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Usually, herpangina is produced by one particular strain of coxsackie virus A (and the term "herpangina virus" refers to coxsackievirus A), [1] but it can also be caused by coxsackievirus B or echoviruses. [2] Most cases of herpangina occur in the summer, [3] affecting mostly children. However, it occasionally occurs in adolescents and adults.
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]
Coxsackie B infection of the heart can lead to pericardial effusion. The development of insulin-dependent diabetes has recently been associated with recent enteroviral infection, particularly coxsackievirus B pancreatitis. This relationship is currently being studied further.
Coxsackie A virus is a subgroup of enterovirus A, which are small, non-enveloped, positive-sense, single-stranded RNA viruses. Its 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.
Patients with Coxsackie B4 virus have seemed to have herpangina, tonsillitis, and pharyngitis. [6] CB4 virus has caused transplacental infections in mice. Infection in the first couple weeks of gestation has been shown to be harmful for dams as well as the fetus, causing reduced litter sizes, abortion, or stillbirth.
Hand, foot, and mouth disease (HFMD) is a common infection caused by a group of enteroviruses. [10] It typically begins with a fever and feeling generally unwell. [10] This is followed a day or two later by flat discolored spots or bumps that may blister, on the hands, feet and mouth and occasionally buttocks and groin.
The amount of virally infected cardiomyocytes varies in different stages of the disease. In a mouse model, at the acute stage (7 days after infection with coxsackievirus B3) approximately 10% of the myocytes are infected and could affect overall cardiac function. In chronic murine infection, the percentage of infected cardiomyocytes are much lower.
sCAR-Fc (Soluble Receptor Analogue) is an experimental prophylactic treatment against coxsackievirus B3 (CVB) infections. Coxsackievirus B3 can cause cardiac damage, eventually resulting in a weakened and enlarged heart that is termed dilated cardiomyopathy. [1]