SARS-CoV-2 utilization of ACE2 from different bat species allows for virus entry and replication in vitro

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is believed to have a zoonotic origin with bats suspected as a natural host. In this work, we individually express the ACE2 of seven bat species including, little brown, great roundleaf, Pearson's horseshoe, greater horseshoe, Brazili...

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Veröffentlicht in:Virology (New York, N.Y.) N.Y.), 2023-09, Vol.586, p.122-129
Hauptverfasser: Briggs, Kelsey, Sweeney, Ryan, Blehert, David S., Spackman, Erica, Suarez, David L., Kapczynski, Darrell R.
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Sprache:eng
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Zusammenfassung:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is believed to have a zoonotic origin with bats suspected as a natural host. In this work, we individually express the ACE2 of seven bat species including, little brown, great roundleaf, Pearson's horseshoe, greater horseshoe, Brazilian free-tailed, Egyptian rousette, and Chinese rufous horseshoe in DF1 cells and determine their ability to support attachment and replication of SARS-CoV-2 viruses. We demonstrate that the ACE2 receptor of all seven species made DF1 cells permissible to SARS-CoV-2. The level of virus replication differed between bat species and variants tested. The Wuhan lineage SARS-CoV-2 virus replicated to higher titers than either variant virus tested. All viruses tested grew to higher titers in cells expressing the human ACE2 gene compared to a bat ACE2. This study provides a practical in vitromethod for further testing of animal species for potential susceptibility to current and emerging SARS-CoV-2 viruses. •Here we demonstrate that SARS2-CoV-2 and its variants can bind to bat ACE2 for entry and replication in avian DF1 cells.•This work examines the ability of SARS-CoV-2 to attach to bat ACE2 and replicate in a non-permissive avian cell line.•Identification of bat species susceptible to SARS-CoV-2 providing data on zoonotic reservoirs and transmission potential.•Results positively correlate with other studies enhancing the predicative capability of the ACE2 expression model.
ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2023.07.002