scholarly journals THE INHIBITORY EFFECT OF POLYSACCHARIDE ON MUMPS VIRUS MULTIPLICATION

1948 ◽  
Vol 87 (5) ◽  
pp. 385-410 ◽  
Author(s):  
Harold S. Ginsberg ◽  
Walther F. Goebel ◽  
Frank L. Horsfall
Keyword(s):  
Chick Embryo ◽  
Inhibitory Effect ◽  
Virus Multiplication ◽  
Mumps Virus ◽  
Viral Multiplication ◽  
Chemical Studies ◽  
Structural Configurations ◽  
Serological Activity

Polysaccharides derived from type-specific Friedländer bacilli cause inhibition of the multiplication of mumps virus in the allantoic sac of the chick embryo. As little as 5 µg. of polysaccharide is effective as an inhibitor. Inhibition of multiplication is obtained when polysaccharide is injected as long as 4 days after inoculation of virus. Chemical studies have shown that the structural configurations of the polysaccharide responsible for specific serological activity are not identical with those which determine the inhibitory effect relative to mumps virus. The possible mechanisms of the inhibition of viral multiplication by means of polysaccharides are discussed.

scholarly journals INHIBITION OF RELEASE OF VACCINIA VIRUS BY N1-ISONICOTINOYL-N2-3-METHYL-4-CHLOROBENZOYLHYDRAZINE

1969 ◽  
Vol 129 (4) ◽  
pp. 795-808 ◽  
Author(s):  
Nobuo Kato ◽  
Hans J. Eggers ◽  
Heinrich Rolly
Keyword(s):  
Chick Embryo ◽  
Vaccinia Virus ◽  
Inhibitory Effect ◽  
Virus Multiplication ◽  
Kidney Cells ◽  
Virus Release ◽  
Single Cycle ◽  
Infected Cells ◽  
Embryo Fibroblasts ◽  
Intracellular Virus

N1-isonicotinoyl-N2-3-methyl-4-chlorobenzoylhydrazine (IMCBH) is a selective inhibitor of vaccinia virus multiplication. In concentrations up to 50 µg/ml, IMCBH causes neither toxic morphologic changes, nor does it inhibit the multiplication of cells. Viruses other than vaccinia are not affected by IMCBH. The virus-inhibitory effect of IMCBH is dependent on the type of host cell used, i.e., the compound is effective in chick embryo fibroblasts and monkey kidney cells but not in L cells. IMCBH does not exhibit any protecting effect on vaccinia virus-infected mice or rabbits. IMCBH interferes with virus release: in single cycle experiments in chick embryo fibroblasts, IMCBH strongly blocks the release of vaccinia virus at concentrations as low as 3 µg/ml, while intracellular virus synthesis is hardly affected. Viral cytopathic changes are completely suppressed by IMCBH within the span of a single cycle infection, although extensive changes eventually occur. By inhibiting virus release from initially infected cells, IMCBH markedly inhibits the multiplication of vaccinia virus in cell cultures infected at low virus/ cell multiplicities. IMCBH does not inhibit the early toxic cytopathic changes induced by large inocula of vaccinia virus in BHK21 cells.

scholarly journals The effects of UK 2054 on the multiplication of influenza viruses

1970 ◽  
Vol 68 (1) ◽  
pp. 151-158 ◽  
Author(s):  
R. D. Barry ◽  
Patricia Davies
Keyword(s):  
Influenza Virus ◽  
Chick Embryo ◽  
Inhibitory Effect ◽  
Virus Multiplication ◽  
Influenza Viruses ◽  
Host Cells ◽  
Virus Infectivity ◽  
Virus Growth ◽  
Virus Particles ◽  
Embryo Fibroblasts

SummaryThe isoquinoline compound UK 2054 prevents the uptake of influenza virus by susceptible cells. Pre-incubation of virus particles with 500μg./ml. UK 2054 at 37°C. for 2 hr. does not reduce virus infectivity. Host cells vary in their responsiveness to the inhibitory effect of UK 2054; virus multiplication is inhibited in chick allantoic cells by lower concentrations than those required to inhibit virus growth in chick embryo fibroblasts. The effectiveness of UK 2054 is reduced by the presence of serum.It is concluded that inhibition of influenza virus multiplication by UK2054 might result from interaction of the inhibitor with both virus and cells. Any direct combination between inhibitor and virus is completely reversible.

