INTRODUCTIONThere is insufficient information on how COVID-19 affects people who already have chronic liver diseases like HBV or HCV (El Kassas et al., 2020). On the other hand, COVID-19 co-infection with viral hepatitis shows a greater potential to cause liver damage with worse results and death. In this regard, according to (Qi et al., 2020), despite receiving intensive care, a 53-yearold man with HBV-related cirrhosis, portal hypertension, and ascites passed away 48 days after the onset of the illness from irreversible multiple organ dysfunction syndromes (Qi et al., 2020). According to a different study, those with HBV infection have a higher risk of dying and a higher prevalence of liver cirrhosis, total bilirubin, severe presentations, and hepatic cirrhosis (Chen et al., 2020).The most frequently reported symptoms of liver injury in COVID-19 patients are abnormal liver function and high levels of aspartate aminotransferase or alanine aminotransferase, (Zhang et al., 2020) which have developed in 16.1-53.1% of SARS-CoV-2-infected patients. Liver damage is a common complication of SARS-CoV-2 infection, which can be caused by a direct viral infection of liver cells (Wang et al., 2020; Huang et al., 2020).Human ACE2 Angiotensin-converting enzyme 2 (ACE2) is the host receptor by SARS-CoV-2 to infect human cells. Coronavirus binds to its specific receptor called. Despite reports that ACE2 is expressed in the lung, liver, stomach, ileum, kidney, and colon, particularly in the lung (Jin et al., 2020).
revealed the discovery of the first case of respiratory illness brought on by a novel coronavirus. The World Health Organization named the disorder coronavirus disease 2019 (COVID-19) dated February 11, 2020, despite the fact that it is still dangerous throughout the entire world (CDC, 2020). As SARS-CoV-2 infected the liver and cause dysfunction and damage to hepatocytes (Fan et al., 2020). Symptoms included cough, fever, pneumonia, وheadache, diarrhea, hemoptysis, and, dyspnea, (Adhikari et al., 2020).SARS-CoV-2 uses the host receptor angiotensin I converting enzyme 2 (ACE2) to infect human cells. Even though it has been claimed that ACE2 is expressed in the lung, liver, stomach, ileum, kidney, and colon, these tissues actually express it at relatively low levels, particularly in the lung) Qi et al., 2020;Lai et al., 2020).When a disease is present, the innate immune system starts to react. Some innate immune cytokines increase, which may help in predicting the subsequent stages of the clinical period (Mason, 2020;Liu et al., 2020). Cytokine storms, which come from increased levels of proinflammatory cytokines and chemokines that affect numerous organs, are the cause of ARDS in COVID-19 disease Merad and Martin, 2020). In the host cell, the type transmembrane protease, serine 2 (TMPRSS2) increases viral uptake by cleaving ACE2 and activating the SARS-CoV-2 S protein, which enables coronavirus entrance into host cells (Hoffmann et al., 2020). ACE2 and TMPRSS2 are present in target cells of the host, specifically alveolar epithelial type II cells (Mancia et al., 2020; Zou et al., 2020).
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