What To Get Out Of An Coronavirus Variants Comparison? Cases Of India And England

     

COVID-19 is not humanity’s first brush with a coronavirus outbreak. A related pathogen, SARS-CoV, first emerged in Foshan, China, in November 2002. In February 2003 the virus was transported to Hong Kong, and from there, severe acute respiratory syndrome (SARS), the disease it causes, spread globally. By May 2004, that epidemic was quelled. Almost a decade later, in April 2012, the first cases of Middle East respiratory syndrome (MERS) occurred in Jordan. Countries in the region hosted persistent epidemics, and cases of MERS popped up in countries outside the Middle East. We can learn a lot about SARS-CoV-2 by comparing and studying the characteristics of these similar coronaviruses and the outbreaks they fueled.

 

SARS-CoV-2 belongs to the diverse family of coronaviruses that are enveloped, single-stranded RNA viruses. Among the four genera (alpha, beta, gamma, and delta), alpha and beta coronaviruses are the most relevant to public health due to their propensity to cross animal-human barriers, thus becoming human pathogens. SARS-CoV, SARS-CoV-2, and MERS-CoV are all beta coronaviruses with high morbidity, mortality, and transmissibility. Other human coronavisures of both the alpha and beta variety, are responsible for up to one-third of common cold cases and sometimes cause gastroenteritis. 

 

SARS-CoV, SARS-CoV-2, and MERS-CoV all consist of nonstructural replicase proteins and four structural proteins: spike (S), envelope (E), membrane (M), and nucleocapsid (N) proteins. The N protein stabilizes the RNA genome, and the S, E, and M proteins together create the viral envelope. Phylogenetic analysis shows that SARS-CoV-2 belongs, together with SARS-CoV and SARS-like coronaviruses isolated in China from horseshoe bats between 2015 and 2018, to a different clade from MERS-CoV, and it is more closely related to the bat SARS-like coronaviruses than to SARS-CoV.

 

The pathogenesis of SARS-CoV-2 and SARS-CoV is related to an immune system phenomenon involving a sharp increase in inflammatory proteins called a cytokine storm, whereas MERS-CoV’s proteins target host interferons to inactivate natural killer cells. In addition to initiating cytokine storms, SARS-CoV-2 promotes various cell death programs, such as pyroptosis, apoptosis, and necrosis, which may contribute to COVID-19 pathogenesis. In the immediate future, an in-depth study of these peculiarities of SARS-CoV-2 requires novel approaches—i.e., omnigenetics, network immunological and biological approaches, etc.—to identify intrinsic factors (genetic risks, immune response kinetics, and other determinants) and biomarkers associated with COVID-19 severity.