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

Abstract

The 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.