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Pandemic SARS-CoV-2 causes a mild to severe respiratory disease called coronavirus disease 2019 (COVID-19). While control of the SARS-CoV-2 spread partly depends on vaccine-induced or naturally acquired protective herd immunity, antiviral strategies are still needed to manage COVID-19. Enisamium is an inhibitor of influenza A and B viruses in cell culture and clinically approved in countries of the Commonwealth of Independent States. In vitro, enisamium acts through metabolite VR17-04 and inhibits the activity of the influenza A virus RNA polymerase. Here we show that enisamium can inhibit coronavirus infections in NHBE and Caco-2 cells, and the activity of the SARS-CoV-2 RNA polymerase in vitro. Docking and molecular dynamics simulations provide insight into the mechanism of action and indicate that enisamium metabolite VR17-04 prevents GTP and UTP incorporation. Overall, these results suggest that enisamium is an inhibitor of SARS-CoV-2 RNA synthesis in vitro.
Since the early 1970s several studies have reported distal splenic artery embolization, better known as partial spleen embolization (PSE), as an efficacious treatment of portal hypertensive variceal bleeding and hypersplenism in cirrhosis.(1, 2) However, the effect of PSE on portal pressure is secondary to the induction of splenic infarction. Depending on both the infarct volume and possible infection, PSE can induce serious complications including death.(2, 3) On the other hand, proximal splenic artery embolization (PSAE), which mimics surgical splenic artery ligation, prevents large infarction of the spleen, favoring collateral perfusion of its intact distal vasculature.(3) For this, PSAE has been extensively preferred over PSE for reducing portal hyperflow and treating refractory ascites (RA) after whole or partial liver transplantation (LT).(3, 4) We report here a case of PSAE used to treat RA in a patient with cirrhosis not eligible for transjugular intrahepatic portosystemic shunt (TIPS) and LT.