Herpes simplex virus: Difference between revisions

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In a 1993 paper in ''Medical Hypotheses (journal)'', P. A. Bond hypothesized that HSV-1 could cause the symptoms of [[chronic fatigue syndrome]] (CFS) in a two-stage process Bond analogized to the relationship of [[HIV/AIDS|HIV to AIDS]]: as (untreated) HIV weakens the immune system and makes the body vulnerable to opportunistic infections and cancers, which then are recognized as the symptoms of AIDS, Bond suggests a variety of conditions could produce immune dysfunction and consequent vulnerability to HSV-1 (either primary infection or reactivation), which in turn could be the cause of a range of CFS symptoms.<ref name=":3">{{Cite journal|last=Bond|first=P. A.|author-link=|author-link2=|author-link3=|author-link4=|author-link5=|date=May 1993|title=A role for herpes simplex virus in the aetiology of chronic fatigue syndrome and related disorders|url=https://www.ncbi.nlm.nih.gov/pubmed/8394501|journal=Medical Hypotheses|volume=40|issue=5|pages=301–308|issn=0306-9877|pmid=8394501|quote=|via=}}</ref>
In a 1993 paper in ''Medical Hypotheses (journal)'', P. A. Bond hypothesized that HSV-1 could cause the symptoms of [[chronic fatigue syndrome]] (CFS) in a two-stage process Bond analogized to the relationship of [[HIV/AIDS|HIV to AIDS]]: as (untreated) HIV weakens the immune system and makes the body vulnerable to opportunistic infections and cancers, which then are recognized as the symptoms of AIDS, Bond suggests a variety of conditions could produce immune dysfunction and consequent vulnerability to HSV-1 (either primary infection or reactivation), which in turn could be the cause of a range of CFS symptoms.<ref name=":3">{{Cite journal|last=Bond|first=P. A.|author-link=|author-link2=|author-link3=|author-link4=|author-link5=|date=May 1993|title=A role for herpes simplex virus in the aetiology of chronic fatigue syndrome and related disorders|url=https://www.ncbi.nlm.nih.gov/pubmed/8394501|journal=Medical Hypotheses|volume=40|issue=5|pages=301–308|issn=0306-9877|pmid=8394501|quote=|via=}}</ref>


In 2018, [[Hector Bonilla]], MD and Clinical Assistant Professor of Medicine in Infectious Diseases at [[Stanford University]], received a [[Ramsay Award Grant]] from the [[Solve ME/CFS Initiative]] for a "Cross-sectional study to assess the prevalence of [[APOE]] e4 alleles in patients with ME/CFS and the association with herpes virus infection”.<ref name=":02">{{Cite web|url=https://solvecfs.org/hector-bonilla/|title=Hector Bonilla|website=Solve ME/CFS Initiative|language=en-US|access-date=2019-03-29}}</ref> The project follows on preliminary findings that HSV-1 infection in the sera of individuals with ME/CFS is related to severity of the disease.<ref name=":02" />
In 2018, [[Hector Bonilla]], MD and Clinical Assistant Professor of Medicine in Infectious Diseases at [[Stanford University]], received a [[Ramsay Award Program|Ramsay Award Grant]] from the [[Solve ME/CFS Initiative]] for a "Cross-sectional study to assess the prevalence of [[APOE]] e4 alleles in patients with ME/CFS and the association with herpes virus infection”.<ref name=":02">{{Cite web|url=https://solvecfs.org/hector-bonilla/|title=Hector Bonilla|website=Solve ME/CFS Initiative|language=en-US|access-date=2019-03-29}}</ref> The project follows on preliminary findings that HSV-1 infection in the sera of individuals with ME/CFS is related to severity of the disease.<ref name=":02" />


Pridgen suggests that an approach related to IMC-1 also merits investigation as an ME/CFS treatment.<ref name=":4" />
Pridgen suggests that an approach related to IMC-1 also merits investigation as an ME/CFS treatment.<ref name=":4" />

Revision as of 19:58, February 21, 2021

Herpes simplex virus 1 and 2 (HSV-1 and HSV-2), also known as human herpesvirus 1 and 2 (HHV-1 and HHV-2), are two members of the eight known members of the herpesviridae family. Both are lifelong infections and mostly asymptomatic.[1]

Overview[edit | edit source]

