Millions of Viruses and Only One Drug

Contributed by Guest Blogger: M. Carraher ’14

A former leader of the Pentagon considers, “Mother Nature among the worst terrorists.” Throughout modern time, the threat of a virus pandemic has seemed more likely, and more deadly than a nuclear war. Swine flu, HIV, and SARS have all frightened average citizens and leading microbiologists into a frenzy. The biggest threats have been the viruses that were least expected. If you don’t see them coming, how can you protect against a deadly outbreak? The general strategy for antivirals is “one bug, one drug”. However, any small mutation of the virus might render the drug useless. Research is currently being poured into developments of a broader range of antivirals. The current hypothesis is that certain proteins inside cells are vital for virus replication. But what if those cellular proteins aren’t necessarily vital for host life? A promising target is the TSG101 protein, which is involved in the transport of viruses out of a cell. A small-molecule drug has been developed to inhibit that interaction between the protein and virus. Researchers have identified more than 30 viruses that rely on this protein, so the drug does protect over a broader range infections. One hundred percent of Ebola-infected mice survive if exposed to the drug, a day after infection. Eighty percent survive if treated two days post infection, and 40% live four days after infection. The early test results seem promising for a strong, broad ranged antiviral drug, that does not hurt the host.
The most promising broad spectrum antiviral targets the host instead of the virus. Healthy cell membranes express a substance called phosphatidylserine on their inner surfaces. When under stress from a viral infection, this substance ends up on the outer surface. All viral infections seem to exhibit this behavior, making it a key target for drugs. An antibody called bavituximab has been developed, which binds to the phosphatidylserine. Once bound, the immune system should clearly recognize the infected cell and destroy, thus limiting viral replication. This method was tested on guinea pigs exposed to a Pichinde virus. Half the animals treated with bavituximab survived, compared 100% death for the control group, not injected with the antibody.
The antibody is currently being tested for a broader range of viruses, such as HIV, hepatitis, and influenza. So far, all infected cells express this molecule on the outside of their membranes, as compared to healthy cells, which maintain the molecule within the cell. This antibody could potentially protect against all known viruses, and some unknown as well, considering all viruses are believed to exhibit this behavior. However, viruses do evolve. Could they evolve to become immune to the antibody at some point? Further testing with humans is also needed to determine any potential side-effects. But, this is one step closer to a universal antiviral.


4 thoughts on “Millions of Viruses and Only One Drug”

  1. I thought this post was very interesting. It never occurred to me that there could exist one broad-ranging antiviral drug that can single out cell structures rather than viral structures. This is certainly possible considering that most, if not all cells share some universal proteins and processes, which can be targeted to inhibit viral infection and transmission between host cells. It seems like with further testing and development, a universal antiviral could soon exist. Of course, there is always the danger that the viruses will evolve and develop resistance to the new antiviral. But if we let that stop us, we’ll never get closer to eradicating the countless diseases caused by viruses.

  2. It seems that phosphatidylserine doesn’t have a signaling purpose. Rather, its expression seems to be a side effect of cell death, because if it had signaling functions, then the viruses would already have tried to inhibit its expression. I think it’s a very good idea to use phosphatidylserine expression as another means of directing immune response to the site of infection. While I’m sure such a method will work well in most diseases, I don’t know if it’ll help in HIV infection since HIV infects the immune cells themselves. Triggering more immune response at the site of infection might cause the infection to spread more rapidly.

  3. I was surprised after reading this post. I had always thought it was impossible to develop a drug that prevents viral infection from multiple types of viruses. Do all cells express the substance phosphatidylserine? If all infected cells express this after infection from a virus, then I think it might truly be possible to have a drug that stops a variety of viruses from infecting cells. Perhaps, for once, viruses will be unable to get creative and evolve around this barrier. Also, as scientists continue to learn more about this antibody, it will be possible for them to develop a similar one that halts, or at least greatly slows down infection rates more so than in the experiment done on mice. The study provides strong evidence for the newly developed bavituximab antibody to prevent infections, but I think more studies need to be done (both on other animal species and humans) to confirm this promising cure for infections.

  4. This post makes me very hopeful. I think that you raise a very good point about the possibility of viruses evolving to somehow become immune to the antibody. Maybe a solution to this would be to find other universals in host cells- it seems likely that phosphatidylserine presentation wouldn’t be the only one- and develop an antiviral that targets these other universals- maybe to be used in conjunction with the one you wrote about, or maybe to be used for hosts who are not cured by the bavituximab (sort of like doctors do once a host becomes immune to HIV).

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