[Prevention and treatment of influenza].
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Humans↗
Biomedical subjects
M Degré
Publications and source records attributed to M Degré.
Coxsackie B1 virus-induced changes in cell membrane-associated functions are not responsible for altered sensitivity to bacterial invasiveness.
To analyze the possible mechanisms by which coxsackie B1 virus infection affects the invasiveness of Shigella flexneri, we have studied the influence of intracellular levels of Na+ and K+, ATPase activity, cytoplasmic membrane potential, cAMP level and cell communication through gap junctions. 3h after adsorption of viable or UV-inactivated coxsackie B1 virus the Na(+)-K+ gradient of the cell collapsed, ATPase activity decreased, the cytoplasmic membranic potential-dependent tetraphosphonium ion uptake were reduced. No changes in cAMP or intercellular cell communication were observed. S. flexneri invasiveness in HEp-2 cell pretreated with viable or UV-inactivated coxsackie B 1 virus was enhanced, but bacterial invasiveness was unchanged in K(+)-depleted HEp-2 cells, cell cultures with high intracellular Na+ content or ouabain pre-treated cells compared to control cells. We found no correlation between the enhanced bacterial invasiveness in the early phase of coxsackie B 1 virus infection in HEp-2 cell cultures and intracellular K+ depletion, high intracellular Na+ content, inhibited Na(+)-K+ ATPase activity or membranic depolarization.
Cell Communication↗
Correlation between Coxsackie B1 virus replication and enhanced invasiveness of Shigella flexneri.
Coxsackie B1 virus infection enhances the susceptibility of cultured HEp-2 cells to Shigella flexneri invasiveness. This can be reproduced partially with UV-inactivated virus, particularly the effect observed shortly after viral inoculation. The following phases of viral multiplication were correlated with the enhancing effect: uncoating of viral particles, synthesis of viral RNA and proteins, and assembly of newly produced virus particles. Uncoating of virus particles was completed within 60 min. This process was not correlated with the development of the early effect on invasiveness. Intact virus capsids seem to be necessary to enhance bacterial invasiveness in the early phase of virus infection. Separated capsid proteins had no effect either when applied to the cell surface or when microinjected into the cells. Virus protein synthesis was not required for the virus effect on bacterial invasiveness in the early infection phase, but it seems to be necessary in the late phase.
Cells, Cultured↗
Interferon-gamma may enhance infection of blood-derived macrophages with HIV-1 in the presence of HIV-positive serum.
HIV multiplication in blood-derived macrophages was slightly inhibited by pretreatment of cells with interferon-gamma or by preincubation of virus with serum containing antibodies against HIV. When these pretreatments were combined, the HIV titres observed a short time after infection were enhanced. This effect was blocked by antibodies against Fc receptors but not by antibodies against CD4 receptors. Interferon enhanced the expression of Fc receptors on macrophages. The results indicate that IFN-gamma, in appropriate combinations with HIV-antibody-containing human serum, may enhance the rate of HIV infection of macrophages.
Antibodies↗
Nonspecific oral immunity in individuals with HIV infection.
Lactoferrin, lysozyme, interferon, and neopterin levels were determined in parotid saliva from 44 individuals with different clinical stages of human immunodeficiency virus (HIV) infection and 19 HIV-seronegative controls. The secretory output of individual components was calculated according to the fluid flow rate. No parotid interferon activity was found in any of the HIV-infected subjects or controls, and no significant differences in parotid lysozyme or neopterin outputs were observed. The lactoferrin output was significantly decreased in HIV-seropositive subjects in parallel with their markedly reduced parotid secretory IgA output. This combined deficiency of parotid lactoferrin and secretory IgA may well contribute to the frequent oral infections seen in subjects with HIV infection.
Adult↗
[Diagnosis of cytomegalovirus infections in hospitalized patients].
