Fig. 3: LRP1 acts as an entry factor for SFTSV.

a A SFTSV-glycoprotein pseudovirus was used to infect WT and LRP1 KO MEFs (MOI = 5, 48 h). VSV-glycoprotein pseudovirus was used as a positive control. n = 3 independent experiments. b An LRP1 neutralizing antibody (anti-LRP1; Invitrogen #MA1-27198) was administered at 30 µg/mL 4 h before, during, and 4 h after SFTSV infection (MOI of 1). The levels of intracellular intracellular viral RNA and protein were measured by RT‒qPCR and Western blotting 48 h post infection. Data are mean ± SD, n = 6 independent experiments. c Overview of the binding and internalization assay (constructed by Figdraw.). Effects of LRP1 deletion on the binding (d) and internalization (e) of SFTSV (MOI of 10) in MEFs. Relative viral RNA was measured by RT‒qPCR, and the data were normalized to the SFTSV S mRNA level in WT cells. Data are mean ± SD, n = 6 independent experiments. Two-tailed unpaired t test, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. ns not significant (binding: WT vs. Lrp1 KO, P < 0.0001; internalization: WT vs. Lrp1 KO, P < 0.0001) f, g Visualization of virion (MOI of 10) binding to cell membranes in WT and LRP1 KO MEFs by confocal microscopy (f). The cell membrane was defined by the membrane protein PDPN, and the virus was stained with a rabbit anti-SFTSV antibody. Scale bars, 20 µm. The number of virions that bound to the cell membrane was quantified and analyzed (g). Data are means ± SD, n = 138 cells examined over three independent experiments. Source data are provided as a Source Data file.