Yes for a short period of time. Viral infection can cause unbearable symptoms and may even lead to death if your immune system is compromised. Few weeks ago, when I was infected with the stomach flu viruses, I had absolutely nothing to do other than waiting patiently for my immune system to be activated. Is there other ways to treat viral infection, other than the well-known antiviral remedy, such as vaccines, Tamiflu and HAART?
A pediatrician pointed out the possibility of deriving viruses to target virus-infected cells last week at a Christmas party. To design such virus, one must recognize the receptors required to enter the cells. To target virus-infected cells, these receptors must be the same for the designed virus to enter. The designed virus can potentially do several things: hijack the replication machinery to repress harmful virus to replicate; repress the transcription of specific cellular factors that are required for the replication of the harmful virus; induce apoptosis (programmed cell death) quickly.
Genetic Testing: What is it?
The first point that I proposed may not be the best due to the fact that harmful viruses can still be replicated but at a slower rate. In contrast, the second point that I proposed can potentially inhibit harmful replication at the maximum level but may be detrimental to uninfected cells if the cellular factors are essential. The last point may not work due to the same reason as the previous point.
Another restriction on the design is the rapid mutation of the viruses. RNA viruses depend on the error-prone RNA polymerase to reproduce its RNA genome. For instance, HIV virus is estimated to have mutation in every single basepairs in its genome in just 24 hours. Thus, restricting the expression of cellular factors may repress viral replication for only a short period of time.
If there weren’t viruses, our cats and dogs would not develop a placenta. A group of researchers from France discovered that in cats and dogs, the gene syncytin, responsible for creating a placenta, is stolen from retroviruses. Syncytin is highly conserved within species in the carnivora. In other words, there is a little DNA variation in the syncytin sequence. By comparing syncytin in species, the gene is stolen from viruses about 70-80 million years ago. Interestingly, syncytin is identified as an envelope gene that belongs to a provirus (provirus means a virus genome integrated into cat’s or dog’s genome). An envelope gene codes for an envelope protein. Go to the figure below: envelope protein is important in binding to cells for the virus to enter the cell. Stealing env gene from viruses is, therefore, an important mechanism for mammals to evolve. Evolution is a slow process. It depends on mutations that give rise to characteristics that may convey fitness to a particular species. By stealing an entire gene from viruses, mammals essentially skip the slow process of accumulating mutations. The researcher wrote,
“Therefore, it seems that, on several occasions in the course of mammalian evolution, env genes from endogenous retroviruses have been co-opted by their host to participate in the formation of the placenta”
The researchers also asked an interesting question after correlating the syncytin gene with the envelope gene of retroviruses. Can viruses use syncytin gene from cats and dogs as their envelope (see figure to see where the envelope protein is) to enter the cell? This group of researchers made virus mutants with cats’ or dogs’ syncytin as their envelope protein (envelope protein is responsible for binding to specific receptor to enter the cells). Then, they measured the number of viruses produced to see if syncytin is functional. In Figure C, you can see that viruses with either cat’s and dog’s syncytin can replicate in cat and dog’s cell. In sum, syncytin gene is still a functional envelope gene for virus replication.
Humans also have syncytin.
What if there are no viruses on Earth? Life would probably be developed with a difference mechanism. Given the slow rate of evolution, forming a placenta is quite unlikely.
Ancestral capture of syncytin-Car1, a fusogenic endogenous retroviral envelope gene involved in placentation and conserved in Carnivora.
To fight off a viral infection, your immune system often mounts a targeted response against the proteins expressed on the virus surface. Dengue virus infects 50-390 million worldwide. While most first cases of infection are asymptomatic, cases infected with more than 1 strain of the virus often results in unwanted immune response, which include dengue hemorrhagic fever. Recently, researchers have found a structural difference when the virus is in mosquito (left) and in human (right). After the virus enters human, the structure of virus is found to be expanded. This structural expansion may explain why our immune system doesn’t do a good job in mounting an effective response, as human antibodies are found to only target the un-expanded orientation of surface protein in the mosquito.