More about COVID-19

COVID-19 is a disease caused by the novel coronavirus SARS-CoV-2. SARS-CoV-2 reportedly originated from bats in an animal market in Wuhan, China, where the outbreak of the virus first occurred. The disease has since been documented in individuals of all age groups, with infection severity ranging from asymptomatic to critical condition to even death. Comorbid cases are more fatal and there is also an age-related susceptibility to the virus with elders developing more critical COVID-19 conditions. Further, certain populations of individuals are more susceptible to the disease including ethnic populations such as those from the Black and Asian community.

SARS-CoV-2 is an enveloped, positive-sense single-stranded RNA virus that is a member of the β-coronavirus family. The SARS-CoV-2 genome encodes for various major viral proteins, some of which are structurally important such as the E (envelope), M (membrane), N (nucleocapsid) and S (spike) proteins. Of these, the S protein is critical for cellular entry by facilitating the attachment and fusion of the viral membrane with the host cell membrane. SARS-CoV-2 gets its Coronavirus (corona: crown) name from the glycosylated S proteins protruding from the viral surface. S protein contains a receptor-binding domain (RBD), a fusion and a transmembrane domain. In humans, the RBD of S binds to the angiotensin converting enzyme 2 (ACE2) receptor, facilitating viral entry in cells. ACE2 receptors are present in a wide variety of human cells including those lining nasal pathways, the lungs and ileum, making these some of the primary target areas. Given that the main transmission route of the virus is through respiratory droplets and/or physical contact with an infected individual, the nasal and lung pathways allow for easy viral entrance and attachment to host cells.

When the S protein binds to the ACE2 receptor, a TM serine protease (TMPRSS2) cleaves S between its two subunits (S1 and S2), thus activating the protein to enter the host cell, which it does upon altering the conformation of its spike. After proteolytic cleavage of S and release of one of its subunits (S2), fusion of the virion and endocytosis can occur. Upon virus entry into the cell, viral RNA is released, and host cell machinery is utilized for replication and transcription of the viral RNA genome. SARS-CoV-2 needs both the S protein and the ACE2 receptor to facilitate cellular entry of the virus for the purposes of its transmission, propagation and spreading in cells and tissues within the body. The interactions of these two proteins leads to a host of physiological changes in the body, including pneumonia-like symptoms of fever, headache, coughing and body pain.

SARS-CoV-2, upon gaining access to the host cell machinery, is initially detected by pathogen recognition receptors (PRRs) which then elicits enhanced interferon production. Like previous SARS-CoV and MERS-CoV infections, the humoral response against SARS-CoV-2 involves characteristic IgG and IgM antibody production. An observational study detected anti-S-RBD IgG in all 16 of the study’s SARS-CoV-2 patients, with additional reporting of anti-N IgG, anti-S-RBD IgM and anti-N IgM antibodies but in slightly decreased presence.

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