PubMed Health⌕ Search

Biomedical subjects

L Seganti

Publications and source records attributed to L Seganti.

At least 55 records · Page 3Linked to original sources
PubMed1991

Effect of antibiotics on polycation-treated Escherichia coli HB101 (pRI203).

In the present paper, we demonstrated that low concentrations of various polycationic agents sensitize E. coli HB 101 harboring the plasmid pRI203, containing the Y. pseudotuberculosis invasion region, to antibiotics rifampicin, amikacin, ceftazidime and cefotaxime. These antibiotics, known to be excluded, to various degrees, by the bacterial outer membrane, resulted several-fold more active towards polycation-treated bacteria by comparison with controls. This increased permeability to antibiotics of E. coli HB 101 (pRI203) probably depends upon the binding of polycations to the acidic moieties of lipopolysaccharide, as already suggested for other gram-negative bacteria.

Anti-Bacterial Agents↗
PubMed1991

Human serum non-antibody inhibitors towards SA-11 rotavirus hemagglutination.

In the present work the non-antibody inhibitory activity of human serum towards SA-11 rotavirus hemagglutination (HA) has been studied. Among human serum protein components, inhibitory activity was recovered in fractions III (beta-globulin), IV (alpha-globulin) and IV (glycoprotein). Additional experiments performed with purified lipoprotein sub-classes and their lipid and apolipoprotein moieties demonstrated the ability of HDL and, HDL1 to prevent SA-11 HA.

Animals↗
PubMed1990

In vitro effect of synthetic flavanoids on astrovirus infection.

In this study we investigated the activity of halogeno-, cyano- and amidino-isoflavenes, isoflavans and flavans on the multiplication of human astroviruses. These are naked small round viruses which have been recognized as causative agents of human gastroenteritis, and whose capsid proteins are similar to those of picornaviruses. Although all drugs tested caused a dose-dependent reduction of viral antigen synthesis as monitored by immunofluorescence, the chloro derivatives were the most effective.

Animals↗
PubMed1990

Effect of polyelectrolytes on entry of Escherichia coli HB101 (pRI203) into HeLa cells.

The role of charged molecules in the entry mechanism of enteroinvasive bacteria was studied using Escherichia coli HB101 harboring a plasmid (pRI203) containing the Yersinia pseudotuberculosis invasion region as an experimental model. We investigated the effect of several anionic and cationic polyelectrolytes on the initial steps of infection of HeLa S3 cells by E. coli HB101 (pRI203). Experiments in which the polyions were added to cell monolayers together with bacteria showed that invasion was only slightly influenced by anions whereas cations strongly enhanced bacterial entry. DEAE-dextran, histone and poly-L-lysine were the most effective enhancers producing an up to five-fold increase in the number of both infected cells and internalized bacteria. Moreover, addition of the active polycations at different stages of infection demonstrated that their action took place during the attachment step, whereas internalization was not affected.

Cell Division↗
PubMed1990

Susceptibility of mammalian, avian, fish, and mosquito cell lines to rabies virus infection.

The relationship between plasma membrane receptor organization and cell susceptibility in vitro was investigated in mammalian, avian, fish, and arthropod cell lines infected with fixed rabies virus. IMR32, HeLa, CER, and EPC cells were widely susceptible to infection with CVS virus, whereas a lower level of specific viral antigens was detectable in A. albopictus cells. In spite of these differences, the amount of infectious virus particles bound to the various cell surfaces was similar. Competition experiments carried out with plasma membranes extracted from ability of these components to bind the virus and to prevent infection. The different cellular permissiveness to rabies infection described here did not correlate with significant differences in number or in chemical structure of the receptor binding sites, but more likely with events following virus adsorption.

Adsorption↗
PubMed1989

Effect of cellular function inhibitors on the infection of Frp/3 cells by hepatitis A virus.

The effect of some cellular function inhibitors on hepatitis A virus (HAV) adsorption and on the successive events of infection in a monkey cell line (Frp/3 cells) was investigated. Treatments of Frp/3 cells with colcemide, vinblastine and cytochalasin D, which affect cytoskeleton organization, indicated that neither microtubules nor microfilaments play an important role in the early events of HAV infection. Monensin, which acts as an ionophore on intracellular vesicle compartments inhibited HAV infection probably at the uncoating step. Inhibition of viral replication to a different degree was observed with both inhibitors of oxidative phosphorylation, such as dinitrophenol and sodium azide, and with an inhibitor of glycolysis, 2-deoxy-D-glucose. However, none of these compounds significantly affected the early steps of infection, thus demonstrating that HAV replication is largely dependent upon cell energy.

