Projects
- Host-parasite interactions in filarial worm infections
- The respiratory microbiome in health and disease
- Omics Profiling of virus infections to identify markers of disease severity
- Influenza and SARS-CoV-2 evolution and transmission
About Us
The Ghedin Lab has recently re-located to the Laboratory of Parasitic Diseases at the National Institute of Allergy and Infectious Diseases (NIAID) of the NIH in Bethesda, MD. The research focus in the Ghedin laboratory is on defining genomic characteristics of human pathogens. Our research is multidisciplinary and draws upon the tools of genomics, molecular virology, and computational biology. Our systems biology research program focuses on the molecular basis of macroparasite (nematodes) adaptation to niches in their human hosts and microparasite (virus and bacteria) diversity and interaction in transmission and virulence.
The overarching question of our research is:
How do pathogens adapt to their hosts and what is the evolutionary basis of this adaptation?
Host-pathogen interactionS
in filarial worm infections
Filarial nematodes infect millions of individuals and represent the leading cause of morbidity in the developing world. Current medications are inadequate for control and elimination, necessitating a better understanding of the basic biology of these worms. Most filarial nematodes, including Brugia malayi and Onchocerca volvulus (causative agents of lymphatic filariasis and river blindness, respectively) have an essential intracellular bacterial endosymbiont, Wolbachia.
Our studies address key questions on the reciprocal cues required in the co-dependency between the worm and the bacteria.
Predictive modeling of clinical
outcomes in respiratory infections
We develop and use new analytical tools to define genetic structure and mechanisms of evolutionary change in respiratory viruses sampled within individual hosts over the course of an infection and across chains of transmission. We have observed that the dynamics of evolution of respiratory viruses like influenza are different in pre-immune versus naïve hosts and in high risk populations, such as immunocompromised and obese individuals. In light of the COVID-19 pandemic, we have expanded our research program to include SARS-CoV-2 to pursue questions on transmission, factors associated with disease severity, and host selection pressure on the evolution of the virus.
Our goal is to integrate systems-wide data and map molecular interaction networks to build predictive models of disease severity.
Lab News
Yearlong infection spawned a striking mutation beyond SARS-CoV-2’s spike protein.
RyeAnne Ricker awarded NSF Fellowship
