Utilizing animals that encode an pRB mutant that lacks non-canonical activities of pRB, i.e., pRBS mutant mice, infection with the RB-binding defective E7D90A mutant MmuPV1 could reveal whether loss of non-canonical activities of pRB complement for the loss of pRB binding and provide evidence on which non-canonical activities of pRB play a role in MmuPV1 pathogenesis [188]. The gene discussed is RB1; the disease is infection.