Viral pathogens have emerged as the most significant microbial agents causing deleterious effects in solid organ transplant recipients (OTRs). Cytomegalovirus (CMV) is the most common opportunistic organism encountered during the one- to six-month posttransplantation period, and prophylactic regimens have been carefully developed to counter its virulence. Several other viruses manifest on mucocutaneous sites, ranging from cosmetically disfiguring facial molluscum contagiosum virus (MCV) to extensive common or genital warts from human papillomavirus (HPV) to invasive or life-threatening HPV-induced squamous cell carcinoma. In the great majority of cases, viral opportunistic infection (OI) represents reactivation of latent viral infection, that is, herpes family of viruses, or proliferation of subclinical infection with HPV or MCV.

HERPETOVIRIDAE (HUMAN HERPES VIRUSES)

Human herpesviruses (HHV), that is, herpes simplex virus (HSV) types 1 and 2; cytomegalovirus (CMV); varicella-zoster virus (VZV); Epstein–Barr virus (EBV); human herpesvirus-6, -7, -8 (HHV-6, HHV-7, HHV-8), share three characteristics in common that make them particularly effective pathogens in the immunocompromised host: (1) latency (once infected with the virus, the individual remains infected for life, with immunosuppression being the major factor responsible for reactivation of the virus from a latent state); (2) cell association (these viruses are highly cell-associated, rendering humoral immunity inefficient as a host defense and cell-mediated immunity paramount in the control of these infections); and (3) oncogenicity (all herpes group viruses should be regarded as potentially oncogenic, with the clearest demonstration of this being EBV-related lymphoproliferative disease).