Hepatobiliary changes in patients infected with coronavirus

At the end of 2019, an outbreak of a new coronavirus infection was observed in the People's Republic of China, with its epicenter located in Wuhan City, Hubei Province. On February 11, 2020, the World Health Organization (WHO) officially named the infection caused by the new coronavirus - COVID-19 (Coronavirus Disease 2019). On the same day, the International Committee on Taxonomy of Viruses assigned the official name SARS-CoV-2 to the causative agent. SARS-CoV-2 is a single-stranded RNA-containing virus belonging to the Coronaviridae family. The S-protein of SARS-CoV-2 is structurally similar to angiotensin-converting enzyme 2 (ACE2). After entering the human body through the upper respiratory tract, the virus affects receptors of the respiratory epithelium, alveolocytes, alveolar monocytes, vascular endothelium, gastrointestinal and urinary tract epithelium, macrophages, as well as other systems and organs such as the myocardium and the central nervous system. The core pathogenic mechanism of this disease includes destructive-productive thrombovasculitis, hypercoagulation syndrome, microangiopathy, and an inadequate immune response. In response to SARS-CoV-2, a hyperergic activation of the immune system develops in patients, leading to a severe systemic inflammatory syndrome, alteration of alveolar lung tissue and other organs, and the development of septic shock.