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At least 19 recordsLinked to original sources
PubMed2004

Differential expression of sialylglycoconjugates and sialidase activity in distinct morphological stages of Fonsecaea pedrosoi.

The expression of sialoglycoconjugates in Fonsecaea pedrosoi conidia, mycelia, and sclerotic cells was analyzed using influenza A and C virus strains, sialidase treatment, and lectin binding. Conidium and mycelium whole cells were recognized by Limax flavus (LFA), Maackia amurensis (MAA), and Sambucus nigra (SNA) lectins, denoting the presence of surface sialoglycoconjugates containing alpha 2,3- and alpha 2,6-sialylgalactosyl sequences. Sialidase-treated conidia reacted more intensively with peanut agglutinin (PNA), confirming the occurrence of sialyl-galactosyl linkages. Conidial cells agglutinated in the presence of influenza A and C virus strains, which confirmed the results obtained from lectin-binding experiments and revealed the presence of sialoglycoconjugates bearing 9-O-acetyl-N-acetylneuraminic acid (Neu5,9Ac(2)) surface structures. Western blotting analysis with peroxidase-labeled LFA demonstrated the occurrence of sialylglycoproteins in protein extracts from conidia and mycelia, with molecular masses corresponding to 56 and 40 kDa. An additional band of 77 kDa was detected in conidial extracts, suggesting an association between sialic acid expression and morphogenesis. Synthesis of sialic acids was correlated with sialidase expression, since both conidial and mycelial morphological stages presented secreted and cell-associated enzyme activity. Sialoglycoconjugates were not detected in F. pedrosoi sclerotic cells from in vitro and in vivo sources, which also do not express sialidase activity. The surface sialyl residues in F. pedrosoi are apparently involved in the fungal interaction with immune effector cells, since sialidase-treated conidia were less resistant to phagocytosis by human neutrophils from healthy individuals. These findings suggest that sialic acid expression in F. pedrosoi varies according to the morphological transition and may protect infecting propagules against immune destruction by host cells.

Ascomycota↗
PubMed2003

Kinetics of influenza virus fusion with the endosomal and plasma membranes of cultured cells. Effect of temperature.

We performed a detailed kinetic analysis of influenza virus fusion with the endosomal and plasma membranes of Madin Darby canine kidney (MDCK) cells and provided a comparison of the kinetic parameters obtained for both cases at 20 degrees C and 37 degrees C. Using our mass action kinetic model, we determined that the fusion rate constant, f, for influenza virus with the endosomal membrane was 0.02 s(-1) at 37 degrees C and 0.0035 s(-1) at 20 degrees C. The analysis of the fusion kinetics of influenza virus with the plasma membrane yielded that the fusion rate constants were close to those deduced with the endosomal membrane. The systematic kinetic analysis performed in this study provides for the first time a biophysical support for studies on influenza virus-cell fusion where the acidic endosomal internal environment is simulated artificially by lowering the pH of the medium.

Animals↗
PubMed2002

Role of influenza A virus hemagglutinin in neurovirulence for mammalians.

Influenza viruses with potential neuroinvasiveness for humans emerged in Hong Kong in 1997. Prophylactic and therapeutic strategies are urgently needed for controlling the central nervous system complications caused by influenza. Here we review recent advances toward understanding of the possible mechanisms of the neuropathogenesis of influenza virus infection, especially focusing on the role of viral hemagglutinin glycoprotein.

Adolescent↗
PubMed2004

The association between life events, social support, and antibody status following thymus-dependent and thymus-independent vaccinations in healthy young adults.

This study determined whether stressful life events and social support were related to antibody status following both thymus-dependent and thymus-independent vaccinations. Life events in the previous year and customary social support were measured in 57 healthy students at baseline. Antibody status was also assessed at baseline and at five weeks and five months following vaccination with the trivalent influenza vaccine and the meningococcal A+C polysaccharide vaccine. Taking into account baseline antibody titre, high life events scores prior to vaccination were associated with lower responses to the B/Shangdong influenza strain at both five weeks and five months and meningococcal C at five weeks. Life event scores were not associated with response to the other two influenza viral strains nor response to meningococcal A. Those with high social support scores had stronger 5-week and 5-month antibody responses to the A/Panama influenza strain, but not to any of the other strains. These associations could not be accounted for by demographic or health behaviour factors, and also emerged from analyses comparing those who exhibited a fourfold increase in antibody titre from baseline with those who did not. Life events and social support were related to antibody status following influenza vaccination in distinctive ways that may be partly determined by vaccine novelty and prior naturalistic exposure. Life events also predicted poor antibody response to meningococcal C polysaccharide vaccination after previous meningococcal C conjugate vaccination. Neither psychosocial factor was associated with response to primary meningococcal A polysaccharide vaccination.

