Complete #genome analysis of a #SARS-like #bat #coronavirus identified in the Republic of #Korea (Virus Genes, abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Virus Genes. 2019 May 10. doi: 10.1007/s11262-019-01668-w. [Epub ahead of print]

Complete genome analysis of a SARS-like bat coronavirus identified in the Republic of Korea.

Kim Y1,2, Son K1, Kim YS2, Lee SY2, Jheong W1, Oem JK3.

Author information: 1 Environmental Health Research Department, National Institute of Environmental Research, Hwangyeong-ro 42, Seo-gu, Incheon, Republic of Korea. 2 Department of Veterinary Infectious Diseases, College of Veterinary Medicine, Chonbuk National University, Jeonju, Republic of Korea. 3 Department of Veterinary Infectious Diseases, College of Veterinary Medicine, Chonbuk National University, Jeonju, Republic of Korea. jku0623@jbnu.ac.kr.

 

Abstract

Bats have been widely known as natural reservoir hosts of zoonotic diseases, such as severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) caused by coronaviruses (CoVs). In the present study, we investigated the whole genomic sequence of a SARS-like bat CoV (16BO133) and found it to be 29,075 nt in length with a 40.9% G+C content. Phylogenetic analysis using amino acid sequences of the ORF 1ab and the spike gene showed that the bat coronavirus strain 16BO133 was grouped with the Beta-CoV lineage B and was closely related to the JTMC15 strain isolated from Rhinolophus ferrumequinum in China. However, 16BO133 was distinctly located in the phylogenetic topology of the human SARS CoV strain (Tor2). Interestingly, 16BO133 showed complete elimination of ORF8 regions induced by a frame shift of the stop codon in ORF7b. The lowest amino acid identity of 16BO133 was identified at the spike region among various ORFs. The spike region of 16BO133 showed 84.7% and 75.2% amino acid identity with Rf1 (SARS-like bat CoV) and Tor2 (human SARS CoV), respectively. In addition, the S gene of 16BO133 was found to contain the amino acid substitution of two critical residues (N479S and T487 V) associated with human infection. In conclusion, we firstly carried out whole genome characterization of the SARS-like bat coronavirus discovered in the Republic of Korea; however, it presumably has no human infectivity. However, continuous surveillance and genomic characterization of coronaviruses from bats are necessary due to potential risks of human infection induced by genetic mutation.

KEYWORDS: Bat; Frame shift; SARS-like coronavirus; Whole genome; Zoonotic disease

PMID: 31076983 DOI: 10.1007/s11262-019-01668-w

Keywords: Coronavirus; SARS; Bats; S. Korea.

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Anti-spike #IgG causes severe acute #lung #injury by skewing #macrophage responses during acute #SARS-CoV infection (JCI Insight, abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

JCI Insight. 2019 Feb 21;4(4). pii: 123158. doi: 10.1172/jci.insight.123158. eCollection 2019 Feb 21.

Anti-spike IgG causes severe acute lung injury by skewing macrophage responses during acute SARS-CoV infection.

Liu L1,2, Wei Q3, Lin Q1, Fang J1, Wang H1, Kwok H1, Tang H1, Nishiura K1, Peng J1, Tan Z1, Wu T1, Cheung KW1, Chan KH1, Alvarez X4, Qin C3, Lackner A4, Perlman S5,6, Yuen KY1, Chen Z1,2.

Author information: 1 AIDS Institute and Department of Microbiology, State Key Laboratory of Emerging Infectious Disease, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. 2 HKU-AIDS Institute Shenzhen Research Laboratory and AIDS Clinical Research Laboratory, Shenzhen Key Laboratory of Infection and Immunity, Shenzhen Key Clinical Department of Emerging Infectious Diseases, Shenzhen Third People’s Hospital, Shenzhen, China. 3 Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences (CAMS) and Peking Union Medical College (PUMC), Beijing, China. 4 Division of Comparative Pathology, Tulane National Primate Research Center, Covington, Louisiana, USA. 5 Department of Microbiology and Immunology, University of Iowa, Iowa City, Iowa, USA. 6 State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.

