Pathophysiology of COVID-19
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The incubation period ranges from 1 day to 14 days. The variation in incubation period is associated with the age of the patients above the age of 60 usually develop the symptoms faster as compared to others.
· SARS-CoV-2 affects the epithelial cells in the alveoli. After the entry of the virus to the respiratory tract, the cilia in the lower respiratory tract facilitate the attachment of the virus to its receptor.
· The cilia move the mucus covering the respiratory epithelium it moved upwards towards the throat. This facilitates the attachment of the virus.
· Multiple SARS-CoV-2 proteins interact with components of the innate immune system to evade an antiviral interferon response.
· The expression of hACE2, the SARS-CoV-2 receptor, on the surface of cells is down-regulated after infection with SARS-CoV-2.
· The mechanism of this down-regulation appears to be due to the internalization of ACE2 during SARS-CoV entry and by induction of TNFα converting enzyme activity of metallo-proteases.
· The enzymes cleave the ACE2 extracellular domain from its transmembrane domain, resulting in shedding of this domain.
· This has led to the hypothesis that the binding of SARS-CoV-2 S protein is a virulence factor for SARS above and beyond its role in viral attachment and entry.
· Patients infected with COVID-19 show higher leukocyte numbers, abnormal respiratory findings, and increased levels of plasma pro-inflammatory cytokines.
· The main pathogenesis of COVID-19 infection as a respiratory system targeting virus is severe pneumonia, RNAaemia, combined with the incidence of acute cardiac injury.
· Significantly high blood levels of cytokines and chemokines are noted in patients with COVID-19 infection that include IL1-β, IL1RA, IL7, IL8, IL9, IL10, basic FGF2, GCSF, GMCSF, IFNγ, IP10, MCP1, MIP1α, MIP1β, PDGFB, TNFα, and VEGFA.
· Besides, high levels of pro-inflammatory cytokines including IL2, IL7, IL10, GCSF, IP10, MCP1, MIP1α, and TNFα that are reasoned to promote disease severity are observed in patients suffering from severe symptoms.
· The association of worsening clinical progression with declining virus loads and the onset of an immunological response, plus the presence of markedly elevated cytokines levels suggest that severe lung damage is largely immunopathological in nature.
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