Herpesviridae

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Herpesviridae

Virus classification

Group:	Group I (dsDNA)
Family:	Herpesviridae

Genera

Subfamily Alphaherpesvirinae
   Simplexvirus
   Varicellovirus
   Mardivirus
   Iltovirus
Subfamily Betaherpesvirinae
   Cytomegalovirus
   Muromegalovirus
   Roseolovirus
Subfamily Gammaherpesvirinae
   Lymphocryptovirus
   Rhadinovirus
Unassigned
   Ictalurivirus

The Herpesviridae are a family of DNA viruses that cause diseases in humans and animals.

There are eight types of viruses in this family known to cause disease in humans. These viruses are (HHV stands for human herpesviruses):

HHV-1 = HSV-1 (herpes simplex virus 1): causes oral and/or genital herpes
HHV-2 = HSV-2 (herpes simplex virus 2): causes oral and/or genital herpes
HHV-3 = VZV (varicella-zoster virus): causes chickenpox and shingles
HHV-4 = EBV (Epstein-Barr virus), lymphocryptovirus: causes infectious mononucleosis, Burkitt's lymphoma and nasopharyngeal carcinoma
HHV-5 = CMV (cytomegalovirus): causes mononucleosis, retinitis, etc.
HHV-6 = roseolovirus: causes "sixth disease" (roseola infantum, exanthem subitum)
HHV-7 = closely related to HHV-6; causes roughly the same symptoms
HHV-8 = rhadinovirus = KSHV = Kaposi's sarcoma herpesvirus

Viral structure

The human herpes viruses all share some common properties. One shared property is virus structure - all herpesviruses are composed of relatively large double stranded linear DNA genomes encoding 100-200 genes encased within an icosahedral protein cage called the capsid which is itself wrapped in a lipid bilayer membrane called the envelope. This particle is known as the virion. Following binding of viral envelope protein to cell membrane receptors, the virion is internalized and dismantled, allowing viral DNA to migrate to the cell nucleus. Within the nucleus, viral DNA undergoes limited replication and transcription of a small number of viral genes termed latent genes. In this fashion the virus can persist in the cell (and thus the host) indefinitely. Reactivation of latent viruses has been implicated in a number of organic diseases. While primary infection is often accompanied by a self-limited period of clinical illness, long-term latency is symptom-free. Following activation, the virus switches on transcription of multiple additional non-latent genes termed lytic genes that lead to enhanced replication and virus production. Often, lytic activation leads to cell death. Clinically, lytic activation is often accompanied by emergence of non-specific symptoms such as low grade fever, headache, sore throat, malaise, rash, etc as well as clinical signs such as swollen or tender lymph nodes and immunological findings such as reduced levels of natural killer cells.