Varicella zoster virus

From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history

Varicella zoster virus (VZV) is one of eight herpesviruses (HHV 3) and is known to only infect humans. It causes varicella (chickenpox) upon initial infection, and can reactivate to cause herpes zoster (shingles). After initial infection, VZV establishes a latent infection in the body.

Initial infection[edit | edit source]

Varicella, more commonly referred to as chickenpox, usually lasts 5-7 days. Chickenpox, as defined by the Centers for Disease Control & Prevention (CDC), "is a very contagious disease caused by the varicella zoster virus (VZV). It causes a blister-like rash, itching, tiredness, and fever. The rash appears first on the stomach, back and face and can spread over the entire body causing between 250 and 500 itchy blisters. Chickenpox can be serious, especially in babies, adults, and people with weakened immune systems. The best way to prevent chickenpox is to get the chickenpox vaccine."[1]

Typical signs and symptoms include:

  • A rash that turns into itchy, fluid-filled blisters (turn into scabs after a week)
  • Fever
  • Tiredness
  • Loss of appetite
  • Headache

People who have been vaccinated against varicella can still get the disease, but it is usually a milder form. Complications can occur, but are not common in healthy, vaccinated people who get the disease. People who are at risk for complications include infants, adolescents, adults, pregnant women, and people with weakened immune systems. Complications include:

  • Bacterial infections of the skin and soft tissues
  • Pneumonia
  • infection/inflammation of the brain
  • Bleeding problems
  • Sepsis
  • Dehydration [2]

Age of infection[edit | edit source]

Similar to Epstein-Barr virus, the age of initial infection affects the severity of the infection. In childhood (except for in infants), varicella is usually significantly less severe than in adolescence and adulthood. As a result, adolescents and adults are at risk for complications. Reactivation (zoster/shingles) also continues this pattern; older adults are more likely to have complications, with longer lasting and more severe pain.[2]

Reactivation: Zoster/Shingles[edit | edit source]

About 1 in 3 people in the U.S. will develop zoster/shingles in their lifetime. Anybody who has had varicella/chickenpox may develop zoster (including children). People who have weakened immune systems or use immunosuppressive drugs (e.g., steroids) are at higher risk to develop zoster. Most people only have one episode of zoster, but multiple reactivations may occur. Zoster causes a painful rash on one side of the face or body. The rash consists of blisters that are accompanied by pain, itching, or tingling. Other symptoms can include fever, headache, chills, and an upset stomach.[2]

Transmission of VZV[edit | edit source]

VZV is a highly contagious virus that spreads through touching or breathing in the virus particles that come from the chickenpox blisters. VZV can also be spread from people with zoster/shingles via the same methods of transmission, resulting in varicella/chickenpox. For most people, getting varicella/chickenpox once provides immunity for life, meaning they will not get chickenpox twice.

The best method of prevention is the chickenpox vaccine.[2]

Latency and reactivation[edit | edit source]

After initial infection, VZV establishes a latent infection in the trigeminal nerve and dorsal root ganglia, most predominantly in 87% of the nuclei of neurons of the trigeminal ganglia, as VZV is neurotropic (preferentially targets neural tissue). VZV infects less than 0.1% of non-neuronal cells. It is present in the ganglia of more than 90% of adults.[3]

Virus gene transcription during latency is epigenetically regulated by at least 6 genes. The expression of gene 63 is the indicator of VZV latency.[4] Thus, reactivation can occur either spontaneously or following a triggering factor.[3]

The latency burden of VZV seems to correlate with the severity of the primary illness.[5]

Complications[edit | edit source]

Neurological complications may follow reactivation (zoster/shingles), especially in immunocompromised individuals. These complications include:

  • Encephalitis
  • Segmental motor weakness
  • Myelitis
  • Asteritis
  • postherpetic neuralgia
  • Vasculopathy
  • Viral infection of cerebral arteries
  • Vision loss
  • Hearing problems [6]

Treatment[edit | edit source]

Antiviral treatment can be curative, even after weeks to months of chronic VZV infection.[7]

VZV as a cause of ME/CFS[edit | edit source]

One medical hypothesis states that for some patients, CFS is a result of infection by a neurotropic virus, particularly VZV. Shapiro argues that virtually all CFS symptoms could be produced by infection of the peripheral ganglia. He further argues that the chronic course of CFS could be explained by how infections of the peripheral ganglia can cause long-term nerve dysfunction.[8]

Dr John Chia says around 1.5% of cases of ME/CFS are due to reactivated varicella zoster virus, and this varicella form of ME/CFS can be very easily treated with antiviral drugs like acyclovir, which can completely cure the ME/CFS in around 3 weeks.[9]

Studies[edit | edit source]

A population cohort study followed a group of VZV-infected and non-infected individuals, and found that the incidence of CFS was higher among the VZV-infected cohort. The authors report that the VZV-infected patients that used antiviral treatment had a 15% reduced risk of CFS compared to patients without antiviral treatment. Overall they concluded that VZV infection may be associated with the risk of CFS, even without a comorbidity.[10]

Lyme Disease[edit | edit source]

Several herpesviruses including varicella-zoster virus[11][12] may cause false positives on Lyme Disease tests.

