Coxsackie B virus infection

A case of a 27-year patient with a clinical syndrome of Coxsackie B viral infection is presented. The symptoms included pleurodynia, myocarditis and the acute gastritis. The diagnosis was confirmed with serological tests which showed high titre of antibodies neutralizing Coxsackie B3. The symptoms of myocardial infarction dominated in both clinical course and autopsy. The authors suggest that serological tests specific for Coxsackie B infection should be performed in the young patients with the symptoms of myocardial infarction.     

Allosteric inhibitors of Coxsackie virus A24 RNA polymerase

Coxsackie virus A24 (CVA24), a causative agent of acute hemorrhagic conjunctivitis, is a prototype of enterovirus (EV) species C. The RNA polymerase (3D^pol) of CVA24 can uridylylate the viral peptide linked to the genome (VPg) from distantly related EV and is thus, a good model for studying this reaction. Once UMP is bound, VPgpU primes RNA elongation. Structural and mutation data have identified a conserved binding surface for VPg on the RNA polymerase (3D^pol), located about 20 Å from the active site. Here, computational docking of over 60,000 small compounds was used to select those with the lowest (best) specific binding energies (BE) for this allosteric site. Compounds with varying structures and low BE were assayed for their effect on formation of VPgU by CVA24-3D^pol. Two compounds with the lowest specific BE for the site inhibited both uridylylation and formation of VPgpolyU at 10–20 μM. These small molecules can be used to probe the role of this allosteric site in polymerase function, and may be the basis for novel antiviral compounds.     

Experimental Coxsackie B-3 virus infection in Citellus lateralis

Coxsackie B-3 virus produces a mild infection which passes unnoticed in the non-hibernating Citellus lateralis. A severe infection occurs in the hibernating animal. The progress of infection in the hiberating animal is related to the number of arousal hours and quite independent of the number of infected days. Nevertheless, it has been shown that the low-temperature hibernation phase has a potentiating effect upon subsequent viral production. Infective virus has not been found in the inoculated brown fat pads during the hibernation phase but very high virus titers are recorded 48 hours after arousal. This results in an earlier viraemia and earlier and higher titers in other organs of the body. A similar effect is noted when virus is inoculated at the very beginning of the arousal phase. While most animals recover with subsequent antibody development, a few succumb. Antibody development is slow and related only to the number of arousal hours experienced. Particular note is made of the fact that an animal may successfully resume hibernation despite complete loss of the axillary brown fat pads.