Energetics based epitope screening in SARS CoV-2 (COVID 19) spike glycoprotein by Immuno-informatic analysis aiming to a suitable vaccine development

Amrita Banerjee; Dipannita Santra; Smarajit Maiti

In a series of medication regimen, 1 (AT1R) blockers is used for reducing the severity and mortality from SARS-CoV-2 virus infections [9] . Chloroquine and Hydroxychloroquine are now being prescribed somewhere to fight COVID-19 for the time being [10, 11] . Human coronaviruses and other influenza viruses resulted in epidemic in last 2 decade in different parts of the world. The anomalies between severity and spreading between the origin site, China and the other parts of the World (European and North America countries) might have some indication. Common human CoVs may have annual peaks of circulation in winter months in the US, and individual human CoVs may show variable circulation from year to year. [12] Colder climate and prior exposure to other human coronaviruses, or influenza or flu viruses or possible vaccination against those might develop antibody dependent enhancement (ADE) of immunological responses during recent SARS CoV-2 exposure. ADE might have modulated immune response and could elicit sustained inflammation, lymphopenia, and/or cytokine storm [13, 14] . Possibly, that could be one of the reasons (more history of exposure with CoVs beside weaker immune system) for older people being more affected by the present SARS CoV-2. Moreover, both helper T cells and suppressor T cells in patients with COVID-19 were below normal levels. The novel coronavirus might mainly act on lymphocytes, especially T . CC-BY-ND 4.0 International license author/funder. It is made available under a The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/2020.04.02.021725 doi: bioRxiv preprint lymphocytes [15] . Strong inflammatory events could be the initiator of the collapsing environment during COVID-19 infection. In most of the death cases in COVID-19 infections, acute respiratory failure is followed by other organs like kidney anomalies. In these cases inflammatory outburst might have worsened the infection and post viral-incubation situations [16, 17] . Recent studies in experimentally infected animal strongly suggest a crucial role for virus-induced immunopathological events in causing fatal pneumonia after human CoV infections [18] . So, combined anti-viral and anti-inflammatory treatment might be beneficial in these cases [19] . SARS-based available immune-therapeutic and prophylactic modalities revealed poor efficacy to neutralize and protect from infection by targeting the novel spike protein. [20] .