 

Abstract

Newly emerging viruses, such as severe acute respiratory syndrome coronavirus (SARS-CoV), Middle Eastern respiratory syndrome CoVs (MERS-CoV), and H7N9, cause fatal acute lung injury (ALI) by driving hypercytokinemia and aggressive inflammation through mechanisms that remain elusive. In SARS-CoV/macaque models, we determined that anti-spike IgG (S-IgG), in productively infected lungs, causes severe ALI by skewing inflammation-resolving response. Alveolar macrophages underwent functional polarization in acutely infected macaques, demonstrating simultaneously both proinflammatory and wound-healing characteristics. The presence of S-IgG prior to viral clearance, however, abrogated wound-healing responses and promoted MCP1 and IL-8 production and proinflammatory monocyte/macrophage recruitment and accumulation. Critically, patients who eventually died of SARS (hereafter referred to as deceased patients) displayed similarly accumulated pulmonary proinflammatory, absence of wound-healing macrophages, and faster neutralizing antibody responses. Their sera enhanced SARS-CoV-induced MCP1 and IL-8 production by human monocyte-derived wound-healing macrophages, whereas blockade of FcγR reduced such effects. Our findings reveal a mechanism responsible for virus-mediated ALI, define a pathological consequence of viral specific antibody response, and provide a potential target for treatment of SARS-CoV or other virus-mediated lung injury.

KEYWORDS: Cytokines; Immunoglobulins; Infectious disease; Macrophages; Pulmonology

PMID: 30830861 DOI: 10.1172/jci.insight.123158

Keywords: Coronavirus; SARS-CoV; Acute Lung Injury; Immunoglobulins.

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#Global #Epidemiology of #Bat #Coronaviruses (Viruses, abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Viruses. 2019 Feb 20;11(2). pii: E174. doi: 10.3390/v11020174.

Global Epidemiology of Bat Coronaviruses.

Wong ACP1, Li X2, Lau SKP3,4,5,6,7, Woo PCY8,9,10,11,12.

Author information: 1 Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong. antonwcp@hku.hk. 2 Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong. lixinlyh@connect.hku.hk. 3 Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong. skplau@hku.hk. 4 State Key Laboratory of Emerging Infectious Diseases, The University of Hong Kong, Pokfulam, Hong Kong. skplau@hku.hk. 5 Research Centre of Infection and Immunology, The University of Hong Kong, Pokfulam, Hong Kong. skplau@hku.hk. 6 Carol Yu Centre for Infection, The University of Hong Kong, Pokfulam, Hong Kong. skplau@hku.hk. 7 Collaborative Innovation Centre for Diagnosis and Treatment of Infectious Diseases, The University of Hong Kong, Pokfulam, Hong Kong. skplau@hku.hk. 8 Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong. pcywoo@hku.hk. 9 State Key Laboratory of Emerging Infectious Diseases, The University of Hong Kong, Pokfulam, Hong Kong. pcywoo@hku.hk. 10 Research Centre of Infection and Immunology, The University of Hong Kong, Pokfulam, Hong Kong. pcywoo@hku.hk. 11 Carol Yu Centre for Infection, The University of Hong Kong, Pokfulam, Hong Kong. pcywoo@hku.hk. 12 Collaborative Innovation Centre for Diagnosis and Treatment of Infectious Diseases, The University of Hong Kong, Pokfulam, Hong Kong. pcywoo@hku.hk.

