From Wikipedia, the free encyclopedia

Viral structure and Genome

Coxsackie A virus is a subgroup of enterovirus A, which are small, non-enveloped, single-stranded RNA viruses. It's protective, icosahedral capsid has an external portion that contains sixty copies of viral proteins (VP1,-2,-3) and an internal portion surrounding the RNA genome containing sixty copies of VP4 viral proteins. This capsid mediates cell entry and illicit the humoral immune responses. [1] Enteroviruses have a depression encircling each fivefold axis (canyon), which is their binding site for immunoglobulin-like receptors. This binding can trigger viral expansion and release of its genome. [2]

A complete genome analysis of Coxsackie virus A2, A4, A5, and A10 strains isolated from patients with hand-foot-mouth disease showed that natural recombination is frequent in the virus's evolution. It's strains in China were related to strains in Mongolia, Taiwan, likely to those that circulated in Europe, and form a distinct lineage from strains imported from Japan and South Korea. [3]

Replication cycle

Replication of the coxsackie virus happens through contributions of the host and virus components. After cell entry of the virus and its internalization into the Golgi and endoplasmic reticulum and viral un-coating, viral RNA is released. Ribosomes on the rough endoplasmic reticulum translate the RNA into viral polyprotein. [4] This polyprotein in processed into structural protein P1 and non-structural proteins P2 and P3. Via the virus-encoded proteinase, P1 is processed into the viral capsid subunit proteins VP0, -1, -3. The 5'-non-coding region contains sequences that control genome replication and translation while the 3'-non-coding region contains polyA tail needed for virus infectivity. [5]

Diseases[edit]

The most well known Coxsackie A disease is hand, foot and mouth disease (unrelated to foot-and-mouth disease), a common childhood illness which affects mostly children aged 5 or under, often produced by Coxsackie A16. In most cases, infection is asymptomatic or causes only mild symptoms. In others, infection produces short-lived (7–10 days) fever and painful blisters in the mouth (a condition known as herpangina), on the palms and fingers of the hand, or on the soles of the feet. There can also be blisters in the throat, or on or above the tonsils. Adults can also be affected. The rash, which can appear several days after high temperature and painful sore throat, can be itchy and painful, especially on the hands/fingers and bottom of feet. [6]

Other diseases include acute haemorrhagic conjunctivitis (A24 specifically), herpangina, and aseptic meningitis (both Coxsackie A and B viruses). Coxsackievirus A7 is associated with neurological diseases and can cause paralytic poliomyelitis [7]

Picture citation and description: A transmission electron microscopic image depicting virions causing acute hemorrhagic conjunctivitis, primarily caused by two enteroviruses: enterovirus 70, and a variant of coxsackievirus A24. [8]

