90K/LGALS3BP Expression is Upregulated in COVID-19 but Does Not Restrict SARS-CoV-2 Infection
Bosquillon de Jarcy, L.; Akbil, B.; Leyens, J.; Postmus, D.; Harnisch, G.; Jansen, J.; Schmidt, M.; Aigner, A.; Pott, F.; Chua, R. L.; Krist, L.; Gentile, R.; Muehlemann, B.; Jones, T. C.; Niemeyer, D.; Fricke, J.; Keil, T.; Pischon, T.; Janke, J.; Conrad, C.; Iacobelli, S.; Drosten, C.; Corman, V. M.; Ralser, M.; Eils, R.; Kurth, F.; Sander, L. E.; Goffinet, C.
Show abstract
Glycoprotein 90K, encoded by the interferon-stimulated gene LGALS3BP, displays broad antiviral activity. It reduces HIV-1 infectivity by interfering with Env maturation and virion incorporation, and increases survival of Influenza A virus-infected mice via antiviral innate immune signaling. Here, we analyzed the expression of 90K/LGALS3BP in 44 hospitalized COVID-19 patients. 90K protein serum levels were significantly elevated in COVID-19 patients compared to uninfected sex- and age-matched controls. Furthermore, PBMC-associated concentrations of 90K protein were overall reduced by SARS-CoV-2 infection in vivo, suggesting enhanced secretion into the extracellular space. Mining of published PBMC scRNA-seq datasets uncovered monocyte-specific induction of LGALS3BP mRNA expression in COVID-19 patients. In functional assays, neither 90K overexpression in susceptible cell lines nor exogenous addition of purified 90K consistently inhibited SARS-CoV-2 infection. Our data suggests that 90K/LGALS3BP contributes to the global type I IFN response during SARS-CoV-2 infection in vivo without displaying detectable antiviral properties.
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