Antonito (Nito) Panganiban, Ph.D.
B.S., Bacteriology, University of Wisconsin, Madison, WI
Ph.D., Microbiology & Immunology, University of Washington, Seattle, WA
The long-term research interests of our lab encompass the replication strategies and pathogenesis of Category A, B, and C bunyaviruses. Most recent published work has centered on Sin nombre hantavirus (SNV), which is a Category A member of the bunyavirus family. There are currently three main research avenues in the lab.
First, we have focused primarily on novel and fundamental replication strategies and RNA-protein function during SNV infection of cells. In addition, we recently expanded our effort to include additional viruses Crimean Congo Hemorrhagic fever (CCHFV) and Rift Valley fever viruses (RVFV), important human pathogens from the nairo- and phlebovirus genera of the family.
Second, along with extending our study of basic replication to these additional bunyaviruses, we have been working on a project that compares the host response to infection by diverse bunyaviruses. This latter effort, which uses approaches including microarray and transcriptome analysis, focuses on the human cellular response to infection. This work is being carried out in collaboration with Alex Freiberg, Director of the BSL-4 lab at UTMB-Galveston, as well as investigators at LSU GeneLab, and computational biologists at Los Alamos National Labs. We are carrying out a complementary project to examine the nonhuman primate response to infection with hantaviruses. This is a direct extension of our project on defining the host response to infection and will enable us to compare our current data with that arising from a relevant in vivo model.
A third project is to identify novel cellular factors that are required for efficient bunyavirus replication. This effort builds on a couple of previous observations from the lab. SNV functionally interfaces with the cellular cytoplasmic mRNA degradation machinery suggesting that some of these cellular components may be required for replication. At the same time, some of our comparative analysis indicates that specific components of the mRNA degradation pathway are up- or down-regulated following infection with SNV, CCHFV, or RVFV. We carried out targeted siRNA-mediated gene knockdown of this gene set and are elucidating the mechanism by which these products of these genes function during replication. The proteins encoded by these genes are candidates for broad spectrum anti-viral drugs, and we will be carrying out high throughput screening to isolate molecules that may inhibit these targets.
The TNPRC is a division of Tulane University (985) 871-6201 email@example.com