Battle of the Viral Mutations

Research Blogging / by Dave Munger /

Viruses like H1N1 and HIV are hard for biomedical researchers to tackle because they mutate so readily. Will scientists uncover new treatments before the viruses adapt again?

Why is it that you have to get immunized against the flu every year, but just two chicken pox shots will do you for a lifetime?

For any disease caused by a virus, the human immune response is similar. White blood cells known as B lymphocytes (B cells) produce antibodies that bind to foreign proteins such as viruses, in effect flagging them to be attacked by T lymphocytes (T cells). Each antibody is specific to a particular protein; a vaccine introduces a non-virulent form of that protein so that the B cells can produce antibodies and be ready when the real virus strikes. This works great for diseases like chicken pox and measles, which don’t change much from year to year. But why doesn’t it work for the flu?

Atila Iamarino is a graduate student researching the evolution of HIV, and an editor for ResearchBlogging.org who blogs about H1N1 for BIREME, a Brazilian affiliate of the World Health Organization.

Iamarino says that the key difference between the flu virus and other more stable viruses is its ability to translate small differences in the virus’s genetic material into big differences when it infects a human. He points to a 2004 study led by Derek J. Smith and published in Science. Smith’s team found that genetic mutations leading to differences as small as a single amino-acid component of a protein could cause the virus to be unrecognizable by the immune system, even if the victim had previously been immune. This ability of the flu virus—as well as other viruses, including HIV—to skirt the immune system means that traditional vaccination may always be nothing more than a temporary fix.

But “Revere,” one of several pseudonymous public health scientists and practitioners that edit the blog Effect Measure, says that there may be another way to treat the flu virus: Changing the human host. Viruses rely on a host cell to spread, hijacking its DNA and protein synthesis apparatus to replicate before moving on to infect other cells. If just one part of that process could be interrupted, then the virus wouldn’t be able to reproduce, and we wouldn’t get sick.

Obviously we don’t want to stop human cells from producing the proteins we need to survive, but a team led by Alexander Karlas published a letter in Nature last month showing how they could identify specific portions of a cell’s RNA required to replicate flu viruses. Deactivating these portions made it impossible for any type of flu to replicate. If a drug could be developed to do this temporarily, then it might be possible to treat all forms of flu with one simple drug—and a similar process could be used to treat many other diseases, even HIV/AIDS. But could the viruses simply mutate to form their own adaptation around this fix?

Ian York, an assistant professor of immunology and virology at Michigan State University, responded to this question with a blog post in response to Revere’s. A study led by Guylaine Haché and published in 2008 in Current Biology examined whether the HIV virus could successfully respond to a dramatic change in its own defense mechanisms. One of the reasons HIV is so pernicious is that it readily defends itself from a type of human protein called APOBEC3G, using its own accessory protein Vif. Haché’s team deleted the Vif from HIV virus and then placed it in cells that had APOBEC3G. For several weeks, the HIV was unable to replicate, but after 45 days, it started to grow again in 3 of the 48 cultures being tested. The strains of HIV that survived had independently developed mutations that allowed them to resist the APOBEC3G. This mutation was quite slow, probably occurring at a rate of less than 3 in 400,000 individual viruses, and these mutated strains were still susceptible to another antiviral agent, APOBEC3F. Nonetheless, the study demonstrated that some viruses have the ability to adapt to extreme measures designed to kill them.

But the study also showed that some mutations are less like to occur than others. If researchers can create drugs that target these less-likely mutations, then we will have more time to develop more effective treatments in the future. No practical drugs have yet been developed using these techniques, but you can follow the research as it progresses on ResearchBlogging.org.

Originally published February 3, 2010

Tags contagion disease virus

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