Coxsackie B virus

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Coxsackie B virus
Coxsackie B4 virus.JPG
Coxsackie B4 virus
Virus classification OOjs UI icon edit-ltr.svg
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum: Pisuviricota
Class: Pisoniviricetes
Order: Picornavirales
Family: Picornaviridae
Genus: Enterovirus
Species:
Enterovirus B
Strain:
Coxsackie B virus

Coxsackie B is a group of six serotypes of coxsackievirus (CVB1-CVB6), a pathogenic enterovirus, that trigger illness ranging from gastrointestinal distress to full-fledged pericarditis and myocarditis (coxsackievirus-induced cardiomyopathy). [1] [2]

Contents

The genome of Coxsackie B virus consists of approximately 7,400 base pairs. [3]

Geographic distribution

The various members of the Coxsackie B group were discovered almost entirely in the United States, appearing originally in Connecticut, Ohio, New York, and Kentucky, although a sixth member of the group has been found in the Philippines. [1] However, all six serotypes have a global distribution and are a relatively common cause of gastrointestinal upset. The name reflects the first isolation from Coxsackie, New York.[ citation needed ]

Transmission

Infections are most commonly spread by the Fecal-oral route, emphasizing the importance of good hygiene, especially hand-washing. [2] Oral-oral and respiratory droplets can also be means of transmission. [4]

Epidemiology

Coxsackie B infections have been reported to account for nearly a quarter of all enterovirus infections. [5] Nearly half of all reported cases of Coxsackie B infections occur before the age of five. [5] For the CBV1 serotype, two-thirds of Centers for Disease Control and Prevention reported infections in the United States were for children under one year of age. [4]

Symptoms

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. This presentation is known as pleurodynia or Bornholm disease in many areas. Patients with chest pain should see a doctor immediately—in some cases, 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. [6] The incubation period for the Coxsackie B viruses ranges from 2 to 6 days, and illness may last for up to 6 months in extreme cases, but may resolve as quickly as two days. Infection usually occurs between the months of May and June, but do not show symptoms until October in temperate Northern Hemisphere regions. People should ideally spend 1 month resting during the height of infection. Another cause of this virus is from a dirty wound from an accident. [1]

Diagnosis

Enterovirus infection is diagnosed mainly via serological tests such as ELISA [7] and from cell culture. [1] Because the same level and type of care is given regardless of type of Coxsackie B infection, it is mostly unnecessary for treatment purposes to diagnose which virus is causing the symptoms in question, though it may be epidemiologically useful.[ citation needed ]

Pathology

Coxsackie B infections usually do not cause serious disease, although for newborns in the first 1–2 weeks of life, Coxsackie B infections can easily be fatal. [2] The pancreas is a frequent target, which can cause pancreatitis. [2]

Coxsackie B3 (CB3) infections are the most common enterovirus cause of myocarditis and sudden cardiac death. [8] CB3 infection causes ion channel pathology in the heart, leading to ventricular arrhythmia. [8] Studies in mice suggest that CB3 enters cells by means of toll-like receptor 4. [9] Both CB3 and CB4 exploit cellular autophagy to promote replication. [9]

Diabetes

The B4 Coxsackie viruses (CB4) serotype was suggested to be a possible cause of diabetes mellitus type 1 (T1D). [10] An autoimmune response to Coxsackie virus B infection upon the islets of Langerhans may be a cause of T1D. [2]

Other research implicates strains B1, A4, A2 and A16 in the destruction of beta cells, [11] [12] with some suggestion that strains B3 and B6 may have protective effects via immunological cross-protection.

Treatment and Prevention

As of 2008, there is no well-accepted treatment for the Coxsackie B group of viruses. [1] Palliative care is available, however, and patients with chest pain or stiffness of the neck should be examined for signs of cardiac or central nervous system involvement, respectively. Some measure of prevention can usually be achieved by basic sanitation on the part of food-service workers, though the viruses are highly contagious. Care should be taken in washing ones hands and in cleaning the body after swimming. In the event of Coxsackie-induced myocarditis or pericarditis, anti-inflammatories can be given to reduce damage to the heart muscle.[ citation needed ]

Persistent Coxsackie B virus (non-cytolytic infection)