Adult↗
PubMed2006

Effects of rutin and quercetin on monooxygenase activities in experimental influenza virus infection.

The aim of this work is to study the effect of the flavonoids rutin and quercetin on hepatic monooxygenase activities in experimental influenza virus infection (EIVI). EIVI causes oxidative stress in the whole organism. This is confirmed by the rapidly increased concentrations of thiobarbituric reactive substances in influenza-infected mice: lungs - 290%; blood plasma - more than 320%; liver - 230%; brain - 50%. Although known for their antioxidant activities, rutin and quercetin exhibit prooxidant effect in healthy and antioxidant activity in influenza-infected animals. The pretreatment with both flavonoids (20 mg/kg b.w.) restores oxidative damage mostly in the target organ of the infection as well as in the liver of all infected mice (lungs: rutin - 30%, quercetin - 40%, combination - 45%; liver: rutin - 12%; quercetin - 40%; combination - 50%). As far as EIVI causes oxidative stress, toxicosis and inhibition of the hepatic monooxygenase activity, it is important to study the effects of rutin and quercetin on these systems. Both flavonoids induce the level of cytochrome P-450 (rutin - 13%, quercetin - 30%, combination - 22%) but inactivate NADPH-cytochrome c reductase, aminopyrine N-demethylase and analgin N-demethylase on the 5th day of EIVI. Probably, these flavonoids affect different components of the monooxygenase system. These effects could be explained with oxidative hepatic intoxication on the 5th critical day of EIVI as well as higher dose treatment. More data are needed on the antioxidant/prooxidant effects of rutin and quercetin, probably due to specific metabolic and physiological activities, chemical structure, etc.

Animals↗
PubMed2002

Induction of proinflammatory cytokines in human macrophages by influenza A (H5N1) viruses: a mechanism for the unusual severity of human disease?

BACKGROUND: In 1997, the first documented instance of human respiratory disease and death associated with a purely avian H5N1 influenza virus resulted in an overall case-fatality rate of 33%. The biological basis for the severity of human H5N1 disease has remained unclear. We tested the hypothesis that virus-induced cytokine dysregulation has a role. METHODS: We used cDNA arrays and quantitative RT-PCR to compare the profile of cytokine gene expression induced by viruses A/HK/486/97 and A/HK/483/97 (both H5N1/97) with that of human H3N2 and H1N1 viruses in human primary monocyte-derived macrophages in vitro. Secretion of tumour necrosis factor alpha (TNF alpha) from macrophages infected with the viruses was compared by ELISA. By use of naturally occurring viral reassortants and recombinant viruses generated by reverse genetic techniques, we investigated the viral genes associated with the TNF-alpha response. FINDINGS: The H5N1/97 viruses induced much higher gene transcription of proinflammatory cytokines than did H3N2 or H1N1 viruses, particularly TNF alpha and interferon beta. The concentration of TNF-alpha protein in culture supernatants of macrophages infected with these viruses was similar to that induced by stimulation with Escherichia coli lipopolysaccharide. The non-structural (NS) gene-segment of H5N1/97 viruses contributed to the increase in TNF alpha induced by the virus. INTERPRETATION: The H5N1/97 viruses are potent inducers of proinflammatory cytokines in macrophages, the most notable being TNF alpha. This characteristic may contribute to the unusual severity of human H5N1 disease.

Cells, Cultured↗
PubMed2002

Structural studies of the resistance of influenza virus neuramindase to inhibitors.

Zanamivir and oseltamivir, specific inhibitors of influenza virus neuraminidase, have significantly different characteristics in resistance studies. In both cases resistance is known to arise through mutations in either the hemagglutinin or neuraminidase surface proteins. A new inhibitor under development by Biocryst Pharmaceuticals, BCX-1812, has both a guanidino group, as in zanamivir, and a bulky hydrophobic group, as in oseltamivir. Using influenza A/NWS/Tern/Australia/G70C/75 (H1N9), neuraminidase variants E119G and R292K have previously been selected by different inhibitors. The sensitivity of these variants to BCX-1812 has now been measured and found in both cases to be intermediate between those of zanamivir and oseltamivir. In addition, the X-ray crystal structures of the complexes of BCX-1812 with the wild type and the two mutant neuraminidases were determined. The ligand is bound in an identical manner in each structure, with a rearrangement of the side chain of E276 from its ligand-free position. A structural explanation of the mechanism of resistance of BCX-1812, relative to zanamivir and oseltamivir in particular, is provided.

