Abstract:SUMMARY:Gastroenteritis, arthralgaia and myalgia are frequently associated with influenza virus infections in humans.One explanation for these symptoms may be extrarespiratory transmission of virus by peripheral blood mononuclear cells (PBMC). We tried to detect genomic viral RNA of the nucleoprotein (NP) and H3 subtype hemagglutinin (HA) genes by the method of RT-PCR in PBMC of 18 children aged 1-14 who sufferred from an influenza outbreak in the Kansai district of Japan between December 1992 and February 199… Show more
“…A number of studies searching for influenza viremia after the onset of illness have failed to detect virus, supporting the notion that influenza viremia is at most a rare event in the post-symptomatic period and if it exists, it is not generally sustained for long periods. However, recent studies employing highly sensitive PCR suggested transient viremia before onset of respiratory is not rare 33,34…”
Problem
Epidemiological data suggested that pandemic influenza increased the risks of spontaneous abortion and premature labor, while seasonal influenza also increased the risk of schizophrenia in adolescence. However, their pathogenesis is so far unknown.
Method of study
The first trimester trophoblast cell lines, namely, Swan71 and HTR8 cells were challenged with A/Udorn/72 influenza virus (H3N2). At indicated time points, cells were examined for expression of influenza proteins. Viral replication in culture media, apoptosis and the expression of human leukocyte antigen (HLA)-G were also examined.
Results
Intracellular localization of viral proteins was observed. Twenty-four hours after inoculation, virus was detected in culture media while most cells fell into apoptosis. During apoptosis, expression of HLA-G was unchanged.
Conclusion
We revealed replication of low pathogenic influenza virus in the first trimester trophoblast cell lines. Placental damages are likely to be induced by direct cytopathic effects of influenza virus and subsequent apoptosis rather than down regulation of HLA-G expression and subsequent rejection by maternal immune system.
“…A number of studies searching for influenza viremia after the onset of illness have failed to detect virus, supporting the notion that influenza viremia is at most a rare event in the post-symptomatic period and if it exists, it is not generally sustained for long periods. However, recent studies employing highly sensitive PCR suggested transient viremia before onset of respiratory is not rare 33,34…”
Problem
Epidemiological data suggested that pandemic influenza increased the risks of spontaneous abortion and premature labor, while seasonal influenza also increased the risk of schizophrenia in adolescence. However, their pathogenesis is so far unknown.
Method of study
The first trimester trophoblast cell lines, namely, Swan71 and HTR8 cells were challenged with A/Udorn/72 influenza virus (H3N2). At indicated time points, cells were examined for expression of influenza proteins. Viral replication in culture media, apoptosis and the expression of human leukocyte antigen (HLA)-G were also examined.
Results
Intracellular localization of viral proteins was observed. Twenty-four hours after inoculation, virus was detected in culture media while most cells fell into apoptosis. During apoptosis, expression of HLA-G was unchanged.
Conclusion
We revealed replication of low pathogenic influenza virus in the first trimester trophoblast cell lines. Placental damages are likely to be induced by direct cytopathic effects of influenza virus and subsequent apoptosis rather than down regulation of HLA-G expression and subsequent rejection by maternal immune system.
“…22 These observations raise the possibility that antigenic cross-reactivity between influenzaspecific epitopes and resident plaque epitopes can develop within the microenvironment of an inflamed plaque. Such a mechanism of antigenic cross-reactivity is not uncommon in the course of longstanding chronic inflammatory processes, but apart from epitope mimicry, it cannot be ruled out that influenza A virus had been present in the plaques but later disappeared, eg, by eradication through the elicited inflammatory response.…”
Background and Purpose-Evidence is accumulating that infection with influenza A virus contributes to atherothrombotic disease. Vaccination against influenza decreases the risk of atherosclerotic syndromes, indicating that inflammatory mechanisms may be involved. We tested the hypothesis that influenza A virus-specific T cells contribute to atherosclerotic plaque inflammation, which mediates the onset of plaque rupture. Methods-T-cell cultures were generated from atherosclerotic segments and peripheral blood of 30 patients with symptomatic carotid artery disease. The response of plaque and peripheral blood T cells to influenza A virus was analyzed and expressed as a stimulation index (SI). Selective outgrowth of intraplaque influenza A-specific T cells was calculated by the ratio of plaque T cell SI and peripheral blood T cell SI for each patient. Accordingly, the patients were categorized as high-(SI ratio Ն5), intermediate-(5 ϽSI ratio Յ2), and non-(SI ratio Ͻ2) responders. The presence of influenza A virus in the vessel fragments was evaluated by reverse transcription-polymerase chain reaction.
Results-High proliferative responses of plaque-derived T cells to influenza
“…The serum level of IL‐6 is also higher in patients with acute influenza virus‐induced encephalopathy. 20 Furthermore, hyperactivated coagulation factors associated with DIC can participate in the pathogenesis. 21,22 …”
The pathologic change induced by the direct viral invasion cannot be responsible for all of the symptoms, especially for the rapid and severe clinical course of the disease within 24-48 h after the initial respiratory symptoms. Together with the rapid production of several inflammatory cytokines, the breakdown of the blood-brain barrier may induce severe brain edema and can be a major pathologic change for the disease. Any therapeutic strategy to control this multistep progression of the disease could be effective.
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