Rapid detection of cytomegalovirus (CMV) infections, especially in immunocompromised patients, is important and sometimes lifesaving. We describe one year's experience of using a combination of several methods: detection of "immediate early" CMV antigen in blood, detection of "early" virus antigen after brief incubation in cell culture, detection of viral DNA by polymerase chain reaction, regular culture in human embryo fibroblasts, and serological detection of IgM and IgG antibodies. A quick and early diagnosis was achieved by all three rapid methods. However, none of the methods is sufficiently sensitive or specific to allow it to be used alone. A combination of several methods is recommended in order to achieve maximum efficiency and safety.
Cytomegalovirus Infections↗
[Antiviral agents for the systemic treatment of herpesvirus infections].
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Acyclovir↗
[Virologic rapid diagnosis].
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Antibodies, Viral↗
Microinjected Coxsackie B1 virus does not replicate in HEp-2 cells.
Coxsackie B1 virus did not replicate when microinjected into HEp-2 cells. Replication was assayed by production of infectious virus particles, synthesis of viral RNA, and lysis of cells. The same virus preparation initiated replication when it was inoculated into HEp-2 cells similarly to that by microinjected purified coxsackie B1 virus RNA.
Cell Death↗
Effect of interferon treatment on expression of gC and gE glycoproteins in herpes simplex virus-infected cells.
The effect of interferon treatment on the herpes simplex virus type 1 (HSV-1)-specific glycoproteins gC and gE in homologous and heterologous cells has been investigated. In human embryonic fibroblastic cells, human leukocyte interferon inhibited virus multiplication and expression of the HSV-1-specific glycoproteins gC and gE on the cell surface in a dose-dependent manner. In heterologous baby hamster kidney cells, the human interferon had no effect on virus multiplication. However, the surface expression of the HSV-1-specific glycoproteins was reduced, as shown by erythrocyte rosette formation, by attachment of monodisperse polystyrene particles coated with antibodies and by immunogold scanning electron microscopy.
Antigens, Viral↗
Tumor necrosis factor production by human granulocytes.
Human polymorphonuclear leukocytes kill WEHI 164 cells in an 18-hour 51Cr release assay. Antibody to human tumor necrosis factor (TNF) blocks the lysis of targets mediated by human granulocytes. Resting granulocytes produce an undetectable amount of TNF, if any. Granulocytes stimulated with Staphylococcus aureus release 250-500 U/ml TNF alpha. The specificity of the released TNF in the WEHI 164 cytotoxicity assay was confirmed by using neutralizing anti-TNF alpha monoclonal antibodies. The thymidine uptake of endothelial cells was inhibited by granulocyte-derived TNF. The identity of TNF alpha was further confirmed by molecular weight determination, by gel filtration on Sephacryl S-200, with a result of approximately 44,000. Besides their antimicrobial capacity, therefore, granulocytes may contribute to tumor rejection, inflammation and septic infections by releasing TNF.
Animals↗
Prevalence of antibodies against parvovirus B19 in Norwegians with congenital coagulation factor defects treated with plasma products from small donor pools.
The seroprevalence of antibodies against parvovirus B19 in 308 Norwegians with coagulation factor defects of different types and severities was assessed by an IgG antibody capture radioimmunoassay (GACRIA). The overall seroprevalence was 62%. The seroprevalence among subjects with different types of coagulation factor defects was related to the type and severity of the coagulation factor defect: severe hemophilia A 64%, moderate and mild hemophilia A 58%, severe hemophilia B 88%, moderate and mild hemophilia B 73%, and von Willebrand's disease 52%. The prevalence of parvovirus B19 antibodies among household contacts and blood donors was 49% and 42% respectively. This study confirms that replacement therapy with coagulation factors is accompanied by an increased risk for acquiring parvovirus B19 infection. However, the prevalence of parvovirus B19 antibodies among Norwegian hemophiliacs is well below the prevalence reported from other countries and probably reflects the small numbers of donors in plasma pools used for the preparation of coagulation factor concentrates.
Adult↗
[Latent and activated viral infections].