Enteroviruses are usually only capable of acute infections that are rapidly cleared by the adaptive immune response. [13] [14] However, mutations which enterovirus B serotypes such as coxsackievirus B and echovirus acquire in the host during the acute phase can transform these viruses into the non-cytolytic form (also known as non-cytopathic or defective enterovirus). [15] This form is a mutated quasispecies [13] of enterovirus which is capable of causing persistent infection in human tissues, and such infections have been found in the pancreas in type 1 diabetes, [16] [17] in chronic myocarditis and dilated cardiomyopathy, [18] [13] [19] in valvular heart disease, [20] in myalgic encephalomyelitis, [21] [22] and in Sjögren's syndrome. [23] In these persistent infections, viral RNA is present at very low levels, and some researchers believe it is just a fading remnant of the acute infection [14] although others scientists believe this persistent viral RNA may have pathological effects and cause disease. [24]

Related Research Articles

<span class="mw-page-title-main">Coxsackie A virus</span> Virus that causes digestive upset and sometimes heart damage

Coxsackie A virus (CAV) is a cytolytic Coxsackievirus of the Picornaviridae family, an enterovirus.

<span class="mw-page-title-main">Bornholm disease</span> Medical condition

Bornholm disease, also known as epidemic pleurodynia, is a condition characterized by myositis of the abdomen or chest caused by the Coxsackie B virus or other viruses. The myositis manifests as an intermittent stabbing pain in the musculature that is seen primarily in children and young adults.

Coxsackie B4 virus are enteroviruses that belong to the Picornaviridae family. These viruses can be found worldwide. They are positive-sense, single-stranded, non-enveloped RNA viruses with icosahedral geometry. Coxsackieviruses have two groups, A and B, each associated with different diseases. Coxsackievirus group A is known for causing hand-foot-and-mouth diseases while Group B, which contains six serotypes, can cause a varying range of symptoms like gastrointestinal distress myocarditis. Coxsackievirus B4 has a cell tropism for natural killer cells and pancreatic islet cells. Infection can lead to beta cell apoptosis which increases the risk of insulitis.

<span class="mw-page-title-main">Coxsackievirus</span> Virus that causes digestive upset and sometimes heart damage

Coxsackieviruses are a few related enteroviruses that belong to the Picornaviridae family of nonenveloped, linear, positive-sense single-stranded RNA viruses, as well as its genus Enterovirus, which also includes poliovirus and echovirus. Enteroviruses are among the most common and important human pathogens, and ordinarily its members are transmitted by the fecal–oral route. Coxsackieviruses share many characteristics with poliovirus. With control of poliovirus infections in much of the world, more attention has been focused on understanding the nonpolio enteroviruses such as coxsackievirus.

<span class="mw-page-title-main">Poliovirus</span> Enterovirus

Poliovirus, the causative agent of polio, is a serotype of the species Enterovirus C, in the family of Picornaviridae. There are three poliovirus serotypes: types 1, 2, and 3.

<span class="mw-page-title-main">Myocarditis</span> Inflammation of the heart muscle

Myocarditis, also known as inflammatory cardiomyopathy, is an acquired cardiomyopathy due to inflammation of the heart muscle. Symptoms can include shortness of breath, chest pain, decreased ability to exercise, and an irregular heartbeat. The duration of problems can vary from hours to months. Complications may include heart failure due to dilated cardiomyopathy or cardiac arrest.

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Enterovirus is a genus of positive-sense single-stranded RNA viruses associated with several human and mammalian diseases. Enteroviruses are named by their transmission-route through the intestine.

<span class="mw-page-title-main">Decay-accelerating factor</span> Mammalian protein found in Homo sapiens

Complement decay-accelerating factor, also known as CD55 or DAF, is a protein that, in humans, is encoded by the CD55 gene.

Keshan disease is a congestive cardiomyopathy caused by a combination of dietary deficiency of selenium and the presence of a mutated strain of Coxsackievirus, named after Keshan County of Heilongjiang province, Northeast China, where symptoms were first noted. These symptoms were later found prevalent in a wide belt extending from northeast to southwest China, all due to selenium-deficient soil. The disease peaked in 1960–1970, killing thousands of people.

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<span class="mw-page-title-main">Coxsackievirus and adenovirus receptor</span> Protein found in humans

Coxsackievirus and adenovirus receptor (CAR) is a protein that in humans is encoded by the CXADR gene. The protein encoded by this gene is a type I membrane receptor for group B coxsackie viruses and subgroup C adenoviruses. CAR protein is expressed in several tissues, including heart, brain, and, more generally, epithelial and endothelial cells. In cardiac muscle, CAR is localized to intercalated disc structures, which electrically and mechanically couple adjacent cardiomyocytes. CAR plays an important role in the pathogenesis of myocarditis, dilated cardiomyopathy, and in arrhythmia susceptibility following myocardial infarction or myocardial ischemia. In addition, an isoform of CAR (CAR-SIV) has been recently identified in the cytoplasm of pancreatic beta cells. It's been suggested that CAR-SIV resides in the insulin secreting granules and might be involved in the virus infection of these cells.

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Coxsackieviruses-induced cardiomyopathy are positive-stranded RNA viruses in picornavirus family and the genus enterovirus, acute enterovirus infections such as Coxsackievirus B3 have been identified as the cause of virally induced acute myocarditis, resulting in dilated cardiomyopathy. Dilated cardiomyopathy in humans can be caused by multiple factors including hereditary defects in the cytoskeletal protein dystrophin in Duchenne muscular dystrophy (DMD) patients). A heart that undergoes dilated cardiomyopathy shows unique enlargement of ventricles, and thinning of the ventricular wall that may lead to heart failure. In addition to the genetic defects in dystrophin or other cytoskeletal proteins, a subset of dilated cardiomyopathy is linked to enteroviral infection in the heart, especially coxsackievirus B. Enterovirus infections are responsible for about 30% of the cases of acquired dilated cardiomyopathy in humans.

Viral cardiomyopathy occurs when viral infections cause myocarditis with a resulting thickening of the myocardium and dilation of the ventricles. These viruses include Coxsackie B and adenovirus, echoviruses, influenza H1N1, Epstein–Barr virus, rubella, varicella, mumps, measles, parvoviruses, yellow fever, dengue fever, polio, rabies and the viruses that cause hepatitis A and C, as well as COVID-19, which has been seen to cause this in persons otherwise thought to have a "low risk" of the virus's effects.