A STUDY OF THE INHIBITORY EFFECTS OF CHICK WHOLE EYE EXTRACT ON THE DEVELOPMENT OF THE LENS OF THE CHICK EMBRYO IN VITRO

1966 ◽  
Vol 44 (4) ◽  
pp. 661-676 ◽  
Author(s):  
Robert P. Thompson
Keyword(s):  
Chick Embryo ◽  
Nutrient Medium ◽  
Inhibitory Effect ◽  
Reactive System ◽  
Vesicle Formation ◽  
Inhibitory Effects ◽  
Muscle Extract ◽  
Lens Vesicle ◽  
And Control

To demonstrate the phenomenon of homologous inhibition by clearly interpretable results in a readily reactive system, experiments were carried out to study the effect of chick whole eye extract on the development of the vesicular lens of the chick embryo in vitro. The heads of embryos of 11 through 13 somites were explanted onto nutrient medium diluted with varying amounts of the extract, and cultured for 30 hours. A total of 35 embryos exposed to concentrations of 1:1, 1:2, and 1:4 (extract to medium) showed complete inhibition of lens vesicle formation. Of a total of 53 embryos on concentrations of 1:8, 1:16, 1:32, and 1:64, more than 50% showed inhibition of vesicle formation. The inhibitory effect disappeared at a concentration of 1:128. Control material exposed to some equivalent concentrations of nutrient medium – saline mixtures showed inhibition of vesicle formation in only 15% of 33 embryos. Of a total of 27 control embryos exposed to ventricular muscle extract, approximately one-third showed inhibition of vesicle formation at concentrations of 1:8 and 1:16, with the inhibitory effect disappearing at 1:32. The implications of this result are discussed. Other factors and control experiments are described and their value is assessed.

scholarly journals CONCURRENT INFECTION WITH INFLUENZA VIRUS AND MUMPS VIRUS OR PNEUMONIA VIRUS OF MICE (PVM) AS BEARING ON THE INHIBITION OF VIRUS MULTIPLICATION BY BACTERIAL POLYSACCHARIDES

1949 ◽  
Vol 89 (1) ◽  
pp. 37-52 ◽  
Author(s):  
Harold S. Ginsberg ◽  
Frank L. Horsfall
Keyword(s):  
Influenza A ◽  
Virus Multiplication ◽  
Mumps Virus ◽  
Influenza Viruses ◽  
Influenza B ◽  
Capsular Polysaccharides ◽  
Concurrent Infection ◽  
Mechanism Of Inhibition ◽  
Metabolic Systems ◽  
Differing Effect

Preexisting infection with PVM or mumps virus does not prevent multiplication of the virus of influenza A or B in the same tissue. Similarly, pre-existing infection with one or another of the influenza viruses does not prevent multiplication of either PVM or mumps virus in the same tissue. The failure of these two groups of viruses to interfere with the multiplication of each other is discussed in relation to the mechanism of inhibition of multiplication of mumps virus and PVM by the capsular polysaccharides of Friedländer bacilli, and the ability of influenza A and influenza B viruses to multiply in the presence of large quantities of these carbohydrates. It is suggested that differences in the requirements of the two groups of viruses for host cell metabolic systems may serve to explain both the lack of interference between them and the differing effect of polysaccharides upon their multiplication.

Identification of Insulin in Chick Embryo Retina During Development and Its Inhibitory Effect on DNA Synthesis

1992 ◽  
Vol 58 (4) ◽  
pp. 1353-1359 ◽  
Author(s):  
Giovanni Tesoriere ◽  
Renza Vento ◽  
Giuseppe Calvaruso ◽  
Gennaro Taibi ◽  
Michela Giuliano
Keyword(s):  
Chick Embryo ◽  
Dna Synthesis ◽  
Inhibitory Effect

scholarly journals Viral-Induced Systemic Necrosis in Plants Involves Both Programmed Cell Death and the Inhibition of Viral Multiplication, Which Are Regulated by Independent Pathways

2010 ◽  
Vol 23 (3) ◽  
pp. 283-293 ◽  
Author(s):  
Ken Komatsu ◽  
Masayoshi Hashimoto ◽  
Johji Ozeki ◽  
Yasuyuki Yamaji ◽  
Kensaku Maejima ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Viral Infection ◽  
Expression Patterns ◽  
Plant Viruses ◽  
Virus Multiplication ◽  
Mitogen Activated Protein Kinase ◽  
Systemic Necrosis ◽  
Viral Multiplication ◽  
Plantago Asiatica