HSV-1 is mainly transmitted by oral contact and causes cold sores, but can also cause genital herpes (persons with oral HSV-1 are unlikely to subsequently contract genital HSV-1.)[1] HSV-1 is a highly common virus, found in an estimated 67% of the worldwide population under the age of 50.[1] HSV-1 is most contagious while symptomatic, but can also be transmitted while asymptomatic.[1]

HSV-2 is sexually transmitted and causes most cases of genital herpes.[1] HSV-2 infection increases the risk of contracting and transmitting HIV.[1] In the age group of 15 to 49, an estimated 11% of the global population has HSV-2.[1]

Treatment[edit | edit source]

Standard treatment for herpes simplex virus include acyclovir, famciclovir, and valacyclovir.[1] These medications can reduce frequency and severity of symptoms (but do not cure the infection).[1]

Basic research[edit | edit source]

An in vitro study found HSV-1 (as well as the influenza virus) inhibited the mitochondrial respiratory chain. In the case of HSV-1, it reduced cellular respiration by targeting a site between complexes II and III, mediated by protein US3, and reduced the oxygen consumption rate by 31%.[2]

Implication in other diseases[edit | edit source]

Dr. William Pridgen hypothesizes that fibromyalgia may be caused by HSV-1 infection in the dorsal root ganglia of the spine (and/or in other nerve ganglia), and treats fibromyalgia with an antiviral protocol, called IMC-1,[3] comprised of famciclovir (Famvir) and the COX-2 inhibitor drug celecoxib.[4] A randomized, double-blinded, placebo-controlled study clinical trial of 143 fibromyalgia patients found the protocol safe and effective[5] and the US Food & Drug Administration (FDA) granted it fast-track designation for development as a fibromyalgia treatment.[6]

In 2016, an international group of 31 researchers and clinicians published an editorial in the Journal of Alzheimer’s Disease hypothesizing that Alzheimer's may be caused by viral or bacterial infection, noting "many studies, mainly on humans, implicating specific microbes in the elderly brain, notably herpes simplex virus type 1, chlamydia pneumoniae and several types of spirochatete."[7] They proposed trials of antimicrobial therapy.[7]

Several herpesviruses including HSV-2 may cause false positives on Lyme disease tests.[8]

Hypothesized role in ME/CFS[edit | edit source]

In a 1993 paper in Medical Hypotheses (journal), P. A. Bond hypothesized that HSV-1 could cause the symptoms of chronic fatigue syndrome (CFS) in a two-stage process Bond analogized to the relationship of HIV to AIDS: as (untreated) HIV weakens the immune system and makes the body vulnerable to opportunistic infections and cancers, which then are recognized as the symptoms of AIDS, Bond suggests a variety of conditions could produce immune dysfunction and consequent vulnerability to HSV-1 (either primary infection or reactivation), which in turn could be the cause of a range of CFS symptoms.[9]

In 2018, Hector Bonilla, MD and Clinical Assistant Professor of Medicine in Infectious Diseases at Stanford University, received a Ramsay Award Grant from the Solve ME/CFS Initiative for a "Cross-sectional study to assess the prevalence of APOE e4 alleles in patients with ME/CFS and the association with herpes virus infection”.[10] The project follows on preliminary findings that HSV-1 infection in the sera of individuals with ME/CFS is related to severity of the disease.[10]

Pridgen suggests that an approach related to IMC-1 also merits investigation as an ME/CFS treatment.[3]

Notable studies[edit | edit source]

  • 1993, A role for herpes simplex virus in the aetiology of chronic fatigue syndrome and related disorders.[9] (Full text)
  • 1994, Simultaneous measurement of antibodies to Epstein-Barr virus, human herpesvirus 6, herpes simplex virus types 1 and 2, and 14 enteroviruses in chronic fatigue syndrome: is there evidence of activation of a nonspecific polyclonal immune response?[11]
  • 1996, Viral serologies in patients with chronic fatigue and chronic fatigue syndrome.[12]
  • 2002, Markers of viral infection in monozygotic twins discordant for chronic fatigue syndrome.[13]
  • 2006, Human herpesvirus 1 protein US3 induces an inhibition of mitochondrial electron transport[2]
  • 2013, Susceptibility genes are enriched in those of the herpes simplex virus 1/host interactome in psychiatric and neurological disorders.[14]

