Epidemiology, Genomic Structure, the Molecular Mechanism of Injury, Diagnosis and Clinical Manifestations of Coronavirus Infection: An Overview

COVID-19 is caused by a novel beta coronavirus (SARS-CoV-2) strain that was first discovered in 2019 in the Wuhan city of China. Based on virus genome sequencing studies, the bat is suspected as the natural host of virus, and infection might be transmitted from bats via unknown intermediate hosts like reptiles and snakes etc., to infect humans. COVID-19 is transmitted from person to person contact, primarily via droplet infection within the incubation period or after clinical manifestations of fever, cough, sneezing, sputum, dyspnea, and pneumonia and through contaminated fomites. COVID-19 enters the respiratory tract through the ACE2 receptor on alveoli through binding of s-protein of the virus and causes injuries though the cytopathic effect, as well as cytokines and other mediators, released after developing sepsis. ACE 2 is almost 100-fold higher in kidneys than lung, and the virus can also involve the kidney in the same manner. Kidney involvement manifests in the form of proteinuria, hematuria, and an acute rise in serum creatinine. Kidney involvement is an independent risk factor for mortality. Diagnosis is primarly made by detecting viral RNA by reverse transcriptase polymerase chain reaction (rtPCR) in nasopharyngeal swab samples. Role of antibodies, both IgM and IgG are still evolving and at best restricted for epidemiological purpose. Though a large number of treatments, including hydroxychloroquine, anti-viral, convalescent plasma etc., are being tried, as of now treatment is symptomatic only.