Prevalence[edit | edit source]

  • 2001, In a Belgian study, 26.8% of patients meeting the Fukuda criteria and 30.7% of patients meeting the Holmes criteria, in a cohort of 2073 CFS patients, reported cold sores and /or shingles.[13]

Learn more[edit | edit source]

See also[edit | edit source]

References[edit | edit source]

  1. "Chickenpox | About | Varicella | CDC". Centers for Disease Control and Prevention. January 15, 2019. Retrieved March 22, 2019.
  2. 2.0 2.1 2.2 2.3 "Chickenpox | Signs and Symptoms | Varicella | CDC". Centers for Disease Control and Prevention. Retrieved December 14, 2018.
  3. 3.0 3.1 Kennedy, Peter G. E.; Gilden, Donald H.; Cohrs, Randall J.; Bloom, David C.; Mitchell, Bradley M. (March 1, 2003). "Herpes simplex virus-1 and varicella-zoster virus latency in ganglia". Journal of NeuroVirology. 9 (2): 194–204. doi:10.1080/13550280390194000. ISSN 1538-2443.
  4. Cohrs, Randall J.; Kennedy, Peter GE (November 1, 2010). "Varicella-zoster virus human ganglionic latency: a current summary". Journal of NeuroVirology. 16 (6): 411–418. doi:10.1007/BF03210846. ISSN 1538-2443.
  5. Levin, Myron J.; Smith, Jeffrey G.; Kaufhold, Robin M.; Barber, Debra; Hayward, Anthony R.; Chan, Christina Y.; Chan, Ivan S.F.; Li, David J.J.; Wang, William (November 1, 2003). "Decline in varicella-zoster virus (VZV)-specific cell-mediated immunity with increasing age and boosting with a high-dose VZV vaccine". The Journal of Infectious Diseases. 188 (9): 1336–1344. doi:10.1086/379048. ISSN 0022-1899. PMID 14593591.
  6. Kennedy, Peter G. E.; Gilden, Donald H.; Cohrs, Randall J.; Bloom, David C.; Mitchell, Bradley M. (March 1, 2003). "Herpes simplex virus-1 and varicella-zoster virus latency in ganglia". Journal of NeuroVirology. 9 (2): 194–204. doi:10.1080/13550280390194000. ISSN 1538-2443.
  7. Kennedy, Peter G. E.; Gilden, Donald H.; Cohrs, Randall J.; Bloom, David C.; Mitchell, Bradley M. (March 1, 2003). "Herpes simplex virus-1 and varicella-zoster virus latency in ganglia". Journal of NeuroVirology. 9 (2): 194–204. doi:10.1080/13550280390194000. ISSN 1538-2443.
  8. "Does varicella-zoster virus infection of the peripheral ganglia cause Chronic Fatigue Syndrome?". Medical Hypotheses. 73 (5): 728–734. November 1, 2009. doi:10.1016/j.mehy.2009.04.043. ISSN 0306-9877.
  9. Chia, John. "ME/CFS Alert With Llewellyn King: Episode 38 - Interview with Dr. John Chia, Part 1. Dec 2012. Timecode: 6:58".
  10. Kao, C.-H.; Kuo, C.-N.; Shen, W.-C.; Lin, W.-M.; Chen, C.-S.; Chen, H.-J.; Yang, T.-Y.; Tsai, S.-Y. (September 1, 2014). "Increased risk of chronic fatigue syndrome following herpes zoster: a population-based study". European Journal of Clinical Microbiology & Infectious Diseases. 33 (9): 1653–1659. doi:10.1007/s10096-014-2095-x. ISSN 1435-4373.
  11. Feder HM Jr, Gerber MA, Luger SW, Ryan RW. False-positive serologic tests for Lyme disease after varicella infection. N Engl J Med 1991;325:1886-7
  12. Woelfle J, Wilske B, Haverkamp F, Bialek R. False-positive serological tests for Lyme disease in facial palsy and varicella zoster meningo-encephalitis. Eur J Pediatr 1998;157:953-4.
  13. De Becker, Pascale; McGregor, Neil; De Meirleir, Kenny (December 2001). "A definition‐based analysis of symptoms in a large cohort of patients with chronic fatigue syndrome". Journal of Internal Medicine. 250 (3): 234–240. doi:10.1046/j.1365-2796.2001.00890.x.