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-19
  • Start & end year

    2016
    2021
  • Known Financial Commitments (USD)

    $1,179,314
  • Funder

    National Institutes of Health (NIH)
  • Principal Investigator

    Joanne Turner
  • Research Location

    United States of America
  • Lead Research Institution

    Texas Biomedical Research Institute
  • Research 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.