File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Attenuated SARS-CoV-2 variants with deletions at the S1/S2 junction

TitleAttenuated SARS-CoV-2 variants with deletions at the S1/S2 junction
Authors
KeywordsCoronavirus
COVID-19
SARS-CoV-2
Spike mutant
Spike S1/S2 mutant
Issue Date2020
PublisherTaylor & Francis Group, on behalf of Shanghai ShangyixunCultural Communication Co., Ltd. The Journal's web site is located at https://www.tandfonline.com/toc/temi20/current
Citation
Emerging Microbes & Infections, 2020, v. 9, p. 837-842 How to Cite?
AbstractThe emergence of SARS-CoV-2 has led to the current global coronavirus pandemic and more than one million infections since December 2019. The exact origin of SARS-CoV-2 remains elusive, but the presence of a distinct motif in the S1/S2 junction region suggests the possible acquisition of cleavage site(s) in the spike protein that promoted cross-species transmission. Through plaque purification of Vero-E6 cultured SARS-CoV-2, we found a series of variants which contain 15-30-bp deletions (Del-mut) or point mutations respectively at the S1/S2 junction. Examination of the original clinical specimen from which the isolate was derived, and 26 additional SARS-CoV-2 positive clinical specimens, failed to detect these variants. Infection of hamsters shows that one of the variants (Del-mut-1) which carries deletion of 10 amino acids (30bp) does not cause the body weight loss or more severe pathological changes in the lungs that is associated with wild type virus infection. We suggest that the unique cleavage motif promoting SARS-CoV-2 infection in humans may be under strong selective pressure, given that replication in permissive Vero-E6 cells leads to the loss of this adaptive function. It would be important to screen the prevalence of these variants in asymptomatic infected cases. The potential of the Del-mut variants as an attenuated vaccine or laboratory tool should be evaluated.
Persistent Identifierhttp://hdl.handle.net/10722/285303
ISSN
2018 Impact Factor: 6.212
2015 SCImago Journal Rankings: 1.774
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorLau, SY-
dc.contributor.authorWang, P-
dc.contributor.authorMok, BWY-
dc.contributor.authorZhang, AJ-
dc.contributor.authorChu, H-
dc.contributor.authorLee, ACY-
dc.contributor.authorDeng, S-
dc.contributor.authorChen, P-
dc.contributor.authorChan, KH-
dc.contributor.authorSong, W-
dc.contributor.authorChen, Z-
dc.contributor.authorTo, KKW-
dc.contributor.authorChan, JFW-
dc.contributor.authorYuen, KY-
dc.contributor.authorChen, H-
dc.date.accessioned2020-08-18T03:52:12Z-
dc.date.available2020-08-18T03:52:12Z-
dc.date.issued2020-
dc.identifier.citationEmerging Microbes & Infections, 2020, v. 9, p. 837-842-
dc.identifier.issn2222-1751-
dc.identifier.urihttp://hdl.handle.net/10722/285303-
dc.description.abstractThe emergence of SARS-CoV-2 has led to the current global coronavirus pandemic and more than one million infections since December 2019. The exact origin of SARS-CoV-2 remains elusive, but the presence of a distinct motif in the S1/S2 junction region suggests the possible acquisition of cleavage site(s) in the spike protein that promoted cross-species transmission. Through plaque purification of Vero-E6 cultured SARS-CoV-2, we found a series of variants which contain 15-30-bp deletions (Del-mut) or point mutations respectively at the S1/S2 junction. Examination of the original clinical specimen from which the isolate was derived, and 26 additional SARS-CoV-2 positive clinical specimens, failed to detect these variants. Infection of hamsters shows that one of the variants (Del-mut-1) which carries deletion of 10 amino acids (30bp) does not cause the body weight loss or more severe pathological changes in the lungs that is associated with wild type virus infection. We suggest that the unique cleavage motif promoting SARS-CoV-2 infection in humans may be under strong selective pressure, given that replication in permissive Vero-E6 cells leads to the loss of this adaptive function. It would be important to screen the prevalence of these variants in asymptomatic infected cases. The potential of the Del-mut variants as an attenuated vaccine or laboratory tool should be evaluated.-
dc.languageeng-
dc.publisherTaylor & Francis Group, on behalf of Shanghai ShangyixunCultural Communication Co., Ltd. The Journal's web site is located at https://www.tandfonline.com/toc/temi20/current-
dc.relation.ispartofEmerging Microbes & Infections-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectCoronavirus-
dc.subjectCOVID-19-
dc.subjectSARS-CoV-2-
dc.subjectSpike mutant-
dc.subjectSpike S1/S2 mutant-
dc.titleAttenuated SARS-CoV-2 variants with deletions at the S1/S2 junction-
dc.typeArticle-
dc.identifier.emailLau, SY: sylau926@hkucc.hku.hk-
dc.identifier.emailWang, P: puiwang@hkucc.hku.hk-
dc.identifier.emailMok, BWY: bobomok@hku.hk-
dc.identifier.emailZhang, AJ: zhangajx@hkucc.hku.hk-
dc.identifier.emailChu, H: hinchu@hku.hk-
dc.identifier.emailLee, ACY: cyalee@hku.hk-
dc.identifier.emailDeng, S: dengsf@hku.hk-
dc.identifier.emailChan, KH: chankh2@hkucc.hku.hk-
dc.identifier.emailSong, W: wjsong@hkucc.hku.hk-
dc.identifier.emailChen, Z: zchenai@hku.hk-
dc.identifier.emailTo, KKW: kelvinto@hku.hk-
dc.identifier.emailChan, JFW: jfwchan@hku.hk-
dc.identifier.emailYuen, KY: kyyuen@hkucc.hku.hk-
dc.identifier.emailChen, H: hlchen@hku.hk-
dc.identifier.authorityZhang, AJ=rp00413-
dc.identifier.authorityChu, H=rp02125-
dc.identifier.authorityChan, KH=rp01921-
dc.identifier.authorityChen, Z=rp00243-
dc.identifier.authorityTo, KKW=rp01384-
dc.identifier.authorityChan, JFW=rp01736-
dc.identifier.authorityYuen, KY=rp00366-
dc.identifier.authorityChen, H=rp00383-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1080/22221751.2020.1756700-
dc.identifier.pmid32301390-
dc.identifier.pmcidPMC7241555-
dc.identifier.scopuseid_2-s2.0-85083865808-
dc.identifier.hkuros312842-
dc.identifier.volume9-
dc.identifier.spage837-
dc.identifier.epage842-
dc.publisher.placeUnited Kingdom-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats