Coxsackie B

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Coxsackie B (also written coxsackievirus B) is a group of six types of enterovirus, causing symptoms ranging from gastrointestinal distress to pericarditis and myocarditis.

Symptoms[edit | edit source]

Symptoms of infection with viruses in the Coxsackie B grouping include fever, headache, sore throat, gastrointestinal distress, extreme fatigue as well as chest and muscle pain. It can also lead to spasms in arms and legs.

Viruses in the Coxsackie B family progress to myocarditis or pericarditis, which can result in permanent heart damage or death. Coxsackie B virus infection may also induce aseptic meningitis. As a group, they are the most common cause of unexpected sudden death, and may account for up to 50% of such cases.[1] Models of persistent infection of the heart (https://link.springer.com/chapter/10.1007%2F978-3-540-75546-3_13) and brain (http://jvi.asm.org/content/83/18/9356.short) have been studied in mice.

Immune system[edit | edit source]

In a mouse model of myocarditis, Coxsackievirus infection was found to upregulate Toll-like receptor 4 on mast cells and macrophages immediately following infection. It also increased numbers of mast cells.[2]

In human disease[edit | edit source]

Myalgic Encephalomyelitis[edit | edit source]

Several studies have patients with ME to have persistently elevated levels of Coxsackie B IgM or IgG antibodies, circulating immune complexes containing viral antigen, or presence of enterovirus by PCR or culture, all indicating the possible presence of a persistent infection.[3][4] Others studies failed to find a difference in rates of positivity between patients and controls. Differences in study outcomes may be due to the criteria used to define study cohorts as well as the techniques used.

Blood testing[edit | edit source]

Elevated Coxsackie B antibodies have been found in patients in at least two ME outbreaks.[5][6] In a retrospective cohort study[7] by Melvin Ramsay and Elizabeth Dowsett, 31% of the patients were found to have elevated enteroviral IgM antibody levels. Sixteen of these patients were retested annually over three years and all showed persistently elevated Coxsackie B neutralizing antibody levels and intermittently positive enteroviral IgM, suggesting a persistent infection was present.

Similarly, a study of of 76 patients with postviral fatigue syndrome (PVFS) found that 76% had detectible IgM responses to enteroviruses. 22% had positive cultures (compared to 7% controls) and VP1 antigen was detected in 51%, all pointing to a chronic infection in many post-viral patients.[8] However, a larger study in Scotland of 243 PVFS patients and matched controls found no difference in IgM and IgG positivity between patients and controls.[9]

PCR[edit | edit source]

In a study of serum samples from 100 CFS patients and 100 healthy controls, 42% of patients were positive for Coxsackie B sequences by PCR, compared to only 9% of the comparison group.[10]

Also using PCR, a study of 236 patients by John Chia found enteroviral RNA in 48% of patients as compared to 8% of controls.To date, Chia reports finding enteroviral RNA in 35% of 518 patients.[4]

Muscle testing[edit | edit source]

Several muscle biopsy studies have also found the presence of Coxsackie B RNA sequences in CFS patients as compared to controls. A study of 60 PVFS patients found 53% had enteroviral RNA in muscle compared to 15% of controls.[11] However, a follow-up study comparing CFS patients to patients with other neuromuscular disorders failed to find a statistically significant difference.[12]

Type 1 diabetes[edit | edit source]

A study of patients with Type 1 Diabetes found that Coxsackie B4 was found to infect β cells and cause inflammation mediated by natural killer cells.[13]

Testing[edit | edit source]

In the United States, ARUP Laboratories offers a serum microneutralization assay that is designed to measure the concentration of serum antibodies to six serotypes of the virus; B1 through B6. This specific assay has been shown to be sensitive for detection of chronic infections in ME patients. A persistent fourfold or greater rise in antibody titer is often found in these patients, which is not often found in healthy controls.

A complement fixation assay for Coxsackie B serotypes is available in the United States from LabCorp and Quest Diagnostics, however this specific type of assay has not been found to be sensitive for the chronic infections found in ME patients.

Treatment[edit | edit source]

There are no approved vaccines or antivirals for Coxsackie viruses. However, preliminary research (often in animal models or in vitro) have been shown various compounds to have potential antiviral effects.

John Chia reported that treatment with Interferon and Ribavirin on patients with B3 or B5 appeared to show some benefit, but patients relapsed after discontinuation of treatment. One patient with B4 experienced moderate improvement on Pleconaril but also relapsed.[4]

Potential coxsackie antivirals
Serotype Pharmaceuticals Herbs Supplements Other
B1 Fluoxetine[14] ursolic acid, Bupleurum kaoi Glycine max *
B2 Fluoxetine[14] simalikalactone D * *
B3 Ampligen[15],Fluoxetine[14], Interferon[16], ribvarin, arbidol, amiloride, itraconazole, oseltamivir, valsartan, olmesartan, lovastatin, mycophenolate, arsenic trioxide shuang huang lian, garlic, curcumin, baicalein, Paris polyphylla, raoulic acid, Dodonaea viscosa, Spatholobus suberectus, Terminalia chebula, Trichosanthes root, Rhodiola rosea, emodin[17], Astragalus membranaceus[18], acemannan, Sophora flavescens, Isatis tinctoria, cinnamaldehyde, Rheum palmatum chlorogenic acid, fatty acid synthase inhibitors
B4 Fluoxetine[19], oseltamivir Yakammaoto[20], raoulic acid[21], emodin[22] Epimedium, Azadirachta indica (Neem)[23] Dihydroquercetin(Taxifolin)[24] DHEA, 5-androstenediol
B5 arbidol Spatholobus suberectus, Terminalia chebula, Epimedium, hyaluronic acid[25] sodium selenite chlorogenic acid, clinoptilolite
B6 * Azadirachta indica * *
Note: Many of the elements in this table were reproduced from a post on Phoenix Rising. See that post for full citations and/or help us fully cite this table.

See also[edit | edit source]

References[edit | edit source]

  1. "Coxsackie B virus". Wikipedia. 
  2. http://www.ncbi.nlm.nih.gov/pubmed/15386590
  3. Landay, AL (September 1991). "Chronic fatigue syndrome: clinical condition associated with immune activation". Lancet. 
  4. 4.0 4.1 4.2 Chia, John (November 2005). "The role of enterovirus in chronic fatigue syndrome". Journal of Clinical Pathology. 
  5. Fegan, KG; Behan, PO; Bell, EJ (1 Jun 1983), "Myalgic encephalomyelitis — report of an epidemic", J R Coll Gen Pract, 33 (251): 335–337, PMID 6310104 
  6. Calder, BD; Warnock, PJ (Jan 1984), "Coxsackie B infection in a Scottish general practice", Jrnl Royal Coll Gen Pract, 34 (258): 15–19, PMID 6319691 
  7. Dowsett, EG; Ramsay, AM; McCartney, RA; Bell, EJ (1 Jul 1990), "Myalgic encephalomyelitis--a persistent enteroviral infection?", Postgraduate Medical Journal, 66 (777): 526–530, doi:10.1136/pgmj.66.777.526, PMID 2170962 
  8. Yousef, G.E. (January 1988). "CHRONIC ENTEROVIRUS INFECTION IN PATIENTS WITH POSTVIRAL FATIGUE SYNDROME". The Lancet. 
  9. Miller, N A (1991). "Antibody to Coxsackie B virus in diagnosing postviral fatigue syndrome". The British Medical Journal. 
  10. Nairn, C (August 1995). "Comparison of coxsackie B neutralisation and enteroviral PCR in chronic fatigue patients". Journal of Medical Virology. 
  11. Gow, JW. "Enteroviral RNA sequences detected by polymerase chain reaction in muscle of patients with postviral fatigue syndrome". British Medical Journal. 
  12. Gow, JW (1994). "Studies on enterovirus in patients with chronic fatigue syndrome". https://www.ncbi.nlm.nih.gov/pubmed/8148439/.  External link in |journal= (help)
  13. http://www.pnas.org/content/104/12/5115.full
  14. 14.0 14.1 14.2 http://www.ncbi.nlm.nih.gov/pubmed/22751539
  15. http://www.ncbi.nlm.nih.gov/pubmed/14693549
  16. http://www.ncbi.nlm.nih.gov/pubmed/1328433
  17. Zhang, HM (February 2016). "Emodin inhibits coxsackievirus B3 replication via multiple signalling cascades leading to suppression of translation". Biochem J. 
  18. http://www.ncbi.nlm.nih.gov/pubmed/8580483
  19. http://www.ncbi.nlm.nih.gov/pubmed/25655448
  20. https://www.ncbi.nlm.nih.gov/pubmed/24361333
  21. Choi, HJ (January 2009). "Antiviral activity of raoulic acid from Raoulia australis against Picornaviruses". Phytomedicine. 
  22. Liu, Zhao (October 2013). "In Vitro and in Vivo Studies of the Inhibitory Effects of Emodin Isolated from Polygonum cuspidatum on Coxsakievirus B-4". Molecules. 
  23. Badam, L (1999). "'In vitro' antiviral activity of neem (Azadirachta indica. A. Juss) leaf extract against group B coxsackieviruses." J Commun Dis. 
  24. http://www.ncbi.nlm.nih.gov/pubmed/27145597
  25. http://www.ncbi.nlm.nih.gov/pubmed/21439070


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