Abstract
Severe acute respiratory syndrome coronavirus 2 did not replicate efficiently in 13 bat cell lines, whereas severe acute respiratory syndrome coronavirus replicated efficiently in kidney cells of its ancestral host, the Rhinolophus sinicus bat, suggesting different evolutionary origins. Structural modeling showed that RBD/RsACE2 binding may contribute to the differential cellular tropism.
Highlights
Severe acute respiratory syndrome coronavirus 2 did not replicate efficiently in 13 bat cell lines, whereas severe acute respiratory syndrome coronavirus replicated efficiently in kidney cells of its ancestral host, the Rhinolophus sinicus bat, suggesting different evolutionary origins
To elucidate whether the receptor-binding interface is a contributing factor for cellular tropism, we modeled the structure of the SARS-CoV-2 receptor binding domain (RBD) with that of human
Was most closely related to SARSr-Rs-BatCoVs from Yunnan, China, suggesting R. sinicus as its primary origin. It could use R. sinicus angiotensin-converting enzyme 2 (Rs-ACE2) as receptor for cell entry [13], which may explain the efficient replication of SARS-CoV in R. sinicus kidney cells
Summary
Severe acute respiratory syndrome coronavirus 2 did not replicate efficiently in 13 bat cell lines, whereas severe acute respiratory syndrome coronavirus replicated efficiently in kidney cells of its ancestral host, the Rhinolophus sinicus bat, suggesting different evolutionary origins. SARS-CoV could replicate efficiently in kidney cells of its primary origin, R. sinicus, but not in other tested bat cells [6]. To elucidate the possible origin of SARS-CoV-2, we tested susceptibilities of bat cell lines developed from different Miniopterus pusillus, Mr, Myotis ricketti; Pa, Pipistrellus abramus, Rl, Rousettus leschenaultii, Rs, Rhinolophus sinicus, Tp, Tylonycteris pachypus.
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