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References

  1. 1 2 3 4 5 Fields, Bernard N.; David M. Knipe; Robert M. Chanock; Joseph L. Melnick; Bernard Roizman; Robert E. Shope (1985). Fields Virology. New York: Raven Press. pp. 739–794. ISBN   978-0-88167-026-4.
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  3. ↑ Liu B, Li Z, Xiang F, Li F, Zheng Y, Wang G (2014). "The whole genome sequence of coxsackievirus B3 MKP strain leading to myocarditis and its molecular phylogenetic analysis". Virol. J. 11: 33. doi: 10.1186/1743-422X-11-33 . PMC   3996064 . PMID   24555514.
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  6. ↑ Maze, S. S.; Adolph, R. J. (February 1990). "Myocarditis: unresolved issues in diagnosis and treatment". Clinical Cardiology. 13 (2): 69–79. doi: 10.1002/clc.4960130203 . PMID   2407397.
  7. ↑ Bell, Eleanor J.; R.A. McCartney; Diane Basquill; A.K.R. Chaudhuri (1986). "Mu-Antibody capture elisa for the rapid diagnosis of enterovirus infections in patients with aseptic meningitis". Journal of Medical Virology. 19 (3): 213–7. doi:10.1002/jmv.1890190303. PMID   3016164. S2CID   32392085.
  8. 1 2 Peischard S, Ho HT, Seebohm G (2019). "A Kidnapping Story: How Coxsackievirus B3 and Its Host Cell Interact". Cellular Physiology and Biochemistry . 53 (1): 121–140. doi: 10.33594/000000125 . PMID   31230428.
  9. 1 2 Kemball CC, Alirezaei M, Whitton JL (2010). "Type B coxsackieviruses and their interactions with the innate and adaptive immune systems". Future Microbiology . 5 (9): 1329–1347. doi:10.2217/fmb.10.101. PMC   3045535 . PMID   20860480.
  10. ↑ "Type of Enterovirus Linked to Type 1 Diabetes". November 2013. Archived from the original on 2013-12-03. Retrieved 2013-11-04.
  11. ↑ Laitinen, Olli H.; Honkanen, Hanna; Pakkanen, Outi; et al. (2014). "Coxsackievirus B1 Is Associated With Induction of β-Cell Autoimmunity That Portends Type 1 Diabetes". Diabetes. 63 (2): 446–455. doi: 10.2337/db13-0619 . PMID   23974921.
  12. ↑ Honkanen, Hanna; Oikarinen, Sami; Nurminen, Noora; et al. (2017). "Detection of enteroviruses in stools precedes islet autoimmunity by several months: possible evidence for slowly operating mechanisms in virus-induced autoimmunity". Diabetologia. 60 (3): 424–431. doi: 10.1007/s00125-016-4177-z . PMID   28070615.
  13. 1 2 3 Kim KS, Tracy S, Tapprich W, Bailey J, Lee CK, Kim K, Barry WH, Chapman NM (June 2005). "5'-Terminal deletions occur in coxsackievirus B3 during replication in murine hearts and cardiac myocyte cultures and correlate with encapsidation of negative-strand viral RNA". Journal of Virology. 79 (11): 7024–41. doi:10.1128/JVI.79.11.7024-7041.2005. PMC   1112132 . PMID   15890942.
  14. 1 2 Flynn CT, Kimura T, Frimpong-Boateng K, Harkins S, Whitton JL (December 2017). "Immunological and pathological consequences of coxsackievirus RNA persistence in the heart". Virology. 512: 104–112. doi:10.1016/j.virol.2017.09.017. PMC   5653433 . PMID   28950225.
  15. ↑ Chapman, Nora M. (2022-05-12). "Persistent Enterovirus Infection: Little Deletions, Long Infections". Vaccines. 10 (5): 770. doi: 10.3390/vaccines10050770 . ISSN   2076-393X. PMC   9143164 . PMID   35632526.
  16. ↑ Krogvold, Lars; Edwin, Bjørn; Buanes, Trond; Frisk, Gun; Skog, Oskar; Anagandula, Mahesh; Korsgren, Olle; Undlien, Dag; Eike, Morten C.; Richardson, Sarah J.; Leete, Pia; Morgan, Noel G.; Oikarinen, Sami; Oikarinen, Maarit; Laiho, Jutta E. (May 2015). "Detection of a low-grade enteroviral infection in the islets of langerhans of living patients newly diagnosed with type 1 diabetes". Diabetes. 64 (5): 1682–1687. doi: 10.2337/db14-1370 . hdl: 10871/17927 . ISSN   1939-327X. PMID   25422108. S2CID   40883074.
  17. ↑ Chehadeh, W.; Kerr-Conte, J.; Pattou, F.; Alm, G.; Lefebvre, J.; Wattré, P.; Hober, D. (November 2000). "Persistent infection of human pancreatic islets by coxsackievirus B is associated with alpha interferon synthesis in beta cells". Journal of Virology. 74 (21): 10153–10164. doi:10.1128/jvi.74.21.10153-10164.2000. ISSN   0022-538X. PMC   102054 . PMID   11024144.
  18. ↑ Chapman, N. M.; Kim, K. S. (2008). "Persistent coxsackievirus infection: enterovirus persistence in chronic myocarditis and dilated cardiomyopathy". Current Topics in Microbiology and Immunology. 323: 275–292. doi:10.1007/978-3-540-75546-3_13. ISBN   978-3-540-75545-6. ISSN   0070-217X. PMID   18357775.
  19. ↑ "Persistent Coxsackievirus Infection: Enterovirus Persistence in Chronic Myocarditis and Dilated Cardiomyopathy". Group B coxsackieviruses . Tracy, S. (Steven), Oberste, M. Steven., Drescher, Kristen M. Berlin: Springer. 2008. pp.  275–286. ISBN   9783540755463. OCLC   233973571.{{cite book}}: CS1 maint: others (link)
  20. ↑ "Enterovirus replication in valvular tissue from patients with chronic rheumatic heart disease". academic.oup.com. Retrieved 2023-10-11.
  21. ↑ O'Neal, Adam J.; Hanson, Maureen R. (2021-06-18). "The Enterovirus Theory of Disease Etiology in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Critical Review". Frontiers in Medicine. 8: 688486. doi: 10.3389/fmed.2021.688486 . ISSN   2296-858X. PMC   8253308 . PMID   34222292.
  22. ↑ Hanson, Maureen R. (2023-08-17). "The viral origin of myalgic encephalomyelitis/chronic fatigue syndrome". PLOS Pathogens. 19 (8): e1011523. doi: 10.1371/journal.ppat.1011523 . ISSN   1553-7366. PMC   10434940 . PMID   37590180.
  23. ↑ Triantafyllopoulou, Antigoni; Tapinos, Nikos; Moutsopoulos, Haralampos M. (September 2004). "Evidence for coxsackievirus infection in primary Sjögren's syndrome". Arthritis and Rheumatism. 50 (9): 2897–2902. doi:10.1002/art.20463. ISSN   0004-3591. PMID   15457458.
  24. ↑ Zhang, Hongyi; Li, Yanwen; McClean, Dougal R; Richardson, Peter J; Latif, Najma; Dunn, Michael J; Archard, Leonard C; Florio, Richard; Sheppard, Mary; Morrison, Karen (2004). "Detection of enterovirus capsid protein VP1 in myocardium from cases of myocarditis or dilated cardiomyopathy by immunohistochemistry: Further evidence of enterovirus persistence in myocytes". Medical Microbiology and Immunology. 193 (2–3): 109–114. doi: 10.1007/s00430-003-0208-8 . PMID   14634804. S2CID   20457715.
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