The genomes of herpesviruses are linear double-stranded DNA molecules that range in size from 125 to 240 kbp, and contain direct or inverted repeats. The genome replicates by circularization, followed by production of concatemers and cleavage of unit-length genomes during packaging into capsids.

A characteristic of herpesviruses is their ability to establish latent infection in specific host cells, either extra-chromosomally or integrated into the host cell DNA. Latent virus may be reactivated to enter a replicative cycle at any point in time. Also, herpesviruses require intimate contact between the individual shedding the virus and the susceptible host.

Infection with an alpha-herpesvirus follows a characteristic pattern. Four to six days after inoculation onto the skin or the mucous membrane, the virus replicates in epithelial cells, causing cell lysis and inflammation with the formation of vesicles. Viremia follows, and the virus ascends the sensory nerves to reach the dorsal root ganglia. This is where latency is established.

During reactivation, replication in the ganglia is followed by retrograde axonal spread back to other skin surfaces via peripheral sensory nerves.

Diseases caused by herpesvirus include oral and genital herpes (HSV-1, HSV-2), herpetic keratitis and conjunctivitis, neonatal herpes simplex, herpes simplex encephalitis, chickenpox, shingles, cytomegalic inclusion disease, CMV mononucleosis syndrome, Epstein-Barr mononucleosis, HHV-6 and HHV-7 roseola, Kaposi’s sarcoma (HHV-8), and B virus encephalitis.

The only vaccine that is currently available is to the varicella-zoster virus; otherwise, therapy consists of treatment with acyclovir, valaciclovir, famciclovir, or ganciclovir for HSV, zoster, and CMV infections. There are no current antiviral agents for the treatment of EBV, HHV-6, HHV-7, or HHV-8.