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Article: Low Environmental Temperature Exacerbates Severe Acute Respiratory Syndrome Coronavirus 2 Infection in Golden Syrian Hamsters

TitleLow Environmental Temperature Exacerbates Severe Acute Respiratory Syndrome Coronavirus 2 Infection in Golden Syrian Hamsters
Authors
Keywordsanimal
coronavirus
COVID-19
SARS-CoV-2
temperature
Issue Date2021
Citation
Clinical Infectious Diseases, 2021 How to Cite?
AbstractBackground. The effect of low environmental temperature on viral shedding and disease severity of Coronavirus Disease 2019 (COVID-19) is uncertain. Methods. We investigated the virological, clinical, pathological, and immunological changes in hamsters housed at room (21 degrees C), low (12-15 degrees C), and high (30-33 degrees C) temperature after challenge by 10(5) plaque-forming units of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Results. The nasal turbinate, trachea, and lung viral load and live virus titer were significantly higher (similar to 0.5-log(10) gene copies/beta-actin, P < .05) in the low-temperature group at 7 days postinfection (dpi). The low-temperature group also demonstrated significantly higher level of tumor necrosis factor-alpha, interferon-gamma (IFN-gamma), interleulcin-1 beta, and C-C motif chemokine ligand 3, and lower level of the antiviral IFN-alpha in lung tissues at 4 dpi than the other 2 groups. Their lungs were grossly and diffusely hemorrhagic, with more severe and diffuse alveolar and peribronchiolar inflammatory infiltration, bronchial epithelial cell death, and significantly higher mean total lung histology scores. By 7 dpi, the low-temperature group still showed persistent and severe alveolar inflammation and hemorrhage, and little alveolar cell proliferative changes of recovery. The viral loads in the oral swabs of the low-temperature group were significantly higher than those of the other two groups from 10 to 17 dpi by about 0.5-1.0 log(10) gene copies/beta-actin. The mean neutralizing antibody titer of the low-temperature group was significantly (P < .05) lower than that of the room temperature group at 7 dpi and 30 dpi. Conclusions. This study provided in vivo evidence that low environmental temperature exacerbated the degree of virus shedding, disease severity, and tissue proinflarrunatory cytokines/chemokines expression, and suppressed the neutralizing antibody response of SARS-CoV-2-infected hamsters. Keeping warm in winter may reduce the severity of COVID-19.
Persistent Identifierhttp://hdl.handle.net/10722/305000
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChan, JFW-
dc.contributor.authorPoon, KM-
dc.contributor.authorChan, CS-
dc.contributor.authorChik, KKH-
dc.contributor.authorTsang, OL-
dc.contributor.authorZou, Z-
dc.contributor.authorChan, CYC-
dc.contributor.authorLee, CY-
dc.contributor.authorLi, C-
dc.contributor.authorLiang, R-
dc.contributor.authorCao, J-
dc.contributor.authorTang, K-
dc.contributor.authorYuen, TT-
dc.contributor.authorHu, B-
dc.contributor.authorHuang, X-
dc.contributor.authorChai, Y-
dc.contributor.authorShuai, HV-
dc.contributor.authorLuo, C-
dc.contributor.authorCai, J-
dc.contributor.authorChan, KH-
dc.contributor.authorSridhar, S-
dc.contributor.authorYin, F-
dc.contributor.authorKok, KH-
dc.contributor.authorChu, H-
dc.contributor.authorZhang, J-
dc.contributor.authorYuan, S-
dc.contributor.authorYuen, KY-
dc.date.accessioned2021-10-05T02:38:18Z-
dc.date.available2021-10-05T02:38:18Z-
dc.date.issued2021-
dc.identifier.citationClinical Infectious Diseases, 2021-
dc.identifier.urihttp://hdl.handle.net/10722/305000-
