Herpes simplex overview

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

Herpes simplex is a viral disease caused by Herpes simplex viruses. Infection of the genitals is commonly known as herpes and predominantly occurs following sexual transmission of the type 2 strain of the virus (HSV-2).[1] Oral herpes, colloquially called cold sores, is usually caused by the type 1 strain of herpes simplex virus (HSV-1).[2] Both viruses cause periods of active disease—presenting as painful blisters containing infectious virus particles—that lasts 2-21 days and is followed by remission when the sores disappear. Most cases of genital herpes are asymptomatic, although viral shedding may still occur.[3] HSV-1 and HSV-2 are transmitted by direct contact with a sore or body fluid of an infected individual. After initial infection, these viruses move to sensory nerves, where they reside as life-long, latent viruses. The viruses lie dormant in trigeminal ganglia that provide sensation to the lips, lower mouth and neck, or in lumbrosacral that supply sensation to the genitals, perineum and upper legs.[4] Occasionally, these viruses reactivate and return to the area of skin infected during the primary infection. Triggers for recurrences are uncertain but may include sunburn, ultraviolet light, wind, trauma, surgery, and stress. Over time, episodes of active disease reduce and the frequency of recurrences is regulated by specific immunity developed against the virus.[5]

Epidemiology and Demographics

Prevalence of HSV-1 and HSV-2 infections varies throughout the world.[4] Socioeconomic status appears to be an important factor associated with HSV-1 infection levels with developing countries, such as those in Sub-Saharan Africa, showing higher levels of HSV-1 and younger acquisition rates than industrialized countries like the United States and countries in Northern Europe. The risk of infection for HSV-1 is associated with lower income and a more crowded living environment. Levels of HSV-2 infections are much lower in the U.S. (20-30%), Australia (12%), the United Kingdom (4%) and Germany (14%).[6] Risk Factors for acquiring HSV-2 include: Female sex; black race; commencement of sexual activity at a younger age; higher number of sexual partners; and lower socioeconomic status.

Clinical Presentation

Disorders such as herpetic whitlow, herpes gladiatorum, and ocular herpes are caused by herpes simplex viruses. Infection of the central nervous system causes serious disorders - these include herpes encephalitis, Mollaret's meningitis, and possibly Bell's palsy.[7][8] In newborn babies, infection by herpes viruses (neonatal herpes) can be highly serious, resulting in brain damage or even death.[9] In immunocompetent people, herpes simplex is not typically life-threatening. However, individuals with compromised immune systems can develop serious HSV infections such as encephalitis.

Treatment

Treatments are available to reduce the symptoms and speed up the healing process of herpes infections but there is currently no cure.[5] Antiviral drugs, such as aciclovir and valaciclovir, taken orally, reduce viral reproduction and shedding, and some topical creams, such as Docosanol and Tromantadine prevent the virus from entering the skin. Some other drugs reduce herpetic symptoms by synergising with oral antiviral medication; Cimetidine and probenecid can reduce aciclovir clearance and aspirin can reduce inflammation associated with viral infection. Some natural remedies may have potential benefits in reducing herpes outbreaks or their symptoms. No vaccine is currently available to prevent or treat herpes.[5]

References

  1. Gupta R, Warren T, Wald A (2007). "Genital herpes". Lancet. 370 (9605): 2127–37. doi:10.1016/S0140-6736(07)61908-4. PMID 18156035.
  2. Bruce AJ, Rogers RS (2004). "Oral manifestations of sexually transmitted diseases". Clin. Dermatol. 22 (6): 520–7. doi:10.1016/j.clindermatol.2004.07.005. PMID 15596324.
  3. Leone P (2005). "Reducing the risk of transmitting genital herpes: advances in understanding and therapy". Curr Med Res Opin. 21 (10): 1577–82. doi:10.1185/030079905X61901. PMID 16238897.
  4. 4.0 4.1 Fatahzadeh M, Schwartz RA (2007). "Human herpes simplex virus infections: epidemiology, pathogenesis, symptomatology, diagnosis, and management". J. Am. Acad. Dermatol. 57 (5): 737–63, quiz 764–6. doi:10.1016/j.jaad.2007.06.027. PMID 17939933.
  5. 5.0 5.1 5.2 Koelle DM, Corey L (2008). "Herpes Simplex: Insights on Pathogenesis and Possible Vaccines". Annu Rev Med. 59: 381–395. doi:10.1146/annurev.med.59.061606.095540. PMID 18186706.
  6. Xu F, Sternberg MR, Kottiri BJ; et al. (2006). "Trends in herpes simplex virus type 1 and type 2 seroprevalence in the United States". JAMA. 296 (8): 964–73. doi:10.1001/jama.296.8.964. PMID 16926356.
  7. Tyler KL (2004). "Herpes simplex virus infections of the central nervous system: encephalitis and meningitis, including Mollaret's". Herpes. 11 Suppl 2: 57A–64A. PMID 15319091.
  8. Schirm J, Mulkens PS (1997). "Bell's palsy and herpes simplex virus". APMIS. 105 (11): 815–23. PMID 9393551.
  9. Kimberlin DW, Whitley RJ (2005). "Neonatal herpes: what have we learned". Semin Pediatr Infect Dis. 16 (1): 7–16. doi:10.1053/j.spid.2004.09.006. PMID 15685144.

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