EBV infection in healthy carriers. EBV infection in healthy carriers. Primary EBV infection begins in the oral cavity. EBV uses different glycoproteins to infect epithelial cells and naïve B cells. Viral entry results in transport of the EBV genome into the B-cell nucleus, where replication by cellular and viral DNA polymerases begins. EBV gene products activate the B-cell growth program, resulting in the proliferation of blasting B cells. Priming of naïve T cells by antigen-presenting cells occurs in parallel. Normally, these blasting B cells are destroyed by cytotoxic T lymphocytes. Once in the circulation, previously activated memory B cells may continue to undergo lytic replication or, if EBV shuts down most of its protein-encoding genes, latency occurs. At a later time, as cells recirculate between the oral and peripheral compartments, resting B cells may be activated, resulting in viral reactivation and shedding. Oludare A. Odumade et al. Clin. Microbiol. Rev. 2011; doi:10.1128/CMR.00044-10