Analogously, in a cell-free virus infection model, viruses bearing Envs isolated from VNPs or RPs showed similar infectivity and similar ability to promote CD4-dependent signals (as measured by α-tubulin acetylation) in permissive CEM.NKR-CCR5 cells, ruling out an active role of a defective interaction between Env and CD4 in the VNP phenotype. This evidence concerns the gene CCR5 and viral infectious disease.