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Currently used drugs successfully target the viral replication within the host cell, but their use is restricted due to side effects and the development of resistance. An alternative approach is the inhibition of virus entry, for which understanding the details of the initial virus-cell interaction is desirable. As binding of the viral gH\/gL\/gO complex to the cellular PDGFR\u03b1 drives infection of fibroblasts, this is a potential target for inhibition of infection. Our mutational mapping approach suggests the N terminus as the receptor binding portion of the protein. The respective mutants were partially resistant to inhibition by PDGFR\u03b1-Fc but also attenuated for infection of fibroblasts, indicating that such mutations have little if any benefit for the virus. 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