Identification of structural features of heparin required for inhibition of herpes simplex virus type 1 binding.

Binding of HSV-1 to cells is mediated by interactions of virion glycoproteins gC and/or gB with heparin sulfate (HS) glycosaminoglycans on cell surface proteoglycans. HS and the related glycosaminoglycan, heparin, comprise a family of heterogeneous carbohydrates composed of long, unbranched polysaccharides modified, for example, by sulfations and acetylations. To define the specific features of HS important for viral binding, we took advantage of the structural similarities between heparin and cell surface HS and compared the ability of chemically modified heparin compounds to inhibit the binding of viral particles to the cell surface and subsequent plaque formation.

Neomycin inhibits glycoprotein C (gC)-dependent binding of herpes simplex virus type 1 to cells and also inhibits postbinding events in entry.

Previous studies have identified requirements for the binding of herpes simplex virus type 1 (HSV-1) to cells, including the presence of particular glycoproteins in the virion envelope (gC or gB) and the presence of particular glycosaminoglycan chains (principally heparan sulfate) on cell surface proteoglycans. We show here that neomycin, a known inhibitor of HSV infection, blocked early events in HSV infection by two mechanisms: partial inhibition of the gC-dependent binding of virions, but not the gB-dependent binding, and inhibition of events that occurred after the binding of virus to cells. Near-maximal (but incomplete) inhibition of virus binding occurred at low concentrations of neomycin (1 mM) for wild-type and gB-negative virions only.

Glycoprotein C-independent binding of herpes simplex virus to cells requires cell surface heparan sulphate and glycoprotein B.

Previous studies have shown that the initial interaction of herpes simplex virus (HSV) with cells is binding to heparan sulphate and that HSV-1 glycoprotein C (gC) is principally responsible for this binding. Although gC-negative viral mutants are impaired for binding and entry, they retain significant infectivity. The purpose of the studies reported here was to explore the requirements for infectivity of gC-negative HSV-1 mutants.

Heparan sulfate glycosaminoglycans as primary cell surface receptors for herpes simplex virus.

Our current incomplete picture of the earliest events in HSV infection may be summarized as follows. The initial interaction of virus with cells is the binding of virion gC to heparan sulfate moieties of cell surface proteoglycans. Stable binding of virus to cells may require the interaction of other virion glycoproteins with other cell surface receptors as well (including the interaction of gB with heparan sulfate).

Glycoprotein C of herpes simplex virus type 1 plays a principal role in the adsorption of virus to cells and in infectivity.

The purpose of this study was to identify the herpes simplex virus glycoprotein(s) that mediates the adsorption of virions to cells. Because heparan sulfate moieties of cell surface proteoglycans serve as the receptors for herpes simplex virus adsorption, we tested whether any of the viral glycoproteins could bind to heparin-Sepharose in affinity chromatography experiments. Two glycoproteins, gB and gC, bound to heparin-Sepharose and could be eluted with soluble heparin.

[Isovolemic hemodilution--an adjuvant treatment principle in patients with chronic cor pulmonale caused by chronic obstructive lung disease].

On the basis of 10 patients with chronic cor pulmonale due to chronic obstructive lung disease and secondary polyglobulia in a clinical and experimental study could be made evident that by limited isovolaemic haemodilution (haematocrit value of 0.58 +/- 0.03 reduced to 0.

Cryoprecipitates in Kawasaki syndrome: association with coronary artery aneurysms.

Cryoprecipitates are postulated to play a role in the pathogenesis of several vasculitis illnesses and infectious diseases. To investigate the presence of cryoprecipitates in Kawasaki syndrome, we studied sera from 25 children with acute Kawasaki syndrome. None of the subjects was treated with intravenous gamma-globulin.

Purity of commercial non-certified European samples of Pyronin Y.

The purity of six European non-certified samples of Pyronin Y was compared with that of two American samples certified by the Biological Stain Commission. The methods used were spectrophotometry and a Methyl Green-Pyronin staining test (both as applied by the Biological Stain Commission), thin layer chromatography, mass spectrometry, determination of pH, and content of some electrolytes. It was found that none of the European batches of Pyronin Y passed the complete test as prescribed by the Biological Stain Commission.

[Ergometric investigations with pressure measurements in the pulmonary arteria for judgment of the severity of the disease in patients suffering from left heart diseases (author's transl)].

Pressure measurements in the pulmonary artery were performed on 34 patients by intracardiac floating catheter during rest and under ergometer load of 51 Watt (corresponding to an oxygen consumption of 750 ml/min). 15 of the patients were suffering from myocardial infarction 4--6 weeks after admission, 12 from chronic coronary heart disease respectively angina pectoris and 7 from affection of the aortic valve. The pressure during rest ranged within the norm.

[About the clinical picture of pulmonary heart disease with special regard to correlations between pulmonary function and pulmonary hemodynamics (author's transl)].

After introducing heart catheterization especially the right heart catheterization according to Grandjean the direct measurement of right ventricular as well as pulmonary artery pressure has been made possible in a relatively simple manner. Thereby the diagnosis cor pulmonale chronicum can be secured or omitted respectively with high confidence. In this regard the exercise--induced increase in pulmonary artery pressure has evident importance especially in case of clinical uncertainty.

[Hemodynamics in chronic cor pulmonale during exercise (author's transl)].

1. In patients with chronic cor pulmonale there is a regression dependence between the amount of exercise-induced increase in pulmonary arterial pressure and the level of resting value. 2.

[Ventilation, gas-exchange and pulmonary arterial pressure during aerosol inhalation of sympathicomimetics (author's transl)].

The effect of inhalation of Novodrin (beta-receptor-stimulus), Phenylephrine (alpha-receptor-stimulus) and of a mixture of both was tested in patients with chronic nonspecific respiratory syndrome. There was no significant difference of pulmonary arterial mean-pressure. Forced expiratory volume and vital capacity rose both after inhalation of Novdrin and after inhalation of the mixture.

[Analysis of pulmonary mechanics in patients with silicosis (author's transl)].

Parameters of pulmonary mechanics were measured at rest and during physical effort in patients with silicosis and normal subjects. Between normal subjects and patients with silicosis of stage I a significant difference could not be found. However, a decrease of dynamic compliance and an increase of elastic work of breathing were found in patients with silicosis III during exercise.

[71. Float catheter and pulmonary work load hypertension in mitral valve defects and cor pulmonale].

In patients with mitral valvular defects as well as with chronic cor pulmonale there exists an ascertained relation between the pulmonary-arterial pressure in rest and the increase of blood pressure under easy physical load. Patients with high initial value or strong increase of blood pressure reveal a retarded return of the blood pressure of the pulmonary artery to the initial value.

[Mechanics of breathing and exertion dyspnea in silicosis (author's transl)].

Mechanics of breathing as studied in patients with different stages of silicosis in rest and during exercise show the following: dynamic compliance and work against elastic and viscous resistances could not be found to be decisive indices of exertion dyspnea. Evidence of exertion dyspnea could only be achieved by means of the ration VT/PT (VT equals tidal volume, PT equals tidal esophageal pressure). Exertion dyspnea was observed at less than 0,081 VT per cm H20 PT.