Oral excretion of Epstein-Barr virus by healthy subjects and patients with infectious mononucleosis.
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Biomedical subjects
Publications and source records attributed to M Nonoyama.
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Infection of Raji cells with Epstein-Barr virus (EBV) causes suppression of cellular deoxyribonucleic acid (DNA) synthesis and fragmentation of the cellular DNA. About 1,000 copies of EBV DNA of normal size (about 5 x 10(7) daltons in a single strand, as shown in an alkaline gradient) are synthesized per cell.
A deoxynucleoprotein complex (DNP-1) isolated from simian virus 40 (SV40) after disruption of the virus in an alkaline buffer contains the viral deoxyribonucleic acid (DNA) and four minor structural polypeptides. Dissociation of DNP-I by equilibrium centrifugation in CsCl yields a complex (DNP-II) that contains a small amount of polypeptide tightly bound to the viral DNA. Studies of the template activity of these deoxynucleoprotein complexes in vitro with Escherichia coli transcriptase show that the rate of transcription of DNP-I and DNP-II is 30 and 80%, respectively, compared with that of deproteinized SV40 DNA component I. In dimethyl sulfoxide gradients, the complementary ribonucleic acid (cRNA) synthesized from DNP-I is one-third to one-half the size of the cRNA species from DNA-I and DNP-II. Competition hybridization experiments show that with the E. coli transcriptase only a portion (about one-half) of the SV40 genome is transcribed with DNP-I as template, whereas most or all of the genome is transcribed with DNP-II as template. The template activity of the deoxynucleoprotein complexes with a highly active form II ribonucleic acid polymerase prepared from SV40-infected permissive cells follows similar transcription kinetics. The results indicate that structural nucleoproteins of SV40 bind nonrandomly to the viral DNA and effect the transcription of some subset of its sequences in vitro.
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When purified preparations of stock reovirus, type 3, were digested with chymotrypsin, the virions were converted into two different types of particle. These new particles could be separated from each other by isopycnic centrifugation in cesium chloride gradients. One particle banded at a buoyant density of 1.43 g/cm(3), the other at a density of 1.415 g/cm(3). The former particle is termed the heavy (H) particle, the latter is the light (L) particle. The ratio of H/L particles varied between 0.5 and 0.25 in various purified preparations of virus. In electron micrographs, both H and L particles had the appearance and dimensions of viral cores. H particles were infectious for L cells. When plaques formed by stock virus, or by H particles, were picked and propagated in L cells, the majority of the clones gave rise only to H particles on chymotrypsin digestion. On continued serial passage of the clones, virions containing L particles again appeared in the progeny. The simplest explanation of these results was that stock virus was comprised of two populations of virions. One type of virion which contained H particles was infectious, whereas the other, which contained L particles, was not itself infectious and could replicate only in cells coinfected with an H particle virion. Added weight was given to this hypothesis by two observations. First, a small but definite separation of H and L virions could be achieved by isopycnic centrifugation in a gradient of cesium chloride. Second, L particles and virions containing L particles were both shown to lack the largest of the ten segments of double-stranded ribonucleic acid genome. Thus, L particle virions have defective genomes.
Virus obtained from five plaques of reovirus was serially passaged in L cells. Defective virions arose in each clone by the seventh passage. Such defective virions lacked the largest of the 10 segments of the double-stranded ribonucleic acid genome.
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Several chemically defined plant extracts were investigated for their antiviral action on herpes simplex virus (HSV-1, HSV-2)-infected African green monkey kidney cells and human adenocarcinoma cells, using a plaque formation assay. Among them, the monomeric hydrolyzable tannins, oligomeric ellagitannins and condensed tannins, having galloyl groups or hexahydroxydiphenoyl groups, had the most potent anti-HSV activity. Their 50% effective doses (0.03-0.1 microgram/ml) were by two-three orders of magnitude lower than their 50% cytotoxic doses (greater than 10 micrograms/ml). On the other hand, gallic acid, neutral polysaccharides, chemically modified (N,N-dimethylaminoethyl-, carboxymethyl-, and sulfated-) glucans, sialic acid-rich glycoproteins, and uronic acid-rich pine cone polysaccharide showed little or no activity. Using radiolabeled virus particles, we demonstrated that the anti-HSV effect of the tannins is due to inhibition of virus adsorption to the cells.
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BACKGROUND: JTV519 is know to protect cardiomyocytes from calcium overloading-induced damage. The aim of this study was to investigate the potential protective effect of JTV519 on myocardium subjected to prolonged ischemia and the underlying mechanism of such protection. The effect of JTV519 was also compared with that of diltiazem, a 1,5-benzothiazepine derivative. METHODS: Isolated rat hearts were randomly divided into three groups. Control hearts were arrested with histidine-tryptophan-ketoglutarat (HTK) cardioplegic solution alone. In the JTV519 group of hearts, cardiac arrest was achieved with JTV519 (10(-3) mmol/L) in the HTK solution. Hearts in the diltiazem group were arrested with diltiazem (0.5 mmol/L) in the HTK solution. All the hearts were then subjected to 6-hour storage in HTK solution at 4 degrees C. RESULTS: After a 30-minute reperfusion, the left ventricular developed pressure in the JTV519 and diltiazem groups were improved significantly compared with the control group. There was a significantly lower left ventricular end-diastolic pressure level and higher recovery of coronary flow in the JTV519 group than in the control group. The postischemic intracellular calcium concentration was attenuated by adding JTV519 or diltiazem to HTK cardioplegia. CONCLUSION: As an adjunct to cardioplegia, JTV519 showed a significant protective effect on myocardium undergoing 6 hours of ischemia. The beneficial protective effects of JTV519 are correlated with its ability to inhibit the postischemic rise in intracellular calcium.