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      ABO blood groups among Coronavirus disease 2019 patients

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      Author(s): ,
      Publication date (Print and electronic):
      Journal: Iberoamerican Journal of Medicine
      Publisher: Hospital San Pedro
      Keywords: ABO blood group, COVID-19, SARS-CoV-2

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          Abstract

          Abstract Introduction: Susceptibility to some infectious diseases has been associated with blood group phenotypes. Coronavirus disease 2019 (COVID-19) is a new infectious disease caused by a novel corona virus designated Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) which has spread rapidly around the world. The objective of this study was to determine if the susceptibility or severity to COVID-19 was associated with ABO blood group distribution among the affected countries. Materials and methods: This retrospective study of COVID-19 disease was based on data from 105 countries collected on the 13th of April 2020 and analysed by SPSS software version 16.0. Spearman correlation coefficient and Kruskal Wallis test were used to assess for associations between ABO blood group with COVID-19. Results: The results indicated that individuals of blood group A are at increased risk of infection by SARS-CoV-2 virus and severity of COVID-19 disease. Blood groups B and O were less likely to be infected and the disease evolves less severe. Conclusions: The results are discussed in relation to the host-parasite interactions that might contribute to susceptibility to these infections.

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          A pneumonia outbreak associated with a new coronavirus of probable bat origin

          Peng Zhou, Xing-Lou Yang, Xian-Guang Wang … (2020)
          Since the outbreak of severe acute respiratory syndrome (SARS) 18 years ago, a large number of SARS-related coronaviruses (SARSr-CoVs) have been discovered in their natural reservoir host, bats 1–4 . Previous studies have shown that some bat SARSr-CoVs have the potential to infect humans 5–7 . Here we report the identification and characterization of a new coronavirus (2019-nCoV), which caused an epidemic of acute respiratory syndrome in humans in Wuhan, China. The epidemic, which started on 12 December 2019, had caused 2,794 laboratory-confirmed infections including 80 deaths by 26 January 2020. Full-length genome sequences were obtained from five patients at an early stage of the outbreak. The sequences are almost identical and share 79.6% sequence identity to SARS-CoV. Furthermore, we show that 2019-nCoV is 96% identical at the whole-genome level to a bat coronavirus. Pairwise protein sequence analysis of seven conserved non-structural proteins domains show that this virus belongs to the species of SARSr-CoV. In addition, 2019-nCoV virus isolated from the bronchoalveolar lavage fluid of a critically ill patient could be neutralized by sera from several patients. Notably, we confirmed that 2019-nCoV uses the same cell entry receptor—angiotensin converting enzyme II (ACE2)—as SARS-CoV.
          Article 0 comments Cited 10580 times – based on 0 reviews     Review now
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            Genomic characterization of the 2019 novel human-pathogenic coronavirus isolated from a patient with atypical pneumonia after visiting Wuhan

            Jasper Chan, Kin-Hang Kok, Zheng Zhu … (2020)
            ABSTRACT A mysterious outbreak of atypical pneumonia in late 2019 was traced to a seafood wholesale market in Wuhan of China. Within a few weeks, a novel coronavirus tentatively named as 2019 novel coronavirus (2019-nCoV) was announced by the World Health Organization. We performed bioinformatics analysis on a virus genome from a patient with 2019-nCoV infection and compared it with other related coronavirus genomes. Overall, the genome of 2019-nCoV has 89% nucleotide identity with bat SARS-like-CoVZXC21 and 82% with that of human SARS-CoV. The phylogenetic trees of their orf1a/b, Spike, Envelope, Membrane and Nucleoprotein also clustered closely with those of the bat, civet and human SARS coronaviruses. However, the external subdomain of Spike’s receptor binding domain of 2019-nCoV shares only 40% amino acid identity with other SARS-related coronaviruses. Remarkably, its orf3b encodes a completely novel short protein. Furthermore, its new orf8 likely encodes a secreted protein with an alpha-helix, following with a beta-sheet(s) containing six strands. Learning from the roles of civet in SARS and camel in MERS, hunting for the animal source of 2019-nCoV and its more ancestral virus would be important for understanding the origin and evolution of this novel lineage B betacoronavirus. These findings provide the basis for starting further studies on the pathogenesis, and optimizing the design of diagnostic, antiviral and vaccination strategies for this emerging infection.
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              A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus–induced lung injury

              Keiji Kuba, Yumiko Imai, Shuan Rao … (2005)
              During several months of 2003, a newly identified illness termed severe acute respiratory syndrome (SARS) spread rapidly through the world 1,2,3 . A new coronavirus (SARS-CoV) was identified as the SARS pathogen 4,5,6,7 , which triggered severe pneumonia and acute, often lethal, lung failure 8 . Moreover, among infected individuals influenza such as the Spanish flu 9,10 and the emergence of new respiratory disease viruses 11,12 have caused high lethality resulting from acute lung failure 13 . In cell lines, angiotensin-converting enzyme 2 (ACE2) has been identified as a potential SARS-CoV receptor 14 . The high lethality of SARS-CoV infections, its enormous economic and social impact, fears of renewed outbreaks as well as the potential misuse of such viruses as biologic weapons make it paramount to understand the pathogenesis of SARS-CoV. Here we provide the first genetic proof that ACE2 is a crucial SARS-CoV receptor in vivo. SARS-CoV infections and the Spike protein of the SARS-CoV reduce ACE2 expression. Notably, injection of SARS-CoV Spike into mice worsens acute lung failure in vivo that can be attenuated by blocking the renin-angiotensin pathway. These results provide a molecular explanation why SARS-CoV infections cause severe and often lethal lung failure and suggest a rational therapy for SARS and possibly other respiratory disease viruses. Supplementary information The online version of this article (doi:10.1038/nm1267) contains supplementary material, which is available to authorized users.
              Article 0 comments Cited 1345 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (publisher-id): ijm
                Title: Iberoamerican Journal of Medicine
                Abbreviated Title: Iberoam J Med
                Publisher: Hospital San Pedro (Logroño, La Rioja, Spain )
                ISSN (Print): 2695-5075
                ISSN (Electronic): 2695-5075
                Publication date (Print and electronic): 2020
                Volume: 2
                Issue: 4
                Pages: 268-274
                Affiliations
                [1] Tripoli orgnameUniversity of Tripoli orgdiv1Faculty of Medicine Libia
                [2] Tripoli orgnameUniversity of Tripoli orgdiv1Faculty of Medicine Libia
                Article
                Publisher ID: S2695-50752020000400004 Publisher ID: S2695-5075(20)00200400004
                DOI: 10.5281/zenodo.3893256
                SO-VID: 98044551-353b-4739-ada9-11b2e7085554
                License:

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                Date accepted : 13 June 2020
                Date received : 22 May 2020
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 27, Pages: 7
                Product

                SciELO Spain

                Categories
                Subject: Original Article

                Keywords: ABO blood group,SARS-CoV-2,COVID-19
                Data availability:
                Keywords: ABO blood group, SARS-CoV-2, COVID-19

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