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SARS‐CoV‐2 evades immune detection in alveolar macrophages
Author(s) -
Dalskov Louise,
Møhlenberg Michelle,
Thyrsted Jacob,
BlayCadanet Julia,
Poulsen Ebbe Toftgaard,
Folkersen Birgitte Holst,
Skaarup Søren Helbo,
Olagnier David,
Reinert Line,
Enghild Jan Johannes,
Hoffmann Hans Jürgen,
Holm Christian Kanstrup,
Hartmann Rune
Publication year - 2020
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.202051252
Subject(s) - immune system , sendai virus , virology , virus , immunology , respiratory tract , biology , respiratory system , lung , interferon , innate immune system , medicine , anatomy
Respiratory infections, like the current COVID‐19 pandemic, target epithelial cells in the respiratory tract. Alveolar macrophages (AMs) are tissue‐resident macrophages located within the lung. They play a key role in the early phases of an immune response to respiratory viruses. AMs are likely the first immune cells to encounter SARS‐CoV‐2 during an infection, and their reaction to the virus will have a profound impact on the outcome of the infection. Interferons (IFNs) are antiviral cytokines and among the first cytokines produced upon viral infection. In this study, AMs from non‐infectious donors are challenged with SARS‐CoV‐2. We demonstrate that challenged AMs are incapable of sensing SARS‐CoV‐2 and of producing an IFN response in contrast to other respiratory viruses, like influenza A virus and Sendai virus, which trigger a robust IFN response. The absence of IFN production in AMs upon challenge with SARS‐CoV‐2 could explain the initial asymptotic phase observed during COVID‐19 and argues against AMs being the sources of pro‐inflammatory cytokines later during infection.