FIGURE 3.

Puumala in virus and platelets bind to each other. In a pull down assay platelets adhere better to PUUV virus particles compared to vesicular stomatitis virus (VSV; A; Mann–Whitney U p 0.0022). When virus was captured with a PUUV glycoprotein antibody (B), platelets were able to bind to the captured virus, in contrast to wells coated with an IgG2 control antibody (anti-coronavirus glycoprotein; Mann–Whitney U p 0.0022), resulting in no capture of PUUV during the incubation process, controlling for potential other factors present in the virus stock medium. When platelets were bound to plates coated with an anti-CD41a antibody (C), the PUUV particles were able to bind to platelets based on the significant increase in PUUV detection OD compared to wells incubated with VSV particles, thus no PUUV present (Mann–Whitney U p 0.0043). The binding between PUUV and platelets could be blocked by the addition of a blocking step with human anti-PUUV serum (D) which show a decreased CD41 expression when compared to the PUUV coated wells incubated with a PUUV negative control serum. In all experiments no difference in OD was measured when an isotype control antibody was used. Data are representative of three independent experiments.**p < 0.01 ***p ≤ 0.001