 

Abstract

Bats are a unique group of mammals of the order Chiroptera. They are highly diversified and are the group of mammals with the second largest number of species. Such highly diversified cell types and receptors facilitate them to be potential hosts of a large variety of viruses. Bats are the only group of mammals capable of sustained flight, which enables them to disseminate the viruses they harbor and enhance the chance of interspecies transmission. This article aims at reviewing the various aspects of the global epidemiology of bat coronaviruses (CoVs). Before the SARS epidemic, bats were not known to be hosts for CoVs. In the last 15 years, bats have been found to be hosts of >30 CoVs with complete genomes sequenced, and many more if those without genome sequences are included. Among the four CoV genera, only alphaCoVs and betaCoVs have been found in bats. As a whole, both alphaCoVs and betaCoVs have been detected from bats in Asia, Europe, Africa, North and South America and Australasia; but alphaCoVs seem to be more widespread than betaCoVs, and their detection rate is also higher. For betaCoVs, only those from subgenera Sarbecovirus, Merbecovirus, Nobecovirus and Hibecovirus have been detected in bats. Most notably, horseshoe bats are the reservoir of SARS-CoV, and several betaCoVs from subgenus Merbecovirus are closely related to MERS-CoV. In addition to the interactions among various bat species themselves, bat⁻animal and bat⁻human interactions, such as the presence of live bats in wildlife wet markets and restaurants in Southern China, are important for interspecies transmission of CoVs and may lead to devastating global outbreaks.

KEYWORDS: Alphacoronavirus; Betacoronavirus; bat; coronavirus; epidemiology; global; host; interspecies transmission

PMID: 30791586 DOI: 10.3390/v11020174

Keywords: Alphacoronavirus; Betacoronavirus; SARS; MERS-CoV; Bats.

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From #SARS to #MERS, Thrusting #Coronaviruses into the Spotlight (Viruses, abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Viruses. 2019 Jan 14;11(1). pii: E59. doi: 10.3390/v11010059.

From SARS to MERS, Thrusting Coronaviruses into the Spotlight.

Song Z1,2,3, Xu Y4,5,6, Bao L7,8,9, Zhang L10,11,12, Yu P13,14,15, Qu Y16,17,18, Zhu H19,20,21, Zhao W22,23,24, Han Y25,26,27, Qin C28,29,30.

