteins and starts the slow destruction of the cell. While the old CD4 proteins are still functional, another virus can recognize the T-cell and infect it. According to the computerized model developed by the scientists AIDS can develop only if a co-infection occurs at high rates.
The co-infection rate is an outcome of the virus load. The more copies of the HIV, the more frequent the co-infection will be. According to the model, in the first stages of infection there aren’t enough copies to achieve co-infections because of the strength of the immune system. As the immune system’s abilities decline more copies of the virus can be spread, allowing a higher rate of co-infection. At the later stage, enough T-cells are depleted and AIDS can be detected. Any one of the strains couldn’t have caused AIDS on its own.
This model is supported by the SIV – a virus similar to the HIV that attacks monkeys and apes. In the case of SIV no disease is caused by the infection. The fitness of the SIV sampled in the beginning of the infection is high while it is lower at later stages. This can be explained, according to the model, by the rarity of co-infection in the case of SIV. According to the model, if co-infection doesn’t happen frequently enough no disease will be caused by the virus.
This new hypothesis is still considered controversial in the scientific community. The concept that two strains of the same virus are essential for causing a disease is uncommon, not to mentioninnovative. However, the hypothesis can be verified and if co-infection is proven necessary for the outbreak of the disease, this information can be used to attack the virus and prevent it from causing AIDS. This new finding, proven so far merely by a computerized model, can change the way we understand viral infections.
TFOT recently covered another HIV related article on a new research dealing with the role of the FP-23 protein in the development of AIDS.
Further discussion of the Two Strains hypothesis can be found on the TFOT forums.