My research laboratory focuses on viral pathogens, mechanisms of virulence (how viruses cause disease) and how viruses can be designed to create improved vaccines against numerous diseases, including cancer, COVID-19 coronaviruses (SARS), and emerging poxvirus threats. The vaccinia virus poxvirus vaccine is administered to all U.S. military personnel for protection against smallpox and monkeypox viruses, Category A biological disease agents identified by the U.S. Government as bioterrorism/biowarfare threats. Recombinant vaccinia is also widely used as the wildlife rabies vaccine in the U.S. and in cancer treatment trials. However, the use of these vaccines is limited by the virulence of these poxvirus vectors in humans. We sequenced the first North American poxvirus, raccoonpox, a new evolutionary branch distinct from Orthopoxviruses, and showed that it is extremely attenuated even in immunocompromised and pregnant mammals, suggesting it will be a very safe vaccine vector. To study how viruses cause disease and to create safer vaccines, we have used bioinformatic genome analysis to identify previously uncharacterized virulence genes (such as A35). We have shown that A35 acts by inhibiting the mammalian immune system, thus allowing the viruses to replicate and spread prior to control by the immune response. We are currently exploring the biochemical mechanisms of action of these immunoregulatory proteins and are using this information to design safer and more effective platform vaccines for pathogens and for cancer treatment (Patent No 8202521). If we can discover how these proteins act, we may be able to create anti-viral drugs to inhibit the functions, and it may be possible to mimic these immunomodulatory functions in order to control deleterious immune responses in human and animal organ transplantation or autoimmunity. We have also analyzed the effects of dietary supplements and viral co-infection on viral replication and disease severity. - https://microbiology-immunology.ecu.edu/rachel-l-roper/
“When a species is co-evolving with its pathogen . . . they tend to come to a detente, where the virus will be surviving in the population, and the population is surviving without that much illness, but when a virus jumps species, then you’ve got a real problem.”
Virologist and Immunologist at East Carolina University
