Welcome to Biomed Bites, a weekly feature that introduces readers to some of Stanford’s most innovative researchers.
Some of the world’s best known viruses use RNA, rather than DNA, to code for proteins, including polio, measles and hepatitis C. There are a few differences: RNA uses a component not used in DNA, and RNA is usually single-stranded, rather than the familiar double helix of DNA.
RNA viruses change rapidly, evading efforts to develop vaccines and therapies. But the change is uneven — some genes evolve with nearly every replication, others stay the same for generations. Molecular biologist Karla Kirkegaard, PhD, wondered why. The chair of Stanford’s Department of Microbiology and Immunology explains her discovery in the video above:
The answer was unusual. It turns out that there are different kinds of selective pressures on these regions, and it is very hard for new variants to arise in certain regions because their family members around them poison their advantage.
Alone, for example, a mutated gene might perform better than one that is unaltered. But when it is mixed with other genes, it might make the resultant virus less competitive.
That offers valuable insight for drug development, she said. Consider the interaction of genes and viruses together, rather than aiming to disable a single player, Kirkegaard advises:
My quest right now is to convince people who target antivirals for the common cold, West Nile virus and SARS to think about those processes the viruses have to cooperate on so we won’t have such a big problem with drug resistance.
Learn more about Stanford Medicine’s Biomedical Innovation Initiative and about other faculty leaders who are driving biomedical innovation here.
Previously: Ending enablers: Stanford researcher examines genes to find virus helpers, A conversation on West Nile virus and its recent California surge and Exploring the role of extracellular RNA communication in human disease