Azides↗
PubMed1989

Membrane lipid components interacting with hepatitis A virus.

The involvement of lipid components in hepatitis A virus (HAV) attachment to host cells has been investigated. Isolated Frp/3 cell membranes and whole lipids, phospholipid and glycolipid fractions extracted from them were able to bind the virus and to prevent infection. Treatment of virus with various phospholipids or glycolipids demonstrated the participation of phosphatidylserine, phosphatidylethanolamine and galactose in HAV binding. Results obtained added further information on the receptor specificity of host cells for HAV.

Animals↗
PubMed1988

Effect of cellular inhibitors on the infection of various susceptible cells with vesicular stomatitis virus.

The effect of some cellular function inhibitors on adsorption and successive events of penetration of vesicular stomatitis virus to phylogenetically unrelated permissive cells was investigated. Treatment of HeLa, CER, EPC and Aedes albopictus cells with colcemide and cytochalasin D which affect cytoskeleton organization indicated that microfilaments but not microtubules were involved in the early events of VSV infection. Inhibitors of oxidative phosphorylation such as dinitrophenol and sodium azide, and the glycolysis inhibitor 2-deoxy-D-glucose, did not allow multiplication of prebound virions, demonstrating that VSV replication is largely energy dependent in either host cells examined.

Adsorption↗
PubMed1987

Study of the chemical nature of Frp/3 cell recognition units for hepatitis A virus.

Research has been carried out in order to clarify the chemical nature of cell receptors interacting with a fast growing strain of hepatitis A virus (HAV) producing a cytopathic effect on Frp/3 cells. Cell surface susceptibility to HAV attachment has been studied after treatment with enzymes acting on different chemical groupings. Results obtained showed a lowering of cell susceptibility to HAV infection following the action of phospholipase A2, phospholipase C, trypsin and beta-galactosidase. These data suggested that phospholipids, proteins and galactose participate to the cellular receptorial area for HAV.

Cell Line↗
PubMed1987

The effect of lipophilic amines on the growth of hepatitis A virus in Frp/3 cells.

The effect of lipophilic amines on hepatitis A virus infection in a monkey cell line (Frp/3 cells) was studied. Ammonium chloride, amantadine, methylamine and dansylcadaverine inhibited viral antigen synthesis when added to the cells at least one hour after the attachment step. Results obtained suggest that the HAV entry pathway in Frp/3 cells follows an endocytic route and that viral uncoating takes probably place in endosomes and/or lysosomes.

Amantadine↗
PubMed1987

Entry pathway of vesicular stomatitis virus into different host cells.

A biochemical and morphological investigation of the mechanism of entry of vesicular stomatitis virus (VSV) into host cells of mammalian (HeLa), avian (CER), piscine (EPC) and arthropod (Aedes albopictus) origin, is described. VSV was capable of infecting all cell lines tested by a endosome- and/or a lysosome-dependent step since ammonium chloride and amantadine blocked the early stages of infection. Complement-dependent immune lysis of infected host cells provided evidence that in none of the four different cell types examined did insertion of VSV antigens occur from the outside to any great extent on the cell surface. When the entry process was studied by electron microscopy, virus particles were seen to be bound to the cell surface at 0 degrees C. After warming at 37 degrees C for homeothermic cells or at 26 degrees C for poikilothermic cells, virus was detected within coated pits and coated vesicles and, later, in lysosomes. VSV entry was seen to take place by endocytosis in all four cell lines, which were derived from phylogenetically unrelated species.

Aedes↗
PubMed1987

Adhesive properties of Pseudomonas aeruginosa isolated from urinary tract infections.

A research was carried out on the adhesive properties of 104 uropathogenic strains of P. aeruginosa. On the basis of the adhesiveness to various types of cell it was possible to identify the most frequent adhesive patterns. Moreover, the ability of some carbohydrates to inhibit the adhesiveness of P. aeruginosa and the effect of some enzymes on the agglutinability of human erythrocytes by non-hemagglutinating bacterial strains was studied.

