FIGURE 3.

Human cytomegalovirus infection of monocytes drives a number of key molecular mechanisms required to enhance survival of normally short-lived monocytes and for the promotion of the differentiation of these infected monocytes into long-lived productively infected macrophaqes. It is important to note that monocytes, although they can be infected, they are not permissive for viral replication; only upon differentiation is de novo viral gene expression observed. HCMV-infected monocytes show enhanced expression of Mcl-1 early after infection (<48 h post infection) to prolong survival through the key 48-h viability gate. Mcl-1 levels then gradually decrease through this 48 h viability gate. Enhanced expression of Bcl-2 is then observed, as well as partial activation of caspase-3, which together seem to promote both long term survival and differentiation of these infected monocytes toward viral replication-permissive tissue macrophages that begin to produce mature virus around 3 weeks after infection.