herpes(redirected from herpes progenitalis)
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Any virus of the herpesvirus group, which comprises a family of 70 species, 5 of which are pathogenic to humans; the term also refers to any infection caused by these viruses. Since these pathogens are ubiquitous in nature, most individuals of all populations are exposed to and thus immunized to these viruses. The five pathogenic groups include herpes simplex I and II, varicella-zoster, cytomegalovirus, and the Epstein-Barr virus.
In nonimmunized hosts, the vast majority of all herpes infections present symptoms of nonspecific viral illnesses which resolve spontaneously. However, the infections that cause clinical disease in fact may cause serious morbidity and mortality in afflicted individuals. Reactivation of herpes infection, characteristic of the immunocompromised host, is an important cause of mortality in the treatment of patients with advanced cancer, and is a potential complication of an otherwise possibly curable systemic disease.
Herpesviruses have a deoxyribonucleic acid (DNA) core and are 150 to 200 nanometers in size with icosahedral symmetry, and are coated by a protein barrier, the capsid, derived from the infected host cells. The surface of the virions in general contains protein-carbohydrate structures which allow cellular attachment and thus cellular penetration. All viruses require living cells for their replication; the virus may replicate and destroy the cell, or replicate and allow cell survival, or incorporate its viral gene structure into the host gene structure. This incorporation phenomenon is designated as latency. For example, herpes simplex virus exhibits the phenomenon of latency within nerve cells in the area of previous infection. The Epstein-Barr virus characteristically causes latent infection in lymphocytes (white blood cells in the circulating blood), and the cytomegalic virus also causes latent infection within lymphocytes and possibly within nerve cells. Once the viral genome is incorporated into the host cell, antiviral drugs are of no use, since therapeutic agents cannot selectively destroy or inhibit the viral genome. Factors which are possibly involved in the reactivation of latent virus generally revolve around some depression of the host immune response system. Viral genome incorporation into host cells is of great interest as several herpesvirus types are implicated in the development of cancer.
The foundation of therapeutic intervention for all herpesviruses involves a series of chemicals with structures similar to the base pairs which compose the viral DNA structure. The base analogs compete with or inhibit viral enzymes necessary for the assembly of DNA. See Virus
Herpes simplex I and II infections are spread by intimate contact of mucocutaneous surfaces during the period of virus shedding from active lesions. They usually affect the genitalia, but may affect the oral mucosa, causing painful ulcerations which crust and heal. Upon healing, the virus resides in latent form within local nerve cells. Viral reactivation is poorly understood, but may relate in part to the host immune system. The type II virus has been linked to the development of uterine cervical carcinoma, however its precise role remains a question.
Herpes simplex virus I (cold sores, fever blisters) afflicts 20–40% of the population in the United States and usually affects the oropharynx, causing pharyngitis, tonsillitis, gingivostomatitis, or keratitis (eye inflammation) as primary infections. Inflammation of the mouth, eye, or brain may occur as a secondary infection.
Primary infection (airborne) due to herpes varicella-zoster usually affects preschool children, causing chickenpox, with rare complications usually affecting the immunocompromised host. Secondary infection usually afflicts the elderly when latent viral reactivation occurs, presumably due to an immune imbalance in the host, and involves the spread of virus along the skin in the anatomic distribution of nerve (this disorder is known as shingles).
Cytomegalovirus is ubiquitous, with the majority of infections remaining subclinical. Adult syndromes include a mononucleosislike syndrome and hepatitis, both of which are self-limited diseases in the normal host. However, reactivation of latent infection is a major source of morbidity and especially mortality in the compromised host, for example, the patient being treated with chemoradiotherapy for advanced malignant disease. See Cytomegalovirus infection, Hepatitis
The characteristic clinical syndrome caused by Epstein-Barr virus infection includes generalized lymphadenopathy, hepatosplenomegaly, pharyngitis, tonsillitis, and general fatigue and fever. This disorder affects individuals of all ages, but predominantly adolescents. The majority of children are subclinically infected. This mononucleosis syndrome is usually a self-limited disorder, and investigational drugs in use for prophylaxis of high-risk individuals include interferons and acyclovir. Epstein-Barr virus is suspected to be of etiologic importance in Burkitt's African lymphoma. See Animal virus, Epstein-Barr virus