[1] Coxsackievirus B4 is one of the six serotypes found in Group B and is a positive sense, single-stranded, non-enveloped RNA virus.

The capsid of Coxsackie viruses have a distinguishable depression around the fivefold axis, termed the “canyon.” The canyon is thought to help with viral attachment through the interaction with cell surface molecules.

[2] Uncoating is unnecessary as it leaves the capsid at the plasma membrane and the genome is simply injected into the cytoplasm.

Upon entry of the genome into the cytoplasm of the host cell, the IRES in the 5’ UTR recruits ribosomal subunits (cap-independent mechanism) which starts the translation process.

[5] The viral protein 2C brings positive sense RNA genomes to the endoplasmic reticulum where assembly and maturation will occur.

[4] While all of this is occurring, viral proteinases are working to turn off host cell protein synthesis by cleaving the eIF-4 initiation factor.

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.

Pups that were born from dams infected on days 4 and 17 of gestation had significantly (p < 0.05) greater pancreatic abnormalities leading to symptoms similar to diabetes.

[11] A 2011 systematic review and meta-analysis showed an association between enterovirus infections and type 1 diabetes, but in contrast, other studies have shown that rather than triggering an autoimmune process, enterovirus infections, as coxsackievirus B, could protect against onset and development of type 1 diabetes.

Common symptoms of neonatal coxsackie B virus infection in children include meningitis and/or encephalitis.

[6] Infection due to Coxsackie B viruses can be determined by measuring the amount of neutralizing antibodies in the blood, PCR, and through microscopic detection.