Literature review on virus and host response proteins in COVID-19: pathobiology, management, diagnosis and treatment.

Coronavirus disease 2019 (COVID-19) is a severe acute respiratory syndrome caused by a novel strain of coronavirus (SARS-CoV-2) which was declared by WHO as a cause of global pandemic. By human-to-human transmission it caused severe damage to mankind with increased mortality rate worldwide. Coronavirus is a spherical enveloped virus with single stranded positive-sense RNA with a size of ~30 kilobases encoding various structural, non-structural and accessory proteins. The entry of coronavirus into the host cells is mediated by spike proteins. SARS-CoV-2 efficiently replicates in host cell and by evading immune surveillance, like innate and adaptive immune responses, in the host cells ultimately leads to increased virulence and disease outcome. In the current review, we highlighted the molecular insights of SARS-CoV-2 and its infection mechanism in the host cell via host-viral protein interactions based on currently available data up to 16thMay 2020 using various research literature databases. The diagnostics of SARS-CoV-2 is mainly done by RT-qPCR and serological tests. There is no effective treatment for COVID-19, however, few methods like plasma therapy and remdesivir treatment are reported to show promising results in improving patient's health and decreasing mortality rate. Keywords: SARS-CoV; spike protein; nucleocapsid; COVID-19; interferon.

Beta-Adrenergic Blockers as a Potential Treatment for COVID-19 Patients.

More than 15 million people have been affected by coronavirus disease 2019 (COVID-19) and it has caused 640 016 deaths as of July 26, 2020. Currently, no effective treatment option is available for COVID-19 patients. Though many drugs have been proposed, none of them has shown particular efficacy in clinical trials. In this article, the relationship between the Adrenergic system and the renin-angiotensin-aldosterone system (RAAS) is focused in COVID-19 and a vicious circle consisting of the Adrenergic system-RAAS-Angiotensin converting enzyme 2 (ACE2)-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (which is referred to as the "ARAS loop") is proposed. Hyperactivation of the ARAS loop may be the underlying pathophysiological mechanism in COVID-19, and beta-adrenergic blockers are proposed as a potential treatment option. Beta-adrenergic blockers may decrease the SARS-CoV-2 cellular entry by decreasing ACE2 receptors expression and cluster of differentiation 147 (CD147) in various cells in the body. Beta-adrenergic blockers may decrease the morbidity and mortality in COVID-19 patients by preventing or reducing acute respiratory distress syndrome (ARDS) and other complications. Retrospective and prospective clinical trials should be conducted to check the validity of the hypothesis. Also see the video abstract here https://youtu.be/uLoy7do5ROo.

Friend turned foe: A curious case of disrupted endosymbiotic homeostasis promoting the Warburg effect in sepsis.

Sepsis is a grievous health concern with limited understanding of its precise etiology. Although studies on sepsis have implicated the Warburg effect (mitigation of mitochondrial oxidative phosphorylation, as evident from aerobic glycolysis), we propose that an evolutionary perspective might further unravel its etiology. The endosymbiotic theory suggests that evolution of a eukaryotic cell is a consequence of the fruitful association between an archaea (Asgard) and an alphaproteobacterium (Rickettsia). We hypothesize that, during pathological conditions like sepsis, such endosymbiotic homeostasis between the two systems is perturbed. We underscore the fact (supported by in silico homology analyses) that during sepsis, the Asgard component of a cell is promoted to trigger aerobic glycolysis as well as the innate immune response (spearheaded by the TLR pathway), while suppressing the Rickettsia counterpart, thereby promoting the Warburg effect. It might be this discord between the two endosymbiotic partners (Asgard and Rickettsia-derived cellular components) that promotes sepsis.