Acetamides↗
PubMed2004

Use of Oseltamivir to control influenza complications after bone marrow transplantation.

Influenza infection can be severe in bone marrow transplant (BMT) recipients. Although yearly epidemics occur worldwide, and a higher risk of complication is expected in these patients, few studies have addressed the impact of the new neuraminidase inhibitors in the prognosis of influenza after BMT. Influenza A or B infections were found in 39 of the 66 patients (59%) showing a positive nasal wash by DFA. Influenza A was diagnosed in 18 patients and influenza B in 23 patients; two patients were infected by influenza A and B with 84- and 90-day intervals between episodes, respectively. Of the 41 episodes (61%) of influenza A or B, 25 infections occurred during the spring and summer months. Oseltamivir was introduced within 48 h of symptoms appearing. Only two patients (5.1%) developed influenza pneumonia, and no patient died of influenza. A total of 22 patients (56.4%) acquired influenza before day +180 when preventive vaccination strategies are precluded owing to poor immunogenicity of the vaccine during this period. Oseltamivir proved to be safe and appears to have played an important role in the outcome of influenza infection in this population. The therapeutic and/or prophylactic benefits of Oseltamivir in BMT recipients remain to be demonstrated in randomized, prospective trials.

Acetamides↗
PubMed2006

Influenza A virus NS1 protein binds p85beta and activates phosphatidylinositol-3-kinase signaling.

Influenza A virus NS1 is a multifunctional protein, and in virus-infected cells NS1 modulates a number of host-cell processes by interacting with cellular factors. Here, we report that NS1 binds directly to p85beta, a regulatory subunit of phosphatidylinositol-3-kinase (PI3K), but not to the related p85alpha subunit. Activation of PI3K in influenza virus-infected cells depended on genome replication, and showed kinetics that correlated with NS1 expression. Additionally, it was found that expression of NS1 alone was sufficient to constitutively activate PI3K, causing the phosphorylation of a downstream mediator of PI3K signal transduction, Akt. Mutational analysis of a potential SH2-binding motif within NS1 indicated that the highly conserved tyrosine at residue 89 is important for both the interaction with p85beta, and the activation of PI3K. A mutant influenza virus (A/Udorn/72) expressing NS1 with the Y89F amino acid substitution exhibited a small-plaque phenotype, and grew more slowly in tissue culture than WT virus. These data suggest that activation of PI3K signaling in influenza A virus-infected cells is important for efficient virus replication.

Amino Acid Substitution↗
PubMed2001

Independent and synergistic effects of interleukin-18 and interleukin-12 in augmenting cytotoxic T lymphocyte responses and IFN-gamma production in aging.

Aged mice exhibit diminished CD8(+) cytotoxic T lymphocyte (CTL) response to influenza virus. Previously, interleukin-12 (IL-12) was shown to partially restore in vitro influenza virus-specific CD8(+) CTL activity and interferon-gamma (IFN-gamma) production in aged mice. The present study investigated IL-18 production and its ability to collaborate with IL-12 to enhance these responses to the levels of young mice. IL-18 protein production and mRNA expression in influenza virus-specific CTL from aged mice were higher than from young mice. In contrast, IL-18 receptor (IL-18R) mRNA expression was significantly reduced in CD8(+) CTL from aged mice. Generation of CTL in the presence of IL-12 alone caused a significant increase in IFN-gamma production in both old and young mice. IL-18 treatment alone significantly increased IFN-gamma in CTL from young but not old mice. However, a combination of IL-18 and IL-12 significantly increased IFN-gamma in both old and young mice. IL-18 and IL-12, either alone or in combination, stimulated significant influenza virus-specific cytotoxicity in both old and young mice, but no significant synergistic effect was observed. These results represent an initial demonstration of downregulated IL-18R expression in aging mice and are consistent with age-related cytotoxic T lymphocyte 1 (Tc1) deficiency. Potentially, IL-18 and IL-12 can augment IFN-gamma production and reverse CD8(+) CTL deficiency in aging, independently or synergistically.

Aging↗