Parallels in the pathogenesis of SARS-CoV-2 and M. tuberculosis: a synergistic or antagonistic alliance?

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dc.contributor.authorTapela, Kesego
dc.contributor.authorOlwa, Charles Ochieng
dc.contributor.authorQuaye, Osbourne
dc.date.accessioned2023-04-26T13:47:08Z
dc.date.available2023-04-26T13:47:08Z
dc.date.issued2021-01-06
dc.description.abstractThe world is facing a major challenge of the new pneumonia condition termed COVID-19 caused by SARSCoV-2, the seventh member of human coronaviruses. The global burden of COVID-19 is rising daily and as of 10 November 2020, there were over 1,275,122 deaths (https://www.worldometers.info/coronavirus/). Coronaviruses are enveloped, positive-sense and single-stranded RNA viruses [1]. Based on 96.2% nucleotide sequence identity with a bat-borne coronavirus (BatCoV RaTG13) that has been identified in Rhinolophus affinis bat species, it is likely that SARS-CoV-2 originated from a bat [2]. COVID-19 is primarily defined by an acute viral pneumonia and cytokine storm leading to respiratory failure[3]. The main transmission route of this virus is droplets blown out through cough and sneezing by an infected person. The common symptoms of COVID-19 include cough, fever, shortness of breath and tiredness [4]. Severe cases manifest in symptoms that are associated with cellular immune deficiency, coagulation activation, myocardia, multiple organ dysfunction and septic shock [5]. SARS-CoV2 is highly pathogenic in persons with underlying medical conditions that reduce their immune competence such as TB [6]. TB, caused by Mycobacterium tuberculosis and transmitted through infected air droplets from cough or sneezing, is one of the top ten causes of death due to infectious diseases globally, with an estimated 10 million infections and 1.5 million deaths in 2018 [7]. Indeed, since TB affects the respiratory system, it could prove catastrophic if present in comorbidity with COVID-19 [6]. In this commentary, we discuss the current state of knowledge on the parallels in the pathogenesis of SARS-CoV-2 and M. tuberculosis and the potential implications of co-infection on the clinical outcomes.en_US
dc.description.sponsorshipACE: Cell Biology of Infectious and Non-Communicable Diseasesen_US
dc.identifier.citationParallels in the pathogenesis of SARS-CoV-2 and M. tuberculosis: a synergistic or antagonistic alliance? Kesego Tapela, Charles Ochieng’ Olwal, and Osbourne Quaye Future Microbiology 2020 15:18, 1691-1695en_US
dc.identifier.issn1746-0913
dc.identifier.issn1746-092
dc.identifier.urihttp://hdl.handle.net/123456789/1569
dc.language.isoenen_US
dc.publisherFuture Medicine Ltden_US
dc.relation.ispartofseriesFuture Microbiol;(2020) 15(18
dc.subjectangiotensin-converting enzyme 2en_US
dc.subjectUniversity of Ghanaen_US
dc.subjectWACCBIP_NCDSen_US
dc.subjectangiotensin-converting enzyme 2 (ACE2) receptoren_US
dc.subjectBCG vaccineen_US
dc.subjectcoronavirusen_US
dc.subjectcytokine stormen_US
dc.subjectlymphocytopeniaen_US
dc.subjectMycobacterium tuberculosisen_US
dc.subjectpathogenesis of SARS-CoV-2en_US
dc.subjectSARS-CoV-2en_US
dc.subjecttuberculosisen_US
dc.titleParallels in the pathogenesis of SARS-CoV-2 and M. tuberculosis: a synergistic or antagonistic alliance?en_US
dc.typeArticleen_US
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