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 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]
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]
![]() | This is a user sandbox of
SMohebbi95. You can use it for testing or practicing edits. This is not the sandbox where you should draft your assigned article for a dashboard.wikiedu.org course. To find the right sandbox for your assignment, visit your Dashboard course page and follow the Sandbox Draft link for your assigned article in the My Articles section. |
{{
cite journal}}
: Check date values in: |date=
(
help)
{{
cite journal}}
: CS1 maint: PMC format (
link)
{{
cite web}}
: CS1 maint: url-status (
link)
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 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]
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]
![]() | This is a user sandbox of
SMohebbi95. You can use it for testing or practicing edits. This is not the sandbox where you should draft your assigned article for a dashboard.wikiedu.org course. To find the right sandbox for your assignment, visit your Dashboard course page and follow the Sandbox Draft link for your assigned article in the My Articles section. |
{{
cite journal}}
: Check date values in: |date=
(
help)
{{
cite journal}}
: CS1 maint: PMC format (
link)
{{
cite web}}
: CS1 maint: url-status (
link)