Agglutination Tests↗
PubMed1986

Role of sialic acid in cell receptors for vesicular stomatitis virus.

The role of sialic acid in the receptors for vesicular stomatitis virus (VSV) was investigated by treating chick embryo related (CER) cells and goose erythrocytes with neuraminidases from different sources and studying the effects produced on both infection and haemagglutination. The virus attachment to CER cells was reduced by their treatment with C. perfringens and A. ureafaciens neuraminidases and the susceptibility to viral infection of desialylated CER cells was recovered by coating with gangliosides immediately after enzymatic treatment. By contrast, enzymatic treatment of goose erythrocytes enhanced their agglutinability by VSV. The experiments carried out to test the ability of sialoglycolipids (gangliosides) and asialoglycolipids (cerebrosides) to inhibit virus attachment to CER cells or to goose erythrocytes showed that only gangliosides were able to inhibit VSV infection and haemagglutination.

Animals↗
PubMed1986

Study of receptors for vesicular stomatitis virus in vertebrate and invertebrate cells.

Early interactions between vesicular stomatitis virus (VSV) and susceptible cells were examined in cell lines of mammalian (HeLa), bird (CER), piscine (EPC) and arthropod (Aedes albopictus) origin showing different permissiveness to VSV growth. The chemical nature of receptors was investigated either by modification of cell surfaces with different enzymes or by competition for VSV binding between extracted membrane components and whole cells. Results obtained indicate that in all cell models, membrane lipid components show receptor activity whereas glycid groups participate to the in virus binding to a different extent.

Aedes↗
PubMed1985

E. coli adherence to CER cells infected by vesicular stomatitis virus.

Research was carried out on the adherence of a mannose-resistant uropathogenic E. coli strain to CER cells infected with vesicular stomatitis virus (vsv). A decrease in the bacterial adhesion was noticed during the early phases of viral infection, probably due to a close relationship between cell receptors for VSV and E. coli, both containing glycolipids and phospholipids. In a later phase of viral infection, on the contrary, corresponding to the appearance on the cell surface of newly synthesized viral antigens, bacterial adherence was enhanced. This last observation suggested a possible predisposition of the host to bacterial colonization during renal viral infection.

Adhesiveness↗
PubMed1985

Gangliosides in early interactions between vesicular stomatitis virus and CER cells.

In the present report an attempt was made to elucidate the role of gangliosides in early interactions between vesicular stomatitis virus (VSV) and CER cells. Research was carried out to test the ability of gangliosides from mammal brains and from CER cells to inhibit viral attachment to susceptible cells. The incubation of VSV in the presence of gangliosides decreased the subsequent infection of CER cells by the virus. When similar experiments were performed with gangliosides inserted in liposomes the inhibition of infection was enhanced. Since carbohydrate moieties could participate to rhabdovirus binding as a part of a glycolipid receptor, CER cells were subjected to the action of glycosidases and these produced a fall in the viral attachment. Deglycosilated CER cells reacquired their susceptibility to virus infection after coating with gangliosides immediately after enzyme treatment. Results obtained show the participation of gangliosides in the receptorial structure for vesiculovirus of susceptible CER cells.

Animals↗
PubMed1985

Effect of amantadine on rhabdovirus infection.

Enveloped viruses enter host cells by fusion or viropexis. The latter mechanism is the prevalent entry pathway of rhabdoviruses into susceptible cells. Amantadine, a lysosomotropic agent, inhibits the multiplication of various groups of viruses. The effect of this drug was investigated on vesicular stomatitis virus and rabies fixed virus strain replication in fibroblasts. Amantadine was added to cells before, during and after infection to detect the phase of viral replication affected by the drug. Cells were inoculated with viruses at 4 degrees C and the incubation temperature was progressively raised to 37 degrees C in order to observe the effect of amantadine on attachment and early stages of viral replication. Experimental results indicated that the compound inhibited rhabdovirus infection in CER cells. Viral attachment and penetration did not appear to be affected by the drug, while later steps were inhibited, probably at the level of uncoating when the virus is released from the lysosomes into the intracytoplasmic compartment.

Amantadine↗