dc.description.abstractBackground. The effect of low environmental temperature on viral shedding and disease severity of Coronavirus Disease 2019 (COVID-19) is uncertain. Methods. We investigated the virological, clinical, pathological, and immunological changes in hamsters housed at room (21 degrees C), low (12-15 degrees C), and high (30-33 degrees C) temperature after challenge by 10(5) plaque-forming units of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Results. The nasal turbinate, trachea, and lung viral load and live virus titer were significantly higher (similar to 0.5-log(10) gene copies/beta-actin, P < .05) in the low-temperature group at 7 days postinfection (dpi). The low-temperature group also demonstrated significantly higher level of tumor necrosis factor-alpha, interferon-gamma (IFN-gamma), interleulcin-1 beta, and C-C motif chemokine ligand 3, and lower level of the antiviral IFN-alpha in lung tissues at 4 dpi than the other 2 groups. Their lungs were grossly and diffusely hemorrhagic, with more severe and diffuse alveolar and peribronchiolar inflammatory infiltration, bronchial epithelial cell death, and significantly higher mean total lung histology scores. By 7 dpi, the low-temperature group still showed persistent and severe alveolar inflammation and hemorrhage, and little alveolar cell proliferative changes of recovery. The viral loads in the oral swabs of the low-temperature group were significantly higher than those of the other two groups from 10 to 17 dpi by about 0.5-1.0 log(10) gene copies/beta-actin. The mean neutralizing antibody titer of the low-temperature group was significantly (P < .05) lower than that of the room temperature group at 7 dpi and 30 dpi. Conclusions. This study provided in vivo evidence that low environmental temperature exacerbated the degree of virus shedding, disease severity, and tissue proinflarrunatory cytokines/chemokines expression, and suppressed the neutralizing antibody response of SARS-CoV-2-infected hamsters. Keeping warm in winter may reduce the severity of COVID-19.-
dc.languageeng-
dc.relation.ispartofClinical Infectious Diseases-
dc.subjectanimal-
dc.subjectcoronavirus-
dc.subjectCOVID-19-
dc.subjectSARS-CoV-2-
dc.subjecttemperature-
dc.titleLow Environmental Temperature Exacerbates Severe Acute Respiratory Syndrome Coronavirus 2 Infection in Golden Syrian Hamsters-
dc.typeArticle-
dc.identifier.emailChan, JFW: jfwchan@hku.hk-
dc.identifier.emailPoon, KM: vinpoon@hku.hk-
dc.identifier.emailChan, CS: cschan@hku.hk-
dc.identifier.emailChik, KKH: kennchik@hku.hk-
dc.identifier.emailTsang, OL: oltsang@hku.hk-
dc.identifier.emailLee, CY: cyalee@hku.hk-
dc.identifier.emailLi, C: canlee@hku.hk-
dc.identifier.emailShuai, HV: shuaihp@connect.hku.hk-
dc.identifier.emailLuo, C: cuiting@hku.hk-
dc.identifier.emailCai, J: caijuice@hku.hk-
dc.identifier.emailChan, KH: chankh2@hkucc.hku.hk-
dc.identifier.emailSridhar, S: sid8998@hku.hk-
dc.identifier.emailKok, KH: khkok@hku.hk-
dc.identifier.emailChu, H: hinchu@hku.hk-
dc.identifier.emailZhang, J: zhangajx@hkucc.hku.hk-
dc.identifier.emailYuan, S: yuansf@hku.hk-
dc.identifier.emailYuen, KY: kyyuen@hkucc.hku.hk-
dc.identifier.authorityChan, JFW=rp01736-
dc.identifier.authorityChan, KH=rp01921-
dc.identifier.authoritySridhar, S=rp02249-
dc.identifier.authorityKok, KH=rp01455-
dc.identifier.authorityChu, H=rp02125-
dc.identifier.authorityZhang, J=rp00413-
dc.identifier.authorityYuan, S=rp02640-
dc.identifier.authorityYuen, KY=rp00366-
dc.identifier.doi10.1093/cid/ciab817-
dc.identifier.pmid34536277-
dc.identifier.hkuros326060-
dc.identifier.isiWOS:000789253800001-

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