학술논문

Genome-wide bidirectional CRISPR screens identify mucins as host factors modulating SARS-CoV-2 infection
Document Type
article
Source
Nature Genetics. 54(8)
Subject
Acute Respiratory Distress Syndrome
Clinical Research
Infectious Diseases
Pneumonia & Influenza
Rare Diseases
Biodefense
Lung
Vaccine Related
Pneumonia
Prevention
Emerging Infectious Diseases
Genetics
2.2 Factors relating to the physical environment
2.1 Biological and endogenous factors
Aetiology
Respiratory
Infection
Good Health and Well Being
Animals
COVID-19
Clustered Regularly Interspaced Short Palindromic Repeats
Epigenesis
Genetic
Humans
Mice
Mucins
SARS-CoV-2
Biological Sciences
Medical and Health Sciences
Developmental Biology
Language
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes a range of symptoms in infected individuals, from mild respiratory illness to acute respiratory distress syndrome. A systematic understanding of host factors influencing viral infection is critical to elucidate SARS-CoV-2-host interactions and the progression of Coronavirus disease 2019 (COVID-19). Here, we conducted genome-wide CRISPR knockout and activation screens in human lung epithelial cells with endogenous expression of the SARS-CoV-2 entry factors ACE2 and TMPRSS2. We uncovered proviral and antiviral factors across highly interconnected host pathways, including clathrin transport, inflammatory signaling, cell-cycle regulation, and transcriptional and epigenetic regulation. We further identified mucins, a family of high molecular weight glycoproteins, as a prominent viral restriction network that inhibits SARS-CoV-2 infection in vitro and in murine models. These mucins also inhibit infection of diverse respiratory viruses. This functional landscape of SARS-CoV-2 host factors provides a physiologically relevant starting point for new host-directed therapeutics and highlights airway mucins as a host defense mechanism.