  1. ^ Ren, Jingshan; Wang, Xiangxi; Zhu, Ling; Hu, Zhongyu; Gao, Qiang; Yang, Pan; Li, Xuemei; Wang, Junzhi; Shen, Xinliang; Fry, Elizabeth E.; Rao, Zihe (2015-08-12). "Structures of Coxsackievirus A16 Capsids with Native Antigenicity: Implications for Particle Expansion, Receptor Binding, and Immunogenicity". Journal of Virology. 89 (20): 10500–10511. doi: 10.1128/JVI.01102-15. ISSN  0022-538X. PMC  4580203. PMID  26269176.
  2. ^ Zhao, Yuguang; Zhou, Daming; Ni, Tao; Karia, Dimple; Kotecha, Abhay; Wang, Xiangxi; Rao, Zihe; Jones, E. Yvonne; Fry, Elizabeth E.; Ren, Jingshan; Stuart, David I. (2020-01-07). "Hand-foot-and-mouth disease virus receptor KREMEN1 binds the canyon of Coxsackie Virus A10". Nature Communications. 11. doi: 10.1038/s41467-019-13936-2. ISSN  2041-1723. PMC  6946704. PMID  31911601.
  3. ^ Hu, Y. F.; Yang, Fan; Du, J.; Dong, J.; Zhang, T.; Wu, Z. Q.; Xue, Y.; Jin, Qi (2011-7). "Complete Genome Analysis of Coxsackievirus A2, A4, A5, and A10 Strains Isolated from Hand, Foot, and Mouth Disease Patients in China Revealing Frequent Recombination of Human Enterovirus A▿". Journal of Clinical Microbiology. 49 (7): 2426–2434. doi: 10.1128/JCM.00007-11. ISSN  0095-1137. PMC  3147834. PMID  21543560. {{ cite journal}}: Check date values in: |date= ( help)
  4. ^ Lincez, Pamela J.; Walic, Marine; Horwitz, Marc S. (2011-10-21). "The Key Players of Coxsackievirus-Induced Myocarditis". Myocarditis. doi: 10.5772/20932.
  5. ^ Mao, Qunying; Wang, Yiping; Yao, Xin; Bian, Lianlian; Wu, Xing; Xu, Miao; Liang, Zhenglun (2014-02-01). "Coxsackievirus A16". Human Vaccines & Immunotherapeutics. 10 (2): 360–367. doi: 10.4161/hv.27087. ISSN  2164-5515. PMC  4185891. PMID  24231751.{{ cite journal}}: CS1 maint: PMC format ( link)
  6. ^ CDC (2020). "Hand, Foot & Mouth Disease Symptoms". U.S. Centers for Disease Control and Prevention. Retrieved 2020-07-30.{{ cite web}}: CS1 maint: url-status ( link)
  7. ^ Yamayoshi S, Iizuka S, Yamashita T, Minagawa H, Mizuta K, Okamoto M, et al. (May 2012). "Human SCARB2-dependent infection by coxsackievirus A7, A14, and A16 and enterovirus 71". Journal of Virology. 86 (10): 5686–96. doi: 10.1128/JVI.00020-12. PMC  3347270. PMID  22438546.
  8. ^ "Details - Public Health Image Library(PHIL)". phil.cdc.gov. Retrieved 2020-07-31.
From Wikipedia, the free encyclopedia

Viral structure and Genome

Coxsackie A virus is a subgroup of enterovirus A, which are small, non-enveloped, single-stranded RNA viruses. It's protective, icosahedral capsid has an external portion that contains sixty copies of viral proteins (VP1,-2,-3) and an internal portion surrounding the RNA genome containing sixty copies of VP4 viral proteins. This capsid mediates cell entry and illicit the humoral immune responses. [1] Enteroviruses have a depression encircling each fivefold axis (canyon), which is their binding site for immunoglobulin-like receptors. This binding can trigger viral expansion and release of its genome. [2]

A complete genome analysis of Coxsackie virus A2, A4, A5, and A10 strains isolated from patients with hand-foot-mouth disease showed that natural recombination is frequent in the virus's evolution. It's strains in China were related to strains in Mongolia, Taiwan, likely to those that circulated in Europe, and form a distinct lineage from strains imported from Japan and South Korea. [3]

Replication cycle

Replication of the coxsackie virus happens through contributions of the host and virus components. After cell entry of the virus and its internalization into the Golgi and endoplasmic reticulum and viral un-coating, viral RNA is released. Ribosomes on the rough endoplasmic reticulum translate the RNA into viral polyprotein. [4] This polyprotein in processed into structural protein P1 and non-structural proteins P2 and P3. Via the virus-encoded proteinase, P1 is processed into the viral capsid subunit proteins VP0, -1, -3. The 5'-non-coding region contains sequences that control genome replication and translation while the 3'-non-coding region contains polyA tail needed for virus infectivity. [5]

Diseases[edit]

The most well known Coxsackie A disease is hand, foot and mouth disease (unrelated to foot-and-mouth disease), a common childhood illness which affects mostly children aged 5 or under, often produced by Coxsackie A16. In most cases, infection is asymptomatic or causes only mild symptoms. In others, infection produces short-lived (7–10 days) fever and painful blisters in the mouth (a condition known as herpangina), on the palms and fingers of the hand, or on the soles of the feet. There can also be blisters in the throat, or on or above the tonsils. Adults can also be affected. The rash, which can appear several days after high temperature and painful sore throat, can be itchy and painful, especially on the hands/fingers and bottom of feet. [6]

