Clinical relevance of serum α-l-fucosidase activity in the SARS-CoV-2 infection.

BACKGROUND AND AIMS: The reduced fucosylation in the spike glycoprotein of SARS-CoV-2 and the IgG antibody has been observed in COVID-19. However, the clinical relevance of α-l-fucosidase, the enzyme for defucosylation has not been discovered. MATERIALS AND METHODS: 585 COVID-19 patients were included to analyze the correlations of α-l-fucosidase activity with the nucleic acid test, IgM/IgG, comorbidities, and disease progression. RESULTS: Among the COVID-19 patients, 5.75% were double-negative for nucleic acid and antibodies. All of them had increased α-l-fucosidase, while only one had abnormal serum amyloid A (SAA) and C-reactive protein (CRP). The abnormal rate of α-l-fucosidase was 81.82% before the presence of IgM, 100% in the presence of IgM, and 66.2% in the presence of IgG. 73.42% of patients with glucometabolic disorders had increased α-l-fucosidase activity and had the highest mortality of 6.33%. The increased α-l-fucosidase was observed in 55.8% of non-severe cases and 72.9% of severe cases, with an odds ratio of 2.118. The α-l-fucosidase mRNA was irrelevant to its serum activity. CONCLUSION: The change in α-l-fucosidase activity in COVID-19 preceded the IgM and SAA and showed a preferable relation with glucometabolic disorders, which may be conducive to virus invasion or invoke an immune response against SARS-CoV-2.

Hydrogen peroxide induces p16(INK4a) through an AUF1-dependent manner.

Elevation of p16(INK4a) has been described as an important mechanism for hydrogen peroxide (H2O2)-induced replicative senescence. However, the mechanisms underlying remain unknown. In this study, we demonstrate an important role of RNA-binding protein AUF1-mediated mRNA turnover in H2O2-induced p16(INK4a) expression. The induction of p16 by H2O2 was accompanied with declined cytoplasmic AUF1 level. Accordingly, exposure of cells to H2O2 remarkably reduced the binding of AUF1 to p16 3'UTR and increased the half-life of an EGFP-p16-3'UTR chimeric transcript. In AUF1-silenced cells, the effect of H2O2 on p16 induction was abolished. Furthermore, in cells co-transfected with vectors expressing AUF1s, treatment with H2O2 failed to significantly reduce the expression of AUF1 and subsequently elevate the levels of p16. Moreover, HeLa cells overexpressing AUF1s were resistant to H2O2-induced senescence. Our results indicate that AUF1 is critical for H2O2-induced p16 expression and cellular senescence.