The requirement of environmental acidification for Ibaraki virus infection to host cells

TSURUTA, Yuya; SHIBUTANI, Shusaku T.; WATANABE, Rie; IWATA, Hiroyuki

To understand the mechanism of this loss of infectivity, virus particle was collected by ultracentrifugation after low pH treatment. Western blot analysis using anti-VP2 antisera and anti-IBAV antisera was performed, and VP2, VP5 and VP7 were visualized (Fig. 2b) . The approximate molecular weights of VP2, VP5 and VP7 are 115, 60 and 38 kDa, respectively. In the case of BTV, it was shown that VP2 and VP5 form outer capsid layer and play important roles for the initial step of infection [24] . VP2 is a protein reported as a sialic acid binding protein and implicated to play a role in the attachment to target cells [24] . VP5 is believed to work as a protein which disturbs the lipid bilayer of target cells [9] . As shown in the left panel of Fig. 2b, VP2 was detected in the virus treated with PBS (pH7), whereas no VP2 was detected in the virus treated with PBS (pH4). Similarly, less VP5 was detected in the virus treated with PBS (pH4) compared to the virus treated with PBS (pH7). The amount of VP7 seemed to be the same between PBS (pH4) and PBS (pH7), and hence, it was suggested that there are the same amounts of viral core in each sample.