Other diseases include acute haemorrhagic conjunctivitis (A24 specifically), herpangina, and aseptic meningitis (both Coxsackie A and B viruses). Coxsackievirus A7 is associated with neurological diseases and can cause paralytic poliomyelitis [7]

Picture citation and description: A transmission electron microscopic image depicting virions causing acute hemorrhagic conjunctivitis, primarily caused by two enteroviruses: enterovirus 70, and a variant of coxsackievirus A24. [8]

  1. ^ Ren, Jingshan; Wang, Xiangxi; Zhu, Ling; Hu, Zhongyu; Gao, Qiang; Yang, Pan; Li, Xuemei; Wang, Junzhi; Shen, Xinliang; Fry, Elizabeth E.; Rao, Zihe (2015-08-12). "Structures of Coxsackievirus A16 Capsids with Native Antigenicity: Implications for Particle Expansion, Receptor Binding, and Immunogenicity". Journal of Virology. 89 (20): 10500–10511. doi: 10.1128/JVI.01102-15. ISSN  0022-538X. PMC  4580203. PMID  26269176.
  2. ^ Zhao, Yuguang; Zhou, Daming; Ni, Tao; Karia, Dimple; Kotecha, Abhay; Wang, Xiangxi; Rao, Zihe; Jones, E. Yvonne; Fry, Elizabeth E.; Ren, Jingshan; Stuart, David I. (2020-01-07). "Hand-foot-and-mouth disease virus receptor KREMEN1 binds the canyon of Coxsackie Virus A10". Nature Communications. 11. doi: 10.1038/s41467-019-13936-2. ISSN  2041-1723. PMC  6946704. PMID  31911601.
  3. ^ Hu, Y. F.; Yang, Fan; Du, J.; Dong, J.; Zhang, T.; Wu, Z. Q.; Xue, Y.; Jin, Qi (2011-7). "Complete Genome Analysis of Coxsackievirus A2, A4, A5, and A10 Strains Isolated from Hand, Foot, and Mouth Disease Patients in China Revealing Frequent Recombination of Human Enterovirus A▿". Journal of Clinical Microbiology. 49 (7): 2426–2434. doi: 10.1128/JCM.00007-11. ISSN  0095-1137. PMC  3147834. PMID  21543560. {{ cite journal}}: Check date values in: |date= ( help)
  4. ^ Lincez, Pamela J.; Walic, Marine; Horwitz, Marc S. (2011-10-21). "The Key Players of Coxsackievirus-Induced Myocarditis". Myocarditis. doi: 10.5772/20932.
  5. ^ Mao, Qunying; Wang, Yiping; Yao, Xin; Bian, Lianlian; Wu, Xing; Xu, Miao; Liang, Zhenglun (2014-02-01). "Coxsackievirus A16". Human Vaccines & Immunotherapeutics. 10 (2): 360–367. doi: 10.4161/hv.27087. ISSN  2164-5515. PMC  4185891. PMID  24231751.{{ cite journal}}: CS1 maint: PMC format ( link)
  6. ^ CDC (2020). "Hand, Foot & Mouth Disease Symptoms". U.S. Centers for Disease Control and Prevention. Retrieved 2020-07-30.{{ cite web}}: CS1 maint: url-status ( link)
  7. ^ Yamayoshi S, Iizuka S, Yamashita T, Minagawa H, Mizuta K, Okamoto M, et al. (May 2012). "Human SCARB2-dependent infection by coxsackievirus A7, A14, and A16 and enterovirus 71". Journal of Virology. 86 (10): 5686–96. doi: 10.1128/JVI.00020-12. PMC  3347270. PMID  22438546.
  8. ^ "Details - Public Health Image Library(PHIL)". phil.cdc.gov. Retrieved 2020-07-31.

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