Interrogating inflammatory responses to SARS-CoV-2 infection in vivo

National Institute Of Allergy And Infectious Diseases

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Abstract

The lungs of patients suffering from severe Coronavirus Disease 2019 (COVID-19) present with pneumonia and significant tissue damage which can lead to acute respiratory distress syndrome (ARDS) and death. This tissue destruction is caused not only by the etiological, cytopathic Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) itself, but also a dysregulated host immune response. A phenomenon termed cytokine storm", which is characterized by high levels of pro-inflammatory cytokines such as IL-6 and IL-1, has been observed as a consequence of this dysregulated antiviral immunity. Understanding the complex host response to SARS-CoV-2 infection is a crucial global challenge. We leverage here our current expertise in inflammatory cytokines and pulmonary pathophysiology, operation in our high-containment (BSL3) research environment and importantly, animal BSL3 facilities, to investigate the host molecular and cellular mechanisms that contribute to pathogenesis during SARS-CoV-2 infection. In particular, we will focus on the very earliest innate immune responses to to viral infection in the lung, with emphasis on tissue-resident myeloid cell subsets and lung epithelial cells.