Author information: 1 Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences (CAMS) & Comparative Medicine Centre, Peking Union Medical Collage (PUMC), Beijing 100021, China. songzhiqi1989@foxmail.com. 2 NHC Key Laboratory of Human Disease Comparative Medicine, the Institute of Laboratory Animal Sciences, CAMS&PUMC, Beijing 100021, China. songzhiqi1989@foxmail.com. 3 Beijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious, Beijing 100021, China. songzhiqi1989@foxmail.com. 4 Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences (CAMS) & Comparative Medicine Centre, Peking Union Medical Collage (PUMC), Beijing 100021, China. xuyanf2009@163.com. 5 NHC Key Laboratory of Human Disease Comparative Medicine, the Institute of Laboratory Animal Sciences, CAMS&PUMC, Beijing 100021, China. xuyanf2009@163.com. 6 Beijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious, Beijing 100021, China. xuyanf2009@163.com. 7 Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences (CAMS) & Comparative Medicine Centre, Peking Union Medical Collage (PUMC), Beijing 100021, China. bllmsl@aliyun.com. 8 NHC Key Laboratory of Human Disease Comparative Medicine, the Institute of Laboratory Animal Sciences, CAMS&PUMC, Beijing 100021, China. bllmsl@aliyun.com. 9 Beijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious, Beijing 100021, China. bllmsl@aliyun.com. 10 Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences (CAMS) & Comparative Medicine Centre, Peking Union Medical Collage (PUMC), Beijing 100021, China. zhangling@cnilas.org. 11 NHC Key Laboratory of Human Disease Comparative Medicine, the Institute of Laboratory Animal Sciences, CAMS&PUMC, Beijing 100021, China. zhangling@cnilas.org. 12 Beijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious, Beijing 100021, China. zhangling@cnilas.org. 13 Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences (CAMS) & Comparative Medicine Centre, Peking Union Medical Collage (PUMC), Beijing 100021, China. pinyucau@gmail.com. 14 NHC Key Laboratory of Human Disease Comparative Medicine, the Institute of Laboratory Animal Sciences, CAMS&PUMC, Beijing 100021, China. pinyucau@gmail.com. 15 Beijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious, Beijing 100021, China. pinyucau@gmail.com. 16 Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences (CAMS) & Comparative Medicine Centre, Peking Union Medical Collage (PUMC), Beijing 100021, China. quyj@cnilas.org. 17 NHC Key Laboratory of Human Disease Comparative Medicine, the Institute of Laboratory Animal Sciences, CAMS&PUMC, Beijing 100021, China. quyj@cnilas.org. 18 Beijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious, Beijing 100021, China. quyj@cnilas.org. 19 Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences (CAMS) & Comparative Medicine Centre, Peking Union Medical Collage (PUMC), Beijing 100021, China. zhuh@cnilas.org. 20 NHC Key Laboratory of Human Disease Comparative Medicine, the Institute of Laboratory Animal Sciences, CAMS&PUMC, Beijing 100021, China. zhuh@cnilas.org. 21 Beijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious, Beijing 100021, China. zhuh@cnilas.org. 22 Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences (CAMS) & Comparative Medicine Centre, Peking Union Medical Collage (PUMC), Beijing 100021, China. hnndwenjiezhao@163.com. 23 NHC Key Laboratory of Human Disease Comparative Medicine, the Institute of Laboratory Animal Sciences, CAMS&PUMC, Beijing 100021, China. hnndwenjiezhao@163.com. 24 Beijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious, Beijing 100021, China. hnndwenjiezhao@163.com. 25 Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences (CAMS) & Comparative Medicine Centre, Peking Union Medical Collage (PUMC), Beijing 100021, China. 18510165683@163.com. 26 NHC Key Laboratory of Human Disease Comparative Medicine, the Institute of Laboratory Animal Sciences, CAMS&PUMC, Beijing 100021, China. 18510165683@163.com. 27 Beijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious, Beijing 100021, China. 18510165683@163.com. 28 Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences (CAMS) & Comparative Medicine Centre, Peking Union Medical Collage (PUMC), Beijing 100021, China. qinchuan@pumc.edu.cn. 29 NHC Key Laboratory of Human Disease Comparative Medicine, the Institute of Laboratory Animal Sciences, CAMS&PUMC, Beijing 100021, China. qinchuan@pumc.edu.cn. 30 Beijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious, Beijing 100021, China. qinchuan@pumc.edu.cn.

 

Abstract

Coronaviruses (CoVs) have formerly been regarded as relatively harmless respiratory pathogens to humans. However, two outbreaks of severe respiratory tract infection, caused by the severe acute respiratory syndrome coronavirus (SARS-CoV) and the Middle East respiratory syndrome coronavirus (MERS-CoV), as a result of zoonotic CoVs crossing the species barrier, caused high pathogenicity and mortality rates in human populations. This brought CoVs global attention and highlighted the importance of controlling infectious pathogens at international borders. In this review, we focus on our current understanding of the epidemiology, pathogenesis, prevention, and treatment of SARS-CoV and MERS-CoV, as well as provides details on the pivotal structure and function of the spike proteins (S proteins) on the surface of each of these viruses. For building up more suitable animal models, we compare the current animal models recapitulating pathogenesis and summarize the potential role of host receptors contributing to diverse host affinity in various species. We outline the research still needed to fully elucidate the pathogenic mechanism of these viruses, to construct reproducible animal models, and ultimately develop countermeasures to conquer not only SARS-CoV and MERS-CoV, but also these emerging coronaviral diseases.

KEYWORDS: MERS-CoV; SARS-CoV; animal model; coronaviruses; prevention and treatment; spike proteins

PMID: 30646565 DOI: 10.3390/v11010059

Keywords: MERS-CoV; SARS; Coronavirus.

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TMPRSS2 contributes to #virus spread and #immunopathology in the #airways of murine models after #coronavirus infection (J Virol., abstract)

[Source: Journal of Virology, full page: (LINK). Abstract, edited.]

