Of particular interest, however, was the additional observation that monolayer cells too early to be infected with MCMV (given the low multiplicity of infection used) were also VEGF-positive, an observation suggesting the attractive hypothesis that uninfected bystander macrophages might also be stimulated by adjacent MCMV-infected macrophages to produce enhanced amounts of VEGF during virus infection. This evidence concerns the gene VEGFA and viral infectious disease.