Downstream sample analyses from 3 NHP species infected with SARS-CoV-2.
- Funded by National Institutes of Health (NIH)
- Total publications:0 publications
Grant number: 3P01AG051428-05S1
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Key facts
Disease
COVID-19Start & end year
20162021Known Financial Commitments (USD)
$1,179,314Funder
National Institutes of Health (NIH)Principal Investigator
Joanne TurnerResearch Location
United States of AmericaLead Research Institution
Texas Biomedical Research InstituteResearch Priority Alignment
N/A
Research Category
Pathogen: natural history, transmission and diagnostics
Research Subcategory
Pathogen morphology, shedding & natural history
Special Interest Tags
N/A
Study Type
Non-Clinical
Clinical Trial Details
N/A
Broad Policy Alignment
Pending
Age Group
Not Applicable
Vulnerable Population
Not applicable
Occupations of Interest
Not applicable
Abstract
Over the last three months, COVID-19 has emerged as a major pandemic. Coronavirus SARS-CoV-2, the causative agent of COVID-19, has remarkable infectiousness and pathogenicity, particularly in the elderly and people with immunocompromising conditions.1 The CDC have reported that 8 out of 10 deaths reported in the US related to COVID-19 are in adults 65 years and older. Similar to many other pulmonaryinfectious diseases, the elderly can present with atypical symptoms and initial signs of SARS-CoV-2 infection may be missed resulting in ongoing infection transmission. Texas Biomed recently infected two different age groups of common marmoset, rhesus macaque and baboon with SARS-CoV-2. Each species had differing infection outcomes. Extensive sample collection occurred throughout the 14-day study, providing an array of banked samples from 3 species of NHP, two age groups, and infected and non infected controls. We propose five Aims using banked samples, to increase our understanding of SARS-CoV-2 infection and the host response in old age. Aim 1 will investigate whether the pulmonary environment during SARS-CoV-2 infection results in oxidation of host innate molecules and a possible link to COVID-19 Acute Respiratory Distress Syndrome (CARDS). Aim 2 will determine the phenotype and function of resident and infiltrating innate immune cells during SARS-CoV-2 infection with a focus on the initiation and maintenance of a cytokine storm. Aim 3 will dissect the Tand B cell response in lung and lymph nodes during early SARS-CoV-2 infection that may lead to relevant information about long term protective immunity. Aim 4 will focus on the virus during infection, determining whether viral mutations occur and whether they differ between species and age. Aim 5 will support in-depth analyses of formalin fixed tissues with a goal of viewing SARS-CoV-2 infection beyond the lung and identifying correlates of infection progression in organs such as the brain, heart and intestine.