Since monoclonal anti-gO antibodies are able to neutralize both fibroblast and epithelial cell infection (Gerna et al., 2016; Kabanova et al., 2016), it is suggested that gO is the critical subunit of the trimer, either for interaction with the recently identified fibroblast-specific platelet-derived growth factor alpha receptor (PDGFRα), or for activation of gB-mediated fusion (Schultz et al., 2015; Zhou et al., 2015). Here, PDGFRA is linked to infection.