Pathogenesis of Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) Respiratory Infection

Document Type : Review Article


1 Department of Biochemistry, University of Ibadan, Ibadan, Nigeria

2 Department of Zoology, University of Ibadan, Ibadan, Nigeria

3 Department of Biochemistry, University of Lagos, Lagos, Nigeria



With the occurrence of a mysterious pneumonia in the Hubei province (Wuhan) of China in December 2019, a different coronavirus, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has commanded global awareness and has been named by the World Health Organization (WHO) as a public health emergency of international concern. Two other coronavirus infections (SARS and MERS) were also characterized by severe respiratory distress in 2002-2003. In addition to the new coronavirus, the emerging infectious diseases resulting in universal spread are caused by the β-coronavirus strains. Even though coronaviruses typically target the upper and/or lower respiratory tract, viral shedding into the plasma or serum is frequent, and the human coronavirus (CoV) represents 15%–30% of respiratory syndromes, including common colds. Based on a recent hypothesis, SARS-CoV-2 has been shown to induce lung injury by inhibiting the angiotensin converting enzyme-2 (ACE-2) and could possibly attack organs with high expression. With the lack of a vaccine or major treatment for the disease, palliative care is provided for individuals already infected with the virus. The aim of this review is to discuss the influence and relationship of the coronavirus, particularly SARS-CoV-2, on the respiratory system with a proposed mechanism of action in lung injury and pathogenesis.