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Difference in receptor usage between severe acute respiratory syndrome (SARS) coronavirus and SARS-like coronavirus of bat origin.
J Virol. 2008 Feb; 82(4):1899-907.JV

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.

Authors+Show Affiliations

State key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, Hubei 430071, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18077725

Citation

Ren, Wuze, et al. "Difference in Receptor Usage Between Severe Acute Respiratory Syndrome (SARS) Coronavirus and SARS-like Coronavirus of Bat Origin." Journal of Virology, vol. 82, no. 4, 2008, pp. 1899-907.
Ren W, Qu X, Li W, et al. Difference in receptor usage between severe acute respiratory syndrome (SARS) coronavirus and SARS-like coronavirus of bat origin. J Virol. 2008;82(4):1899-907.
Ren, W., Qu, X., Li, W., Han, Z., Yu, M., Zhou, P., Zhang, S. Y., Wang, L. F., Deng, H., & Shi, Z. (2008). Difference in receptor usage between severe acute respiratory syndrome (SARS) coronavirus and SARS-like coronavirus of bat origin. Journal of Virology, 82(4), 1899-907.
Ren W, et al. Difference in Receptor Usage Between Severe Acute Respiratory Syndrome (SARS) Coronavirus and SARS-like Coronavirus of Bat Origin. J Virol. 2008;82(4):1899-907. PubMed PMID: 18077725.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Difference in receptor usage between severe acute respiratory syndrome (SARS) coronavirus and SARS-like coronavirus of bat origin. AU - Ren,Wuze, AU - Qu,Xiuxia, AU - Li,Wendong, AU - Han,Zhenggang, AU - Yu,Meng, AU - Zhou,Peng, AU - Zhang,Shu-Yi, AU - Wang,Lin-Fa, AU - Deng,Hongkui, AU - Shi,Zhengli, Y1 - 2007/12/12/ PY - 2007/12/14/pubmed PY - 2008/3/6/medline PY - 2007/12/14/entrez SP - 1899 EP - 907 JF - Journal of virology JO - J Virol VL - 82 IS - 4 N2 - 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. SN - 1098-5514 UR - https://www.unboundmedicine.com/medline/citation/18077725/Difference_in_receptor_usage_between_severe_acute_respiratory_syndrome__SARS__coronavirus_and_SARS_like_coronavirus_of_bat_origin_ L2 - https://journals.asm.org/doi/10.1128/JVI.01085-07?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -