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Results for “COXSACKIE VIRUSES”

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At least 19 recordsLinked to original sources
PubMed1995

Differential diagnosis and genetic analysis of the antigenically related swine vesicular disease virus and coxsackie viruses.

Monoclonal antibodies directed against an isolate of swine vesicular disease virus (SVDV), characterized by virus neutralization tests and competition assays, were used to compare SVDV isolates and isolates of the antigenically related Coxsackie viruses by ELISA. SVDV-specific reaction patterns and one specific for Coxsackie viruses were observed. This provided a method for distinguishing between these enteroviruses. In addition, RT-PCRs were undertaken with Coxsackie virus and SVDV genomes. Different product patterns were obtained which correlated with the genetic differences revealed by nucleotide sequence determination. RT-PCR distinguished between SVDV and Coxsackie viruses by pattern differences. Further SVDV-specific PCRs were carried out with clinical samples. Viral genomes were detected with a sensitivity equivalent to that of virus isolation in cell culture. Sequencing of the Coxsackie virus-derived 2A-coding PCR products resulted in a not previously described sequence of a B5 isolate and in SVDV-specific sequence of two Coxsackie virus A16 isolates. The differences of the isolates by ELISA and PCR reactivity, as well as the nucleotide sequence differences are consistent with the quasispecies concept of RNA viruses.

Animals↗
PubMed1998

The intestinal absorption of cadmium increases during a common viral infection (coxsackie virus B3) in mice.

Murine intestinal absorption, tissue accumulation and redistribution of 109Cd during infection were studied using the common human virus Coxsackie virus B3 (CB3) adapted to the mouse. Female Balb/c mice were infected with CB3 and, on day 4 of the infection, dosed orally with 0.3 or 750 microgram Cd/kg body weight, with 109Cd as a tracer, in order to study intestinal absorption and tissue distribution of Cd during infection (Experiment 1). Other mice were dosed with 0.3 microgram Cd/kg body weight 3 days before being infected and, on day 4 of the infection, Cd redistribution was studied (Experiment 2). In both experiments non-infected control animals received the same treatment as infected animals. Results showed that the infected animals had a higher gastrointestinal absorption of Cd than noninfected animals when Cd was administered during infection. In the infected animals the absorption at the low Cd dosage was increased by 70% and was tripled at the high dosage. The increased absorption enhanced the accumulation of Cd in all organs studied. Moreover, the infection caused a Cd dose-dependent change in the organ distribution of Cd, when Cd was administered during the infection. However, no redistribution of previously accumulated Cd occurred during ongoing disease, indicating that Cd was not mobilised from body stores by the infection. These results show, for the first time, that an invading micro-organism can increase the intestinal absorption and concomitantly alter the tissue distribution of an environmental pollutant (Cd) if exposure occurs during the course of viral infection.

Administration, Oral↗
PubMed1986

Coxsackie virus B4 produces transient diabetes in nonhuman primates.

Cynomolgus, rhesus, and Cebus monkeys failed to show glucose tolerance or insulin secretion abnormalities after infection with encephalomyocarditis virus or Coxsackie virus B4. Patas monkeys also showed no abnormalities after infection with encephalomyocarditis virus. However, patas monkeys infected with Coxsackie virus B4 or treated first with a subdiabetogenic dose of streptozocin and then infected sequentially with Coxsackie viruses B4 and B3 showed transient elevation of glucose tolerance tests, depressed insulin secretion, and glucose in the urine. Our experiments in nonhuman primates support earlier studies in mice and humans that under certain circumstances, Coxsackie viruses can cause abnormalities in glucose homeostasis.

Animals↗