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The arms race between viruses and their hosts shaped the evolutionary history and the genome composition of both parties. Restriction factors are the first-line antiviral effectors encoded by the host genomes and are often conserved through evolution to protect the hosts from morbidity, mortality, and even extinction associated with viral infections. There are a number of restriction factors identified so far to counteract HIV infection of the humans. PSGL-1 is a recently characterized human restriction factor that acts both early and late in the viral life cycle, the latter of which is antagonized by the HIV-1 Vpu protein. Here we show in vitro and in a knockout mouse model that PSGL-1's antiviral function is conserved in mice for combating the murine leukemia virus (MLV). In counter-strike, the glycogag or glycoMA proteins encoded by MLV can interact with mouse PSGL-1, which leads to Cul3-KLHL20 E3 ligase-dependent ubiquitination and degradation of PSGL-1. The amino acids involved in this interaction demonstrate the evidence of positive selection, manifesting the evolution pressure from the antagonism between PSGL-1 and glycogag/glycoMA. Our data support that PSGL-1 is an evolutionarily conserved antiviral restriction factor.
Jacques Fellay, Bruno Emanuel Ferreira De Sousa Correia, Zhi Ming Xu, Andreas Scheck, Dylan Lawless, Olivier Noël Marie Naret, Arne Schneuing, David Gfeller, Thomas Junier, Sina Rüeger
Paolo De Los Rios, Daniel Maria Busiello, Stefano Zamuner, Adélaïde Alice Mohr