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Humans↗
Immunogenicity of yeast-derived hepatitis B vaccine from two different producers.
The immunogenicity and reactogenicity of two preparations of yeast-derived hepatitis B vaccines were compared in healthy adult populations. The two groups were vaccinated in parallel, but they were not matched for age and sex. All subjects seroconverted, and 9 months after the first vaccine dose, all had anti HBs titres of at least 10 IU/l. The anti-HBs titres were higher in the group of subjects given 20 micrograms vaccine antigen made by Smith Kline & RIT (GMT 2943 at 9 months) compared to those who received 10 micrograms of vaccine made by Merck, Sharp & Dohme (GMT 729 at 9 months). Adverse effects were recorded in 32.0 and 44.7% of the participants, but these were limited to minor local and general reactions. In the present study both preparations were safe and efficient.
Adult↗
Interferon treatment reduces endocytosis of virus and facultatively intracellular bacteria in various cell lines.
Previous studies have shown that interferons (IFNs) specifically interact with a number of cells cultured in vitro and reduce the invasiveness of facultatively intracellular bacteria. IFN treatment also reduced the internalization of vesicular stomatitis virus (VSV) in cell cultures. Here we show that the anti-invasive effect of IFN on bacteria is eliminated in an L-cell variant where its effect on the uptake of vesicular stomatitis virus is lost. The data strongly suggest that the anti-invasive effect of IFN is mediated through inhibition of endocytosis.
Animals↗
Coxsackie B1 virus infection enhances the bacterial invasiveness, the phagocytosis and the membrane permeability in HEp-2 cells.
To analyze the effect of coxsackie B1 virus infection on bacterial invasiveness, phagocytosis and cytoplasma membrane permeability, we have studied invasiveness of Shigella flexneri, unspecific phagocytosis of latex particles and release of the non-metabolizible amino acid, alpha-aminoisobutyric acid (AIB). Virus infection enhanced invasiveness of S. flexneri and phagocytosis of latex beads and increased plasma membrane permeability as measured by release of AIB. The effect on all three functions increased with virus concentration, but the kinetics were different. During the early phase of virus infection there was no difference between the effect on invasiveness, phagocytosis and permeability in cell cultures pretreated with viable or with UV-inactivated virus. However, after 6 h, 5 h and 2 h respectively, there was an increased response in cell cultures pretreated with viable virus compared to cells inoculated with UV-inactivated virus. The results indicate that the virus effect on bacterial invasiveness is a function of several parameters, including phagocytosis and membrane function changes.
Cell Line↗
Lack of activity of fusidic acid against human immunodeficiency virus in monocytes.
The effect of fusidic acid on the multiplication of human immunodeficiency virus in monocyte-derived macrophages was examined in in vitro cultures. Virus titers, measured by reverse transcriptase and by p24 antigen in the supernatants and in lysed cells, were reduced in some experiments by 50 micrograms/ml or more; in other experiments, 10 micrograms of fusidic acid per ml added to the cells simultaneously with the virus inoculation reduced virus titers. The effect was comparable in peripheral blood lymphocytes. The drug was generally toxic to the cells, both macrophages and peripheral blood lymphocytes, in concentrations of 50 micrograms/ml or more.
Fusidic Acid↗
Involvement of tumor necrosis factor in human granulocyte-mediated killing of WEHI 164 cells.
Human polymorphonuclear leukocytes (PMNLs) kill WEHI 164 clone 13 cells in an 18-hour 51Cr release assay. Antibody to human tumor necrosis factor (TNF) blocks the lysis of targets mediated by human granulocytes. PMNLs triggered by sensitive targets not only displayed cytotoxic activity, but also released a soluble factor capable of selectively lysing WEHI 164 cells. The killing of these cells by supernatants of triggered granulocytes was totally inhibited by anti-TNF antibody. These experiments suggest that the killing of WEHI 164 sarcoma cells by human PMNLs involves TNF or TNF-like molecules.
Antigen-Antibody Reactions↗