Investigators Diagnostic Tests Vaccines Therapeutics Clinical Trials Infections and Pathogenesis Host Response Public Health COVID-19 Resources Seed Projects

 

PROJECT: To determine is serum concentrations of choline can serve as a biomarker of excess acetylcholine production by T cells driving respiratory distress in Covid-19.


Cox, Maureen
Microbiology/Immunology
maureen-cox@ouhsc.edu


 

 

PROJECT: Single cell sequencing technology to determine the repertoire and function of B cells in patients after recovery from Covid-19. This work is funded through a supplement to the OMRF U19 Program (Grant Number: 2 U19 AI062629 16)

 

Smith, Ken
OMRF
ken-smith@omrf.org

Lang, Mark L.
Microbiology/Immunology
Mark-Lang@ouhsc.edu

Shah, Hemangi

 

 

Microbiology and Immunology

Hemangi-Shah@ouhsc.edu
 

 


 

 

PROJECT: Dr. Richardson hypothesizes that the increased vulnerability of older individuals to COVID-19 is because they are more prone to generate a “cytokine storm” when infected by the virus.  It is proposed that this is because lung cells of old individuals are more prone to undergo necroptosis releasing DAMPs that generate inflammatory cytokines.   The group has observed that tissues from old mice show increased markers of necroptosis that are associated with the age-related increase in inflammation.  Importantly, they have shown that blocking/reducing necroptosis leads to reduction in inflammation.

NEEDS:   A mouse model of COVID-19 and a source of blood from patients who have been hospitalized from COVID-19 to determine if they show increased levels of DAMPs, an indication that necroptosis is induced in these patients compared to patients not hospitalized or not infected.


Richardson, Arlan
 

Sathyaseelan, Deepa
 


 

 

PROJECT: Over 1/3rd of patients with COVID-19 display neurological symptoms however little is known about how the virus, or dysregulated host defenses against it, trigger neurological symptoms.  We hypothesize that COVID-19 triggers production of pro-inflammatory cytokines from CD8-T-resident memory cells already residing in the brain that then causes CNS dysfunction directly, or through excessive activation of microglia.   This mechanism is particularly relevant to COVID-19 in the elderly due to the fact that CD8-T-resident memory cells accumulate in the brain during normal aging, thus increased numbers of these cells would cause increased amounts of CNS dysfunction.

NEEDS: If anyone is planning infection of live mice, the would like to collaborate and study the central nervous system.


Drevets, Douglas A
Infectious Diseases
Douglas-Drevets@ouhsc.edu

Sonntag, Bill