Mild SARS-CoV-2 infection in rhesus macaques is associated with viral control prior to antigen-specific T cell responses in tissues
Christine E. Nelson; Sivaranjani Namasivayam; Taylor W. Foreman; Keith D. Kauffman; Shunsuke Sakai; Danielle E. Dorosky; Nickiana E. Lora; - NIAID/DIR Tuberculosis Imaging Program; Kelsie Brooks; E. Lake Potter; Mario Roederer; Alan Sher; Daniela Weiskopf; Alessandro Sette; Emmie de Wit; Heather D. Hickman; Jason M. Brenchley; Laura E. Via; Daniel L. Barber.
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| PREPRINT-BIORXIV | ID: ppbiorxiv-475282
SARS-CoV-2 primarily replicates in mucosal sites, and more information is needed about immune responses in infected tissues. We used rhesus macaques to model protective primary immune responses in tissues during mild COVID-19. Viral RNA levels were highest on days 1-2 post-infection and fell precipitously thereafter. 18F-fluorodeoxyglucose (FDG)-avid lung abnormalities and interferon (IFN)-activated myeloid cells in the bronchoalveolar lavage (BAL) were found on days [~]3-4. Virus-specific effector CD8 and CD4 T cells were detectable in the BAL and lung tissue on days [~]7-10, after viral RNA, lung inflammation, and IFN-activated myeloid cells had declined. Notably, SARS-CoV-2-specific T cells were not detectable in the nasal turbinates, salivary glands, and tonsils on day 10 post-infection. Thus, SARS-CoV-2 replication wanes in the lungs prior to T cell responses, and in the nasal and oral mucosa despite the apparent lack of Ag-specific T cells, suggesting that innate immunity efficiently restricts viral replication during mild COVID-19. ONE SENTENCE SUMMARYSARS-CoV-2 infection leads to mild, focal lung inflammation, and type I IFN activated myeloid cells that mostly resolve prior to the influx of virus-specific effector T cells or antibody responses in rhesus macaques.
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