Resistant plants respond rapidly to invading avirulent plant viruses by triggering a hypersensitive response (HR). An HR is accompanied by a restraint of virus multiplication and programmed cell death (PCD), both of which have been observed in systemic necrosis triggered by a successful viral infection. Here, we analyzed signaling pathways underlying the HR in resistance genotype plants and those leading to systemic necrosis. We show that systemic necrosis in Nicotiana benthamiana, induced by Plantago asiatica mosaic virus (PlAMV) infection, was associated with PCD, biochemical features, and gene expression patterns that are characteristic of HR. The induction of necrosis caused by PlAMV infection was dependent on SGT1, RAR1, and the downstream mitogen-activated protein kinase (MAPK) cascade involving MAPKKKα and MEK2. However, although SGT1 and RAR1 silencing led to an increased accumulation of PlAMV, silencing of the MAPKKKα-MEK2 cascade did not. This observation indicates that viral multiplication is partly restrained even in systemic necrosis induced by viral infection, and that this restraint requires SGT1 and RAR1 but not the MAPKKKα-MEK2 cascade. Similarly, although both SGT1 and MAPKKKα were essential for the Rx-mediated HR to Potato virus X (PVX), SGT1 but not MAPKKKα was involved in the restraint of PVX multiplication. These results suggest that systemic necrosis and HR consist of PCD and a restraint of virus multiplication, and that the latter is induced through unknown pathways independent from the former.

scholarly journals INHIBITION OF INFLUENZA VIRUS MULTIPLICATION BY N-GLYCOSIDES OF BENZIMIDAZOLES

1954 ◽  
Vol 99 (3) ◽  
pp. 227-250 ◽  
Author(s):  
Igor Tamm ◽  
Karl Folkers ◽  
Clifford H. Shunk ◽  
Frank L. Horsfall
Keyword(s):  
Influenza Virus ◽  
Influenza A ◽  
Benzimidazole Derivative ◽  
Chorioallantoic Membrane ◽  
Inhibitory Effect ◽  
Virus Multiplication ◽  
Cellular Growth ◽  
Tissue Proliferation ◽  
Fresh Culture Medium

Chloro derivatives of benzimidazole were found to be 2 to 3 times more active than corresponding methyl derivatives in causing inhibition of Lee virus multiplication in chorioallantoic membrane cultures in vitro. The most active benzimidazole derivative thus far tested is 5,6-dichloro-1-ß-D-ribofuranosylbenzimidazole (DRB); it caused 75 per cent inhibition of Lee virus multiplication in membrane cultures at a concentration of 0.38 x 10–4 M. On the other hand, 5,6-dimethyl-1-alpha;-D-ribofuranosylbenzimidazole, the moiety present in vitamin B12, failed to inhibit Lee virus multiplication at a concentration of 35 x 10–4 M. Other N-glycosides of 5,6-dichlorobenzimidazole were considerably less active than DRB. In single cycle experiments, the degree of inhibition of Lee virus multiplication by DRB in membrane cultures was not dependent on the amount of virus in the inoculum. This compound did not inactivate the infectivity of extracellular Lee virus, had no effect on virus-erythrocyte interaction, did not interfere with the adsorption of the virus by the host tissue, nor affect the release of newly formed virus from the membrane. The inhibitory effect of DRB on Lee virus multiplication, in contrast to that of 2,5-dimethylbenzimidazole, persisted after transfer of infected membranes into fresh culture medium not containing the compound. Both DRB and the 2,5-dimethyl compound caused 99 per cent inhibition of Lee virus multiplication without affecting oxygen uptake of the membrane. Tissue proliferation of membrane pieces in roller tube culture was not significantly affected by DRB at inhibitory concentration, whereas at equivalent concentration the 2,5-dimethyl compound did restrict cellular growth. At higher concentrations, both compounds caused retardation of cell proliferation. This effect was reversible on removal of either compound from the medium. The multiplication of several strains of influenza A and B viruses, i.e. Lee, MB, PR8, and FM1, was inhibited to the same degree by each of the two compounds; DRB was 35 times more active than the 2,5-dimethyl compound relative to each of the strains. DRB caused inhibition of Lee virus multiplication in intact embryonated chicken eggs and in mice without causing significant signs of toxicity in either host. Some of the implications of these findings are discussed in relation to the mechanism of the inhibition of influenza virus multiplication.

STUDIES OF INFECTIOUS BOVINE RHINOTRACHEITIS VIRUS: II. EFFECT OF METABOLIC INHIBITORS ON VIRUS MULTIPLICATION

1965 ◽  
Vol 11 (6) ◽  
pp. 887-892 ◽  
Author(s):  
Leslie R. Sabina
Keyword(s):  
Nucleic Acid ◽  
Experimental Evidence ◽  
Inhibitory Effect ◽  
Virus Multiplication ◽  
Metabolic Inhibitors ◽  
Infectious Bovine Rhinotracheitis ◽  
Viral Inhibition ◽  
Infectious Bovine Rhinotracheitis Virus

The suppression of infectious bovine rhinotracheitis (IBR) virus multiplication by certain metabolic inhibitors was studied. Viral inhibition with analogues of deoxyuridine and the reversal of this inhibitory effect by thymidine indicates a deoxyribose type of nucleic acid in IBR. Experimental evidence showed no difference in antigenic constitution between IBR and analogue-resistant IBR viruses.

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