LAUSR

Long before reaching its peak, the SARS-CoV-2 pandemic has already met the 1 million death toll worldwide. Since whether and when an effective vaccine will be available is unknown, there is an urgent need for therapeutic approaches to target this novel viral disease. The repurposing of drugs approved for clinical use of other diseases or of compounds that are in advanced pre-clinical development can help to accelerate drug development, which otherwise takes many years [1]. A respective approach has been pursued for the antiviral compound remdesivir. This broad-spectrum antiviral drug represents an already twice-repurposed compound. It had been unsuccessful as an anti-hepatitis C medication before also failing to meet expectations as an anti-Ebola drug. It has now, however, shown positive actions against COVID-19. Although detailed knowledge on the complex immune response towards SARS-CoV-2 is constantly evolving, it is widely established that a cytokine storm resulting from amyeloid overactivation in combination with thrombosis and vascular leakage contribute to morbidity and mortality [2]. Therefore, the search for therapeutic strategies has strongly focused on the suppression of the innate immune response. In this context one recently suggested approach focuses on the innate immune protein CD14 [2]. CD14, which exists in a membrane-bound (mCD14) and a soluble form (sCD14), represents a critical factor for the activation of innate immune cells [3]. It can act as an adaptor or co-receptor for either bacterial or viral molecular structures termed pathogen-associated molecular patterns (PAMPs). CD14 also represents an accessory protein to recognize host-derived factors during inflammation and cell lysis, termed damage-associated molecular patterns (DAMPs). SARSCoV-2 induces cell lysis especially in the early phase of the disease, while the later phase of COVID-19 is governed by severe acute respiratory distress syndrome (ARDS), which is widely independent of viral replication [2]. CD14 levels are increased in lung lavage fluids of patients with ARDS and plasma concentrations of sCD14 correlate with disease severity [2, 3]. Higher activity of the inflammatory