Difference in Receptor Usage between Severe Acute Respiratory Syndrome (SARS) Coronavirus and SARS-Like Coronavirus of Bat Origin

Citation

Material Information

Title:
Difference in Receptor Usage between Severe Acute Respiratory Syndrome (SARS) Coronavirus and SARS-Like Coronavirus of Bat Origin
Series Title:
Journal of Virology
Creator:
Ren, Wuze
Qu, Xiuxia
Li, Wendong
Han, Zhenggang
Yu, Meng
Zhou, Peng
Zhang, Shi-yu
Wang, Lin-Fa
Deng, Hongkui
Shi, Zhengli
Publisher:
American Society for Microbiology
Publication Date:
Language:
English

Subjects

Subjects / Keywords:
Difference In Receptor Usage ( local )
Sars ( local )
Sars-Like Coronavirus ( local )
Genre:
serial ( sobekcm )

Notes

Abstract:
Severe acute respiratory syndrome (SARS) is caused by the SARS-associated coronavirus (SARS-CoV), which uses angiotensin-converting enzyme 2 (ACE2) as its receptor for cell entry. A group of SARS-like CoVs (SL-CoVs) has been identified in horseshoe bats. SL-CoVs and SARS-CoVs share identical genome organizations and high sequence identities, with the main exception of the N terminus of the spike protein (S), known to be responsible for receptor binding in CoVs. In this study, we investigated the receptor usage of the SL-CoV S by combining a human immunodeficiency virus-based pseudovirus system with cell lines expressing the ACE2 molecules of human, civet, or horseshoe bat. In addition to full-length S of SL-CoV and SARS-CoV, a series of S chimeras was constructed by inserting different sequences of the SARS-CoV S into the SL-CoV S backbone. Several important observations were made from this study. First, the SL-CoV S was unable to use any of the three ACE2 molecules as its receptor. Second, the SARS-CoV S failed to enter cells expressing the bat ACE2. Third, the chimeric S covering the previously defined receptor-binding domain gained its ability to enter cells via human ACE2, albeit with different efficiencies for different constructs. Fourth, a minimal insert region (amino acids 310 to 518) was found to be sufficient to convert the SL-CoV S from non-ACE2 binding to human ACE2 binding, indicating that the SL-CoV S is largely compatible with SARS-CoV S protein both in structure and in function. The significance of these findings in relation to virus origin, virus recombination, and host switching is discussed. The outbreaks of severe acute respiratory syndrome (SARS) in 2002-2003, which resulted in over 8,000 infections and close to 800 deaths, was caused by a novel coronavirus (CoV), now known as the SARS-associated CoV (SARS-CoV) (12, 25, 33, 36). The association of SARS-CoV with animals was first revealed by the isolation and identification of very closely related viruses in several Himalayan palm civets (Pagu
Original Version:
Journal of Virology, Vol. 82, no. 4 (2008-01-30).

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Holding Location:
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