The herpesvirus family contains six important human pathogens: herpes simplex virus types 1 and 2, varicella-zoster virus, cytomegalovirus, Epstein–Barr virus, and human herpesvirus 8 (the cause of Kaposi’s sarcoma).
All herpesviruses are structurally similar. Each has an icosahedral core surrounded by a lipoprotein envelope (Figure 37–1). The genome is linear double-stranded DNA. The virion does not contain a polymerase. They are large (120–200 nm in diameter), second in size only to poxviruses.
Herpes simplex virus (HSV)—electron micrograph. Three HSV virions are visible. Short arrow points to the envelope of an HSV virion. Long arrow points to the nucleocapsid of the virion. The dark area between the inner nucleocapsid and the outer envelope is the tegument. (Source: Dr. John Hierholzer, Public Health Image Library, Centers for Disease Control and Prevention.)
They replicate in the nucleus, form intranuclear inclusions, and are the only viruses that obtain their envelope by budding from the nuclear membrane. The virions of herpesviruses possess a tegument located between the nucleocapsid and the envelope. This structure contains regulatory proteins, such as transcription and translation factors, which play a role in viral replication.
Herpesviruses are noted for their ability to cause latent infections. In these infections, the acute disease is followed by an asymptomatic period during which the virus remains in a quiescent (latent) state. When the patient is exposed to an inciting agent or immunosuppression occurs, reactivation of virus replication and disease can occur.1 With some herpesviruses (e.g., herpes simplex virus), the symptoms of the subsequent episodes are similar to those of the initial one; however, with others (e.g., varicella-zoster virus), they are different (Table 37–1).
TABLE 37–1Important Features of Common Herpesvirus Infections |Favorite Table|Download (.pdf) TABLE 37–1 Important Features of Common Herpesvirus Infections
|Virus ||Primary Infection ||Usual Site of Latency ||Recurrent Infection ||Route of Transmission |
|HSV-1 ||Gingivostomatitis1 ||Cranial sensory ganglia ||Herpes labialis,2,3 encephalitis, keratitis ||Via respiratory secretions and saliva |
|HSV-2 ||Herpes genitalis, perinatal disseminated disease ||Lumbar or sacral sensory ganglia ||Herpes genitalis2,3 ||Sexual contact, perinatal infection |
|VZV ||Varicella ||Cranial or thoracic sensory ganglia ||Zoster2 ||Via respiratory secretions |
|EBV ||Infectious mononucleosis1 ||B lymphocytes ||Asymptomatic shedding3,4 ||Via respiratory secretions and saliva |
|CMV ||Congenital infection (in utero), mononucleosis1 ||Monocytes ||Asymptomatic shedding2 ||Intrauterine infection, transfusions, sexual contact, via secretions (e.g., saliva and urine) |
|HHV-85 ||Uncertain6 ||Uncertain ||Kaposi’s sarcoma ||Sexual or organ transplantation |