See also[edit | edit source]

References[edit | edit source]

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 "Herpes simplex virus". www.who.int. Retrieved April 22, 2019.
  2. 2.0 2.1 Derakhshan, Mohammad; Willcocks, Margaret M.; Salako, Michael A.; Kass, George E. N.; Carter, Michael J. (2006). "Human herpesvirus 1 protein US3 induces an inhibition of mitochondrial electron transport". Journal of General Virology. 87 (8): 2155–2159. doi:10.1099/vir.0.81949-0.
  3. 3.0 3.1 "Innovative Med Concepts - Pipeline". innovativemedconcepts.com. Retrieved April 22, 2019.
  4. Pridgen, William L. "Patent: Antiviral compound and cox-2 inhibitor combination therapy for functional somatic syndromes, including combination of famciclovir and celecoxib". Cite has empty unknown parameter: |dead-url= (help)
  5. Pridgen, William L; Duffy, Carol; Gendreau, Judy F; Gendreau, R Michael (February 22, 2017). "A famciclovir + celecoxib combination treatment is safe and efficacious in the treatment of fibromyalgia". Journal of Pain Research. 10: 451–460. doi:10.2147/JPR.S127288. ISSN 1178-7090. PMC 5328426. PMID 28260944.
  6. Moore, Charles (February 2, 2016). "Novel Fibromyalgia Treatment Granted FDA Fast Track Designation". Fibromyalgia News Today. Retrieved April 22, 2019. Cite has empty unknown parameter: |dead-url= (help)
  7. 7.0 7.1 Knapton, Sarah (March 9, 2016). "Alzheimer's disease could be caused by herpes virus, warn experts". The Telegraph. ISSN 0307-1235. Retrieved April 22, 2019. Cite has empty unknown parameter: |dead-url= (help)
  8. Berardi, Victor P.; Seder, Richard H.; Romanzi, Lauri; Strasfeld, Lynne (December 15, 2005). "False-Positive Serological Test Results for Lyme Disease in a Patient with Acute Herpes Simplex Virus Type 2 Infection". Clinical Infectious Diseases. 41 (12): 1826–1827. doi:10.1086/498319. ISSN 1058-4838.
  9. 9.0 9.1 Bond, P. A. (May 1993). "A role for herpes simplex virus in the aetiology of chronic fatigue syndrome and related disorders". Medical Hypotheses. 40 (5): 301–308. ISSN 0306-9877. PMID 8394501.
  10. 10.0 10.1 "Hector Bonilla". Solve ME/CFS Initiative. Retrieved March 29, 2019.
  11. Manian, F. A. (September 1994). "Simultaneous measurement of antibodies to Epstein-Barr virus, human herpesvirus 6, herpes simplex virus types 1 and 2, and 14 enteroviruses in chronic fatigue syndrome: is there evidence of activation of a nonspecific polyclonal immune response?". Clinical Infectious Diseases: An Official Publication of the Infectious Diseases Society of America. 19 (3): 448–453. ISSN 1058-4838. PMID 7811864.
  12. Buchwald, D.; Ashley, R. L.; Pearlman, T.; Kith, P.; Komaroff, A. L. (September 1996). "Viral serologies in patients with chronic fatigue and chronic fatigue syndrome". Journal of Medical Virology. 50 (1): 25–30. doi:10.1002/(SICI)1096-9071(199609)50:13.0.CO;2-V. ISSN 0146-6615. PMID 8890037.
  13. Koelle, David M.; Barcy, Serge; Huang, Meei-Li; Ashley, Rhoda L.; Corey, Lawrence; Zeh, Judy; Ashton, Suzanne; Buchwald, Dedra (September 1, 2002). "Markers of viral infection in monozygotic twins discordant for chronic fatigue syndrome". Clinical Infectious Diseases: An Official Publication of the Infectious Diseases Society of America. 35 (5): 518–525. doi:10.1086/341774. ISSN 1537-6591. PMID 12173124.
  14. Carter, Chris J. (December 2013). "Susceptibility genes are enriched in those of the herpes simplex virus 1/host interactome in psychiatric and neurological disorders". Pathogens and Disease. 69 (3): 240–261. doi:10.1111/2049-632X.12077. ISSN 2049-632X. PMID 23913659.