Xaira Rivera Gutierrez, Baylor College of Medicine

Xaira Rivera-Gutierrez, Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, United States of America Julia D Hankins, Department of Pathology, University of Kansas Health System, Kansas City, Kansas, United States of America Ketki Patil, Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, United States of America Vanessa Harris, Department of Global Health, Amsterdam Institute of Infection and Immunity, Amsterdam University Medical Centers, Amsterdam, the Netherlands, Division of Infectious Diseases, Department of Internal Medicine, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands Megan T. Baldridge, Department of Molecular Microbiology, Washington University School of Medicine in St. Louis, St. Louis, United States of America, Division of Infectious Diseases, Department of Medicine, Edison Family Center for Genome Sciences & Systems Biology, Washington University School of Medicine, St. Louis, United States of America Sasirekha Ramani, Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, United States of America

Vaccines

Rotavirus is the leading cause of morbidity and mortality associated with acute gastroenteritis in children under 5 years old. Live, attenuated oral rotavirus vaccines (ORV) have been introduced into immunization programs in over 100 countries. However, ORV effectiveness against severe gastroenteritis in the first year of life is poor in many low-income countries. Enterovirus, a genus of positive-sense single-stranded RNA viruses, has been associated with poor response to oral vaccines. Population studies have demonstrated that co-administration of the oral poliovirus vaccine (OPV), an Enterovirus coxsackiepol, and/or the presence of non-polio enteroviruses such as Enterovirus betacoxsackie are associated with poor vaccine response to ORV in many low-income settings. We previously demonstrated that jejunal human intestinal enteroids (HIEs) recapitulate OPV-mediated interference of ORV replication through faster replication kinetics, production of secreted factors and exclusion of ORV in OPV infected cells. We have now leveraged the HIE model to investigate ORV interference by non-polio enteroviruses. In new studies, we are exploring the effect of two sub-species from the Enterovirus betacoxsackie, CVB3 and CVB5, on ORV replication in infant HIE’s with the goal of understanding the possible mechanisms of interference. Together, these studies will provide new insight into how the eukaryotic virome can modulate live, oral vaccines.