The Herpesviridae are a large family of DNA viruses that cause diseases in animals, including humans.[1][2][3] The family name is derived from the Greek word herpein ("to creep"), referring to the latent, re-occurring infections typical of this group of viruses. Herpesviridae can cause latent or lytic infections.
Herpes viruses all share a common structure—all herpes viruses are composed of relatively large double-stranded, linear DNAgenomes 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.
Herpes virus life-cycle
All Herpes viruses are nuclear-replicating—the viral DNA is transcribed to RNA within the infected cell's nucleus.
Infection is initiated when a viral particle contacts a cell with specific types of receptor molecules on the cell surface. Following binding of viral envelope glycoproteins to cell membrane receptors, the virion is internalized and dismantled, allowing viral DNA to migrate to the cell nucleus. Within the nucleus, replication of viral DNA and transcription of viral genes occurs.
During symptomatic infection, infected cells transcribe lytic viral genes. In some host cells, a small number of viral genes termed latency associated transcript (LAT) accumulate instead. 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.
Reactivation of latent viruses has been implicated in a number of diseases (e.g. Shingles). Following activation, transcription of viral genes transitions from latency-associated LAT to multiple lytic genes; these 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, and rash as well as clinical signs such as swollen or tender lymph nodes and immunological findings such as reduced levels of natural killer cells.
Human herpesviridae infections
There are eight distinct viruses in this family known to cause disease in humans.[4]
In addition to the Herpes viruses considered endemic in humans, some viruses associated primarily with animals may infect humans. These are zoonotic infections:
Very unusual, with only approximately 25 human cases reported.[6] Untreated infection is often deadly; sixteen of the 25 cases resulted in fatal encephalomyelitis. At least four cases resulted in survival with severe neurologic impairment.[6][7] Symptom awareness and early treatment are important for laboratory workers facing exposure.[8]
Zoonotic infection found in 4.5% of general population and more common in laboratory workers handling infected mice.[9] ELISA tests show factor-of-four (x4) false positive results, due to antibody cross-reaction with other Herpes viruses.[9]
Animal herpesviridae
In animal virology the most important herpesviruses belong to the Alphaherpesvirinae. Research on pseudorabies virus (PrV), the causative agent of Aujeszky's disease in pigs, has pioneered animal disease control with genetically modified vaccines. PrV is now extensively studied as a model for basic processes during lytic herpesvirus infection, and for unravelling molecular mechanisms of herpesvirus neurotropism, whereas bovine herpesvirus 1, the causative agent of bovine infectious rhinotracheitis and pustular vulvovaginitis, is analyzed to elucidate molecular mechanisms of latency. The avian infectious laryngotracheitis virus is phylogenetically distant from these two viruses and serves to underline similarity and diversity within the Alphaherpesvirinae.[2][3]
^ Bottieau E, Clerinx J, Van den Enden E, Van Esbroeck M, Colebunders R, Van Gompel A, Van den Ende J (2006). "Infectious mononucleosis-like syndromes in febrile travelers returning from the tropics.". J Travel Med13 (4): 191–7. PMID 16884400.
^ ab Weigler BJ (1992 Feb). "Biology of B virus in macaque and human hosts: a review". Clinical infectious diseases : an official publication of the Infectious Diseases Society of America14 (2): 555–67. PMID 1313312.
^ Huff J, Barry P (2003). "B-virus (Cercopithecine herpesvirus 1) infection in humans and macaques: potential for zoonotic disease". Emerg Infect Dis9 (2): 246–50. PMID 12603998.
^ ab Hricova M, Mistrikova J (2007). "Murine gammaherpesvirus 68 serum antibodies in general human population". Acta virologica51 (4): 283–7. PMID 18197737.
^ Fenner, Frank J.; Gibbs, E. Paul J.; Murphy, Frederick A.; Rott, Rudolph; Studdert, Michael J.; White, David O. (1993). Veterinary Virology (2nd ed.). Academic Press, Inc. ISBN 0-12-253056-X.