Allied Health Sciences

Education

• Ph.D., Biomedical Sciences, University at Albany
• B.Sc., Biotechnology, Rochester Institute of Technology

Courses Taught at ACPHS

• Immunology
• Virology
• Biomedical Laboratory Techniques I & II
• Flow Cytometry

Research Interests

Research in my laboratory is focused on the pathogenesis of, and host defense against, human enveloped RNA viruses. Several notable human diseases are caused by enveloped RNA viruses: influenza, AIDS, hepatitis C, dengue hemorrhagic fever, congenital Zika syndrome, and COVID-19. Novel insights into the relationship between viruses and human cells has the potential to lead to improved therapeutics and vaccines against these diseases. Currently, my team of undergraduate and graduate students are following these avenues of research:  

1. Role of host lipid biosynthesis in RNA virus infection. Viruses are obligatory intracellular parasites that hijack cellular factors and biosynthetic pathways to complete their life cycle. Emerging studies have revealed the importance of virus-host lipid interactions in the life cycle of several clinically important human RNA viruses. Specifically, viruses can target lipid metabolism, signaling, and trafficking to remodel host cells into an environment favorable for viral replication. Data from collaborative studies with Dr. Kouacou Konan (Albany Medical College) have revealed that the production of infectious influenza and Zika virus particles is dependent on host glycosphingolipid biosynthesis. Elucidating the impact of viral infection on the regulation of glycosphingolipid metabolism and identifying biosynthetic enzymes and metabolites critical for various stages viral life cycle may result in the development of antiviral therapies targeting these, and perhaps additional, human enveloped RNA viruses.
2. Molecular Regulation of inflammation during influenza virus infection. The body’s innate immune system is critical for the rapid control of pulmonary influenza infection as well as the induction of protective T cell and B cell immune responses. Innate immune cells express a collection of molecular “sensors” that allow them to detect influenza viruses early during infection. The cytoplasmic NLRP3 inflammasome complex triggers the production of the inflammatory cytokines interleukin 1-β (IL-1β) and interleukin 18 (IL-18) after sensing the virus. Several reports support that timely NLRP3 inflammasome activity is critical for antiviral immunity, whereas other reports have linked excessive NLRP3 inflammasome activity with cell death and tissue damage observed during infection by highly pathogenic strains of flu. Recent studies have identified small molecules (pyrin-only proteins or POPs) that are capable of modulating inflammasome activity in humans. Studies focused on the expression and function of POPs during human influenza virus infection will aid our understanding of the regulatory mechanisms that finely tune inflammatory responses to favor protection over pathology.
3. Impact of aging on anti-viral immunity. It is estimated that by 2030, nearly one of out every five Americans will be 65 years or older. Such a dramatic increase in the size of the aged population poses new challenges to the U.S. healthcare system as aged individuals exhibit increased susceptibility to infectious disease and are less responsive to contemporary vaccine strategies. We are interested in understanding the intrinsic and extrinsic factors responsible for age-related changes in anti-viral immunity. Data from my postdoctoral studies showed that the naturally occurring contraction of the naïve T cell repertoire can result in impaired CD8 T cell responses to known immunodominant epitopes critical for protection against influenza virus infection. These data have implications for the design of vaccines for the elderly. Since aging is associated with diminished innate immunity, chronic inflammation, and an increased susceptibility to viral infection, our current studies are directed towards evaluating the impact of biological aging on the ability of the NLRP3 inflammasome to properly regulate inflammation and host defense. Results from these studies have the potential to facilitate the identification of new drug targets for the effective treatment of chronic inflammation, and/or the development of vaccination strategies to augment immunity and restore health in the rapidly growing elderly population.

Honors and Awards

• Organizer, 53rd Annual Regional Meeting, American Society for Microbiology, October 16, 2018
• President, Eastern New York Branch of the American Society for Microbiology, 2017-2019
• AAI Early Career Faculty Travel Grant, 2015
• AAI Young Investigator Award, 2014