Coxsackie B virus

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Coxsackie B virus
Coxsackie B4 virus.JPG
Coxsackie B4 virus
Virus classification
Group: Group IV ((+)ssRNA)
Order: unassigned
Family: Picornaviridae
Genus: Enterovirus
Species: Enterovirus B
Subtype

Coxsackie B virus

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

The genome of Coxsackie B virus consists of approximately 7400 base pairs.[2]

Geographic distribution[edit]

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.

Symptoms[edit]

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. Can also lead to spasms in arms and legs. This presentation is known as pleurodynia or Bornholm disease in many areas. Sufferers of 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.[3] 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[edit]

Enterovirus infection is diagnosed mainly via serological tests such as ELISA[4] 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.

Diabetes[edit]

The B4 strain of Coxsackie viruses was suggested to be a possible cause of Diabetes mellitus type 1.[5] More recent research implicates strains B1, A4, A2 and A16 in the destruction of beta cells,[6][7] with some suggestion that strains B3 and B6 may have protective effects via immunological cross-protection.

Treatment and prevention[edit]

As of 2008, there is no well-accepted treatment for the Coxsackie B group of viruses.[1] Palliative care is available, however, and patients suffering 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, antiinflammatories can be given to reduce damage to the heart muscle.

Persistent Coxsackie B virus (non-cytolytic infection)[edit]

Enteroviruses are usually only capable of acute infections that are rapidly cleared by the adaptive immune response.[8][9] 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). This form is a mutated quasispecies[8] of enterovirus which is capable of causing persistent infection in human tissues, and such infections have been found in chronic myocarditis or dilated cardiomyopathy.[10][8] 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[9] although others think it may have pathological effects.[11]

References[edit]

  1. ^ a b c d e 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 0-88167-026-X. 
  2. ^ 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 3996064Freely accessible. PMID 24555514. 
  3. ^ 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. 
  4. ^ 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. 
  5. ^ http://www.diabetesincontrol.com/articles/diabetes-news/15408-type-of-enterovirus-linked-to-type-1-diabetes
  6. ^ 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. American Diabetes Association. 63 (2): 446–455. doi:10.2337/db13-0619. 
  7. ^ 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. Springer. 60 (3): 424–431. doi:10.1007/s00125-016-4177-z. PMID 28070615. 
  8. ^ a b c 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 1112132Freely accessible. PMID 15890942. 
  9. ^ a b 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 5653433Freely accessible. PMID 28950225. 
  10. ^ "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. 
  11. ^ 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.