The outbreak of coronavirus disease 2019 (COVID-19) starting last December in China placed emphasis on liver involvement during infection. This review discusses the underlying mechanisms linking COVID-19 to liver dysfunction, according to recent available information, while waiting further studies. The manifestations of liver damage are usually mild (moderately elevated serum aspartate aminotransferase activities), and generally asymptomatic. Few patients can still develop severe liver problems, and therapeutic options can be limited. Liver dysfunction may affect about one-third of the patients, with prevalence greater in men than women, and in elderly. Mechanisms of damage are complex and include direct cholangiocyte damage and other coexisting conditions such as the use of antiviral drugs, systemic inflammatory response, respiratory distress syndromeinduced hypoxia, sepsis, and multiple organ dysfunction. During new COVID-19 infections, liver injury may be observed. If liver involvement appears during COVID-19 infection, however, attention is required. This is particularly true if patients are older or have a pre-existing history of liver diseases. During COVID-19 infection, the onset of liver damage impairs the prognosis, and hospital stay is longer. SymptomsDuring COVID-19 infection, patients can be asymptomatic or present clinical symptoms ranging from fever, dry cough, headache to dyspnea and fatigue, to acute respiratory distress syndrome (ARDS), shock, and cardiac failure [9,16]. A nasopharyngeal swab is the collection method used to obtain a specimen for testing. Because the likelihood of the SARS-CoV-2 being present in the nasopharynx increases over time, repeated testing is often used [17]. Multi-organ

Sir, with great interest we read the paper by Bianco et al, 1 presenting the association between genetic modifiers of liver injury and outcomes in patients with COVID-19. Whilst Bianco et al 1 showed that the PRS-HFC genetic score does not affect studied phenotypes, they also demonstrated that C3 and AB0 genetic variants are associated with the severity of COVID-19. In this study, we would like to add to these interesting observations and present first data concerning the MBOAT7 polymorphism rs641738 (which is included among other variants in the PRS-HFC score), a known risk factor for liver steatosis and fibrosis. 2Prospectively, we analysed a cohort of 44 patients with COVID-19 (64% men; median age 62 years, range 21-91 years) hospital-