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1. Elevated temperature inhibits SARS-CoV-2 replication in respiratory epithelium independently of IFN-mediated innate immune defenses.

Author

Herder V, Dee K, Wojtus JK, Epifano I, Goldfarb D, Rozario C, Gu Q, Da Silva Filipe A, Nomikou K, Nichols J, Jarrett RF, Stevenson A, McFarlane S, Stewart ME, Szemiel AM, Pinto RM, Masdefiol Garriga A, Davis C, Allan J, Graham SV, Murcia PR, and Boutell C

Subjects
Adolescent, Animals, COVID-19 genetics, COVID-19 immunology, COVID-19 virology, Chlorocebus aethiops, Epithelial Cells metabolism, Epithelial Cells virology, Female, Gene Expression Profiling methods, Host-Pathogen Interactions genetics, Host-Pathogen Interactions immunology, Humans, Immunity, Innate genetics, Interferons genetics, Interferons metabolism, Male, Middle Aged, Models, Biological, RNA-Seq methods, Respiratory Mucosa metabolism, Respiratory Mucosa virology, SARS-CoV-2 genetics, SARS-CoV-2 physiology, Tissue Culture Techniques, Vero Cells, Virus Replication genetics, Virus Replication physiology, Epithelial Cells immunology, Hot Temperature, Immunity, Innate immunology, Interferons immunology, Respiratory Mucosa immunology, SARS-CoV-2 immunology, Virus Replication immunology
Abstract

The pandemic spread of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the etiological agent of Coronavirus Disease 2019 (COVID-19), represents an ongoing international health crisis. A key symptom of SARS-CoV-2 infection is the onset of fever, with a hyperthermic temperature range of 38 to 41°C. Fever is an evolutionarily conserved host response to microbial infection that can influence the outcome of viral pathogenicity and regulation of host innate and adaptive immune responses. However, it remains to be determined what effect elevated temperature has on SARS-CoV-2 replication. Utilizing a three-dimensional (3D) air-liquid interface (ALI) model that closely mimics the natural tissue physiology of SARS-CoV-2 infection in the respiratory airway, we identify tissue temperature to play an important role in the regulation of SARS-CoV-2 infection. Respiratory tissue incubated at 40°C remained permissive to SARS-CoV-2 entry but refractory to viral transcription, leading to significantly reduced levels of viral RNA replication and apical shedding of infectious virus. We identify tissue temperature to play an important role in the differential regulation of epithelial host responses to SARS-CoV-2 infection that impact upon multiple pathways, including intracellular immune regulation, without disruption to general transcription or epithelium integrity. We present the first evidence that febrile temperatures associated with COVID-19 inhibit SARS-CoV-2 replication in respiratory epithelia. Our data identify an important role for tissue temperature in the epithelial restriction of SARS-CoV-2 independently of canonical interferon (IFN)-mediated antiviral immune defenses., Competing Interests: The authors have declared that no competing interests exist.

Published
2021
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2. Elevated temperature inhibits SARS-CoV-2 replication in respiratory epithelium independently of IFN-mediated innate immune defenses

Author

Vanessa Herder, Kieran Dee, Joanna K. Wojtus, Ilaria Epifano, Daniel Goldfarb, Christoforos Rozario, Quan Gu, Ana Da Silva Filipe, Kyriaki Nomikou, Jenna Nichols, Ruth F. Jarrett, Andrew Stevenson, Steven McFarlane, Meredith E. Stewart, Agnieszka M. Szemiel, Rute M. Pinto, Andreu Masdefiol Garriga, Chris Davis, Jay Allan, Sheila V. Graham, Pablo R. Murcia, and Chris Boutell

Subjects
Male, RNA viruses, Viral Diseases, Hot Temperature, Pulmonology, Coronaviruses, Molecular biology, Physiology, viruses, Virus Replication, Body Temperature, Tissue Culture Techniques, Medical Conditions, Sequencing techniques, Chlorocebus aethiops, RNA-Seq, Biology (General), Pathology and laboratory medicine, Virus Testing, General Neuroscience, RNA sequencing, Cell Differentiation, Middle Aged, Medical microbiology, Infectious Diseases, Physiological Parameters, Host-Pathogen Interactions, Viruses, Female, SARS CoV 2, Pathogens, General Agricultural and Biological Sciences, Research Article, Adolescent, SARS coronavirus, QH301-705.5, Respiratory Mucosa, Models, Biological, Microbiology, General Biochemistry, Genetics and Molecular Biology, Respiratory Disorders, Diagnostic Medicine, Virology, Animals, Humans, Vero Cells, Medicine and health sciences, General Immunology and Microbiology, Biology and life sciences, SARS-CoV-2, Gene Expression Profiling, fungi, Organisms, Viral pathogens, COVID-19, Epithelial Cells, Covid 19, Immunity, Innate, Viral Replication, respiratory tract diseases, Microbial pathogens, Research and analysis methods, Molecular biology techniques, Respiratory Infections, Interferons, Developmental Biology
Abstract

The pandemic spread of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the etiological agent of Coronavirus Disease 2019 (COVID-19), represents an ongoing international health crisis. A key symptom of SARS-CoV-2 infection is the onset of fever, with a hyperthermic temperature range of 38 to 41°C. Fever is an evolutionarily conserved host response to microbial infection that can influence the outcome of viral pathogenicity and regulation of host innate and adaptive immune responses. However, it remains to be determined what effect elevated temperature has on SARS-CoV-2 replication. Utilizing a three-dimensional (3D) air–liquid interface (ALI) model that closely mimics the natural tissue physiology of SARS-CoV-2 infection in the respiratory airway, we identify tissue temperature to play an important role in the regulation of SARS-CoV-2 infection. Respiratory tissue incubated at 40°C remained permissive to SARS-CoV-2 entry but refractory to viral transcription, leading to significantly reduced levels of viral RNA replication and apical shedding of infectious virus. We identify tissue temperature to play an important role in the differential regulation of epithelial host responses to SARS-CoV-2 infection that impact upon multiple pathways, including intracellular immune regulation, without disruption to general transcription or epithelium integrity. We present the first evidence that febrile temperatures associated with COVID-19 inhibit SARS-CoV-2 replication in respiratory epithelia. Our data identify an important role for tissue temperature in the epithelial restriction of SARS-CoV-2 independently of canonical interferon (IFN)-mediated antiviral immune defenses., A clinical feature of COVID-19 is the onset of fever, raising the body temperature to 38-41°C. This study demonstrates that temperature elevation to 40°C limits the replication of SARS-CoV-2 in respiratory airway cultures, independently of the induction of interferon-mediated antiviral immune defences.

Published
2020

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