Luis M. Schang, MV, PhD
Animals and humans alike suffer from viral infections, and new viruses continue to emerge on the scene year after year. To learn about viral diseases, Institute Director Dr. Luis Schang uses small molecules with drug-like properties to probe the ways viruses cause infections. He is most interested in finding common features among the many viruses that cause disease in animals or humans. With his research, Schang is learning more and more about how viruses, despite their tiny size, make big problems in health. He’s also uncovering important information on how to use only a few drugs to fight infections with many different viruses, or even stop them before they start.
- Learning how viruses enter cells. Any virus – from Zika virus to herpesviruses – needs to enter cells to cause disease. Although every virus takes a different approach, there are some common tools that all or many viruses use for this microscopic act of breaking and entering. To identify these shared approaches, Schang and his team are testing different types of chemical compounds on a broad array of different viruses to see whether they have an effect on the ability of these viruses to enter cells. This information helps us understand viruses and the way the cause infections, and it also points the way toward new antiviral drugs. Compounds that work against a variety of different viruses are good candidates for the development of broad-spectrum antivirals, a possibility that Schang pursues whenever they discover a potentially useful compound.
- Studying how viruses turn DNA into action to replicate and cause disease. Schang is seeking to better understand how viruses ensure their genetic information gets turned into action by studying herpesviruses. All mammals suffer from their own particular set of herpesviruses, and while these infections are fatal only on occasion, the viruses cause painful and debilitating diseases that curb quality of life and leave the person or animal vulnerable to other infections. When certain types of viruses, including herpesviruses, invade a cell, their DNA gets bundled up tight into coils and wrapped around barrel-shaped proteins very much like the DNA that belongs to the host cell. This “chromatinized” viral DNA is mostly inaccessible, which forces the virus to go dormant and prevents it from spreading to other cells. These seemingly dead-end viruses are not helpless, however. Herpesviruses have found ways to thrive during this dormant period. What’s more, they occasionally bypass the process, disrupt the chromatin, and transcribe their genetic information to replicate themselves, spreading the infection to other cells and causing new outbreaks of disease. Together with his team, Schang is working to determine how the virus manages this end-run around chromatin and causes full-blown infections. By exploring the way the virus gets this done, they may also discern ways to prevent the virus from disrupting chromatin, ending a herpesvirus reactivation before it can produce a new outbreak of disease.