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 cold sores/genital herpes
• HHV-2 = HSV-2 (herpes simplex virus 2): causes cold sores/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

The human herpesviruses all share some common properties. One shared property is virus structure - all herpesviruses are composed of relatively large double stranded circular 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. 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 fever, headache, malaise, rash, etc.

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