Group B coxsackievirus virulence.

That which is understood of virulence phenotypes in the picornaviruses derives in large part from studies of artificially attenuating phenotypes rather than through examination of naturally occurring virus strains. The CVB replicate well in a variety of different murine and human cell cultures, making them excellent viruses with which to engage the problem of how the host environment interacts with specific viral genetics to promote varying efficiencies of viral replication. It is not known how highly virulent CVB strains may arise but evidence suggests such strains are not the norm.

Terson syndrome with bilateral optic nerve sheath hemorrhage.

A 53-year-old man presented with an acute headache and mental status changes due to rupture of an anterior choroidal artery aneurysm. A preoperative CT scan demonstrated subarachnoid hemorrhage, bilateral optic nerve sheath hemorrhage, and bilateral intraocular hemorrhage. Ophthalmoscopy and B-scan ocular ultrasound disclosed vitreous hemorrhages, features consistent with Terson syndrome.

Diabetes acceleration or prevention by a coxsackievirus B4 infection: critical requirements for both interleukin-4 and gamma interferon.

Type 1 diabetes acceleration in nonobese diabetic (NOD) mice through coxsackievirus B4 (CVB4) infection requires a preexisting critical mass of autoreactive T cells in pancreatic islets, and in the absence of this insulitic threshold, CVB4 infection leads to long-term disease protection. To understand this acceleration and protection process, we challenged 8- and 12-week-old NOD mice containing a disruption in interleukin-4 (IL-4) or gamma interferon (IFN-gamma) genes (NOD IL-4-/- and NOD IFN-gamma-/-, respectively) with a diabetogenic, pancreatropic Edwards strain of CVB4. The elimination of IL-4 did not alter the rate of insulitis or diabetes development in NOD mice, while the elimination of IFN-gamma delayed these events several weeks.

Coxsackievirus experimental heart diseases.

Many microorganisms, particularly viruses, can cause myocarditis, an inflammatory disease of the heart. The frequency of and major factors that contribute to this disease, including a pronounced gender (male) bias, age and genetic background parameters are discussed, along with signs and symptoms of disease in infants to adults. Individuals with acute disease generally recover without sequelae; the chronic form can develop into idiopathic dilated cardiomyopathy and death can follow.

Evaluation of coxsackievirus infection in children with human immunodeficiency virus type 1-associated cardiomyopathy.

In a matched case-control study of the association between coxsackieviruses and cardiac impairment, 24 human immunodeficiency virus (HIV) type 1-infected children with cardiac impairment were compared with 24 HIV-1-infected control subjects. Serologic evidence of coxsackievirus infection was present in all children, with no significant difference in geometric mean antibody titers between case patients and control subjects. Conditional logistic regression to test for an association between coxsackievirus antibody titer and the presence or absence of cardiac impairment, by any indicator, showed an odds ratio of 1.