TMPRSS2 contributes to virus spread and immunopathology in the airways of murine models after coronavirus infection

Naoko Iwata-Yoshikawa, Tadashi Okamura, Yukiko Shimizu, Hideki Hasegawa, Makoto Takeda, Noriyo Nagata

DOI: 10.1128/JVI.01815-18

 

ABSTRACT

Transmembrane serine protease TMPRSS2 activates the spike protein of highly pathogenic human coronaviruses such as severe acute respiratory syndrome-related coronavirus (SARS-CoV) and Middle East respiratory syndrome-related coronavirus (MERS-CoV). In vitro, activation induces virus-cell membrane fusion at the cell surface. However, the roles of TMPRSS2 during coronavirus infection in vivo are unclear. Here, we used animal models of SARS-CoV and MERS-CoV infection to investigate the role of TMPRSS2. Th-1-prone C57BL/6 mice and TMPRSS2-knockout (KO) mice were used for SARS-CoV infection, and transgenic mice expressing the human MERS-CoV receptor, hDPP4-Tg mice, and TMPRSS2-KO hDPP4-Tg mice were used for MERS-CoV infection. After experimental infection, TMPRSS2-deficient mouse strains showed reduced body weight loss and viral kinetics in the lungs. Lack of TMPRSS2 affected the primary sites of infection and virus spread within the airway, accompanied by less severe immunopathology. However, TMPRSS2-KO mice showed weakened inflammatory chemokine and/or cytokine responses to intranasal stimulation with poly (I:C), a Toll-like receptor 3 agonist. In conclusion, TMPRSS2 plays a crucial role in viral spread within the airway of murine models infected by SARS-CoV and MERS-CoV and in the resulting immunopathology.

 

IMPORTANCE

Broad-spectrum antiviral drugs against highly pathogenic coronaviruses and other emerging viruses are desirable to enable a rapid response to pandemic threats. Transmembrane protease serine type2 (TMPRSS2), a protease belonging to the type II transmembrane serine protease family, cleaves the coronavirus spike protein, making it a potential therapeutic target for coronavirus infections. Here, we examined the role of TMPRSS2 using animal models of SARS-CoV and MERS-CoV infection. The results suggest that lack of TMPRSS2 in the airways reduces the severity of lung pathology after infection by SARS-CoV and MERS-CoV. Taken together, the results will facilitate development of novel targets for coronavirus therapy.

Copyright © 2019 American Society for Microbiology. All Rights Reserved.

Keywords: Coronavirus; MERS-CoV; SARS; Viral pathogenesis.

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#Replication of #MERS and #SARS #coronaviruses in #bat cells offers insights to their ancestral origins (Emerg Microbes Infect., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Emerg Microbes Infect. 2018 Dec 10;7(1):209. doi: 10.1038/s41426-018-0208-9.

Replication of MERS and SARS coronaviruses in bat cells offers insights to their ancestral origins.

Lau SKP1,2,3,4, Fan RYY5, Luk HKH5, Zhu L5, Fung J5, Li KSM5, Wong EYM5, Ahmed SS5, Chan JFW6,5,7,8, Kok RKH6,5,7,8, Chan KH6,5,7,8, Wernery U9, Yuen KY6,5,7,8, Woo PCY10,11,12,13.

Author information: 1 State Key Laboratory of Emerging Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. skplau@hku.hk. 2 Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. skplau@hku.hk. 3 Carol Yu Centre for Infection, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. skplau@hku.hk. 4 Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. skplau@hku.hk. 5 Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. 6 State Key Laboratory of Emerging Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. 7 Carol Yu Centre for Infection, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. 8 Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. 9 Central Veterinary Research Laboratory, Dubai, United Arab Emirates. 10 State Key Laboratory of Emerging Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. pcywoo@hku.hk. 11 Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. pcywoo@hku.hk. 12 Carol Yu Centre for Infection, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. pcywoo@hku.hk. 13 Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. pcywoo@hku.hk.

