Abstract

SARS-CoV-2, the causative agent of Coronavirus disease 2019 (COVID-19), has infected
more than 22 million people around the globe. Although this pandemic pathogen spreads
with enormous efficiency it seems to be highly sensitive to interferons. Here, I will discuss
some of the mechanisms allowing SARS CoV-2 to prevent control by the innate immune
response and to escape or even highjack specific cellular antiviral factors. In collaborative
studies, we found that the non-structural protein 1 (Nsp1) of SARS CoV-2 targets ribosomes
to shutdown cellular mRNA translation and consequently the antiviral immune response. I
will show that the Zinc finger antiviral protein (ZAP) that specifically targets CpG
dinucleotides in viral RNA sequences restricts SARS-CoV-2, although this pandemic
pathogen emerged from zoonosis of a coronavirus that was preadapted to the low CpG
environment in humans. Finally, I will provide evidence that SARS CoV-2 may actually
highjack specific “antiviral” factor for efficient infection of human lung cells.