Dr. Laurie A. Silva, Ph.D., is a Research Assistant Professor. Dr. Silva's lab studies chikungunya virus, a reemerging arbovirus that has recently caused explosive epidemics of febrile arthritis throughout many parts of the world. Dr. Silva’s research interests are focused on virus-host interactions that dictate chikungunya virus entry, tropism, replication compartment formation, and pathogenesis. Dr. Silva also serves as the Team Lead for chikungunya virus projects within the Dermody lab and as the Facility Manager for the A-BSL3 laboratory at Rangos Research Center.
Dr. Silva received her Bachelor of Science degrees in Microbiology and Molecular & Cell Biology from Oklahoma State University in 2000 and her doctoral degree in Virology from Harvard University in 2009. She completed 4 years of training with Dr. Dermody as a postdoctoral fellow at Vanderbilt University, after which she was promoted to Research Instructor. Working with Dr, Dermody, Dr. Silva established the lab’s research program on chikungunya virus and served as the BSL3 Facility Manager for the Division. She was promoted to Research Assistant Professor in 2015. Dr. Silva joined the Children’s Hospital in 2016. In July of 2019, the Silva lab was initiated.
Professional Affiliations/Society Memberships
- American Society for Virology
Education & Training
- Ph.D.: Harvard University
Dr. Laurie Silva joined the division as a research scientist in May 2016. She leads two teams focused on Chikungunya virus (CHIKV). She also serves as the Rangos BSL3 Facility Manager and oversaw the extensive renovation of the BSL3 lab at Rangos Research Building.
Dr. Silva’s research focuses on replication and pathogenesis of CHIKV, an arthritogenic alphavirus that causes debilitating musculoskeletal inflammatory disease. It is transmitted by Aedes albopictus and Aedes aegypti mosquitoes and is capable of an epidemic, urban transmission between mosquitoes and humans. Since 2004, CHIKV has caused epidemics involving millions of persons and expanded into new areas including Europe, the Middle East, the Pacific region, and most recently in the Americas. No licensed vaccines or specific therapeutics are available for this globally important pathogen.
The CHIKV research program seeks to discover mechanisms by which host cell factors contribute to CHIKV replication and pathogenesis. Dr. Silva’s main project focuses on elucidating the role of COP-I trafficking pathway proteins in the replication cycle of CHIKV. In a genome-wide siRNA screen to identify host factors that are required for efficient CHIKV replication, COP-I coatomer and regulatory factors were some of the top putative hits. Validation experiments using golgicide A (GCA), a specific inhibitor of the COP-I regulatory factor GBF1, supported a function for this host factor in the replication cycle of CHIKV. Further experiments suggest GBF1 may be acting in a non-canonical manner to enhance CHIKV replication. Microscopy experiments suggest GBF1 localizes to sites of CHIKV RNA synthesis early in infection and may be critical for the establishment or maturation of viral replication factories. Current experiments aim to determine the precise stage in the CHIKV replication cycle GBF1 is required and whether GBF1 is necessary for the virus to form viral replication factories in the infected cell. Genetic experiments to determine which domains of GBF1 contribute to CHIKV replication are also underway. Collectively, these experiments will illuminate mechanisms by which an important host factor is usurped by CHIKV, provide support for a noncanonical role for GBF1 in viral replication and perhaps host cell function, and guide intervention strategies based on this host target.
Dr. Silva mentors two graduate students, Anthony Lentscher and Nicole McAllister, a post-doc, Adaeze Izuogu, within the Dermody Lab. Other CHIKV projects to which Dr. Silva contributes include:
- Identification of specific host cell glycosaminoglycans to which CHIKV virions bind
- Elucidation of the role of glycosaminoglycans in the pathogenesis of CHIKV
- Validation of other host proteins that were putative hits for CHIKV proviral factors in a high-throughput siRNA screen
- Determination of specific tissues within an infected host that contribute to the immunopathology of CHIKV
- Candidate vaccines for CHIKV