 

Abstract

Previous findings of Middle East Respiratory Syndrome coronavirus (MERS-CoV)-related viruses in bats, and the ability of Tylonycteris-BatCoV HKU4 spike protein to utilize MERS-CoV receptor, human dipeptidyl peptidase 4 hDPP4, suggest a bat ancestral origin of MERS-CoV. We developed 12 primary bat cell lines from seven bat species, including Tylonycteris pachypus, Pipistrellus abramus and Rhinolophus sinicus (hosts of Tylonycteris-BatCoV HKU4, Pipistrellus-BatCoV HKU5, and SARS-related-CoV respectively), and tested their susceptibilities to MERS-CoVs, SARS-CoV, and human coronavirus 229E (HCoV-229E). Five cell lines, including P. abramus and R. sinicus but not T. pachypus cells, were susceptible to human MERS-CoV EMC/2012. However, three tested camel MERS-CoV strains showed different infectivities, with only two strains capable of infecting three and one cell lines respectively. SARS-CoV can only replicate in R. sinicus cells, while HCoV-229E cannot replicate in any bat cells. Bat dipeptidyl peptidase 4 (DPP4) sequences were closely related to those of human and non-human primates but distinct from dromedary DPP4 sequence. Critical residues for binding to MERS-CoV spike protein were mostly conserved in bat DPP4. DPP4 was expressed in the five bat cells susceptible to MERS-CoV, with significantly higher mRNA expression levels than those in non-susceptible cells (P = 0.0174), supporting that DPP4 expression is critical for MERS-CoV infection in bats. However, overexpression of T. pachypus DPP4 failed to confer MERS-CoV susceptibility in T. pachypus cells, suggesting other cellular factors in determining viral replication. The broad cellular tropism of MERS-CoV should prompt further exploration of host diversity of related viruses to identify its ancestral origin.

PMID: 30531999 DOI: 10.1038/s41426-018-0208-9

Keywords: Coronavirus; MERS-CoV; SARS; Bats.

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Middle East respiratory syndrome #coronavirus (#MERS-CoV): #Impact on #Saudi Arabia, 2015 (Saudi J Biol Sci., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Saudi J Biol Sci. 2018 Nov;25(7):1402-1405. doi: 10.1016/j.sjbs.2016.09.020. Epub 2016 Oct 1.

Middle East respiratory syndrome coronavirus (MERS-CoV): Impact on Saudi Arabia, 2015.

Faridi U1.

Author information: 1 Department of Biochemistry, Tabuk University, Tabuk, Saudi Arabia.

 

Abstract

Middle East respiratory syndrome is the acute respiratory syndrome caused by betacoronavirus MERS-CoV. The first case of this disease was reported from Saudi Arabia in 2012. This virus is lethal and is a close relative of a severe acute respiratory syndrome (SARS), which is responsible for more than 3000 deaths in 2002-2003. According to Ministry of Health, Saudi Arabia. The number of new cases is 457 in 2015. Riyadh has the highest number of reports in comparison to the other cities. According to this report, males are more susceptible than female, especially after the age of 40. Because of the awareness and early diagnosis the incidence is falling gradually. The pre-existence of another disease like cancer or diabetic etc. boosts the infection. MERS is a zoonotic disease and human to human transmission is low. The MERS-CoV is a RNA virus with protein envelope. On the outer surface, virus has spike like glycoprotein which is responsible for the attachment and entrance inside host cells. There is no specific treatment for the MERS-CoV till now, but drugs are in pipeline which bind with the spike glycoprotein and inhibit its entrance host cells. MERS-CoV and SAR-CoV are from the same genus, so it was thought that the drugs which inhibit the growth of SARS-CoV can also inhibit the growth of MERS-CoV but those drugs are not completely inhibiting virus activity. Until we don’t have proper structure and the treatment of MERS-CoV, We should take precautions, especially the health care workers, Camel owners and Pilgrims during Hajj and Umrah, because they are at a higher risk of getting infected.

KEYWORDS: Betacoronavirus; MERS-CoV; SARS; Saudi Arabia

PMID: 30505188 PMCID: PMC6252006  DOI: 10.1016/j.sjbs.2016.09.020

Keywords: Coronavirus; Betacoronavirus; MERS-CoV; SARS; Saudi Arabia; Human; Camels.

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