Peripheral blood mononuclear cells PBMCs were isolated from patients and stimulated with various bacterial stimuli. Infection by H1N1 was accompanied by an increase of monocytes. PBMCs of patients evoked strong cytokine production after stimulation with most of bacterial stimuli. Defective cytokine responses were shown in response to stimulation with phytohemagglutin and with heat-killed Streptococcus pneumoniae. Macrolides could mediate this effect by inhibiting intracellular hemagglutinin HA0 proteolysis.
The inhibitory effect on influenza virus replication of macrolides has been known since the 80s [ 50 - 54 ]. N-acetylcysteine NAC is a thiol-containing compound which non-enzymatically interacts and detoxifies reactive electrophiles and free radicals. NAC has already been shown to effectively protect human bronchial fibroblasts against the toxic effects of tobacco smoke condensates and the isolated perfused lung against the glutathione GSH -depleting effect of tobacco smoke.
NAC has also been demonstrated to reduce the reactive oxygen intermediate hydrogen peroxide H 2 O 2 and to confer protection from the toxic effects of H 2 O 2. In vivo studies, however, have demonstrated that orally administered NAC has very low bioavailability due to its rapid metabolism mainly to GSH but also other metabolites. Thus, even though NAC is very effective in protecting cells of different origins from the toxicity of reactive components in tobacco smoke and reactive oxygen species, a direct scavenging effect by NAC in vivo, does not seem likely.
This holds especially true for oral administration. A more relevant mechanism in vivo for any protective effect of NAC may be attributable to its activity as a precursor of GSH, thereby facilitating its biosynthesis. GSH will then serve as the protective agent and detoxify reactive species both enzymatically and non-enzymatically [ 55 , 56 ]. Finally, the efficacy of vaccination for H1N1 has been documented by assessing antibody formation in the vaccinated elderly subjects from the pandemic in contrast to the younger ones who were not vaccinated.
Nonetheless, antibodies from older subjects previous encounter with pandemic influenza A strains may be a confounding factor [ 57 ]. This study has a number of limitations. First, our patient series was small, but it should be borne in mind that since these H1N1 positive patients represent a population of Furthermore, diagnostic tests with procalcitonine, urine antigen and blood cultures were given only upon suspicion of an infection.
The respiratory capacity tests represented a small number of patients in each group, and so no correlations could be preformed between the four subgroups. In addition, the baseline condition of each patient was not evaluated; this was either because they did not have a respiratory underlying condition or because they were patients that admitted in our hospital for the first time. Respiratory capacity differed between categories of patients at least for the first three months of observation, probably due to the inflammatory factors that are released with the influenza A H1N1 infection and underlying disease.
Importantly, the respiratory inflammation lasted almost two months, as evidenced by the fact that respiratory capacity remained stable between the second and third measurement. Several treatment modalities can be administered to confer protection and suppress the inflammation. Vaccination and early treatment with antiviral agents represent the mainstay of management.
All authors read and approved the manuscript. The authors would like to thank their colleagues in the Unit of Infectious Diseases in the University Hospital of Alexandroupolis, Greece. National Center for Biotechnology Information , U. Journal List Virol J v.
Virol J. Published online Jun Author information Article notes Copyright and License information Disclaimer. Corresponding author. Paul Zarogoulidis: moc. Received Jun 6; Accepted Jun This article has been cited by other articles in PMC.
Abstract Background The first case of pandemic influenza A H1N1 virus infection was documented in our Hospital on 10th August Metdods and findings Real-time reverse-transcriptase-polymerase-chain-reaction RT-PCR testing was used to confirm the diagnosis.
Conclusions An improvement of pulmonary function tests was observed between the first two measurements, implicating an inflammatory pathogenesis of influenza A H1N1 to the respiratory tract.
Introduction The first human infections with the new influenza A H1N1 virus were confirmed in April in America, but the infection had been rapidly spreading around the world and in June World Health Organization WHO declared a pandemic [ 1 - 5 ].
Patients and methods Methods of establishing H1N1 and precaution measures Pharyngeal or nasopharyngeal swabs were taken upon admission in accordance with the protocol from the U. Results Mean patient age was 36 years Table 1 Patients characteristics.
Open in a separate window. Figure 1. Table 2 Statistical findings as mean values between follow ups. Conclusions Respiratory capacity differed between categories of patients at least for the first three months of observation, probably due to the inflammatory factors that are released with the influenza A H1N1 infection and underlying disease. Conflicts of interests The authors declare that they have no competing interests.
Acknowledgements The authors would like to thank their colleagues in the Unit of Infectious Diseases in the University Hospital of Alexandroupolis, Greece. Pandemic H1N1 update ECDC influenza surveillance group; national coordinators for influenza surveillance.
Initial surveillance of influenza A H1N1 pandemic in the european union and European economic area, April-September Euro Surveill. A new pandemic influenza A H1N1 genetic variant predominated in the winter influenza season in Australia, New Zealand and Singapore.
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N Engl J Med. Characterization of the influenza virus polymerase genes. Risk factors for disease severity among hospitalized patients with pandemic influenza A H1N1 in spain, April-December National surveillance of pandemic influenza A H1N1 infection-related admissions to intensive care units during the winter peak in Denmark: two complementary approaches.
Are there any differences in clinical and laboratory findings on admission between H1N1 positive and negative patients with flu-like symptoms? BMC Res Notes. A new common mutation in the hemagglutin of the H1N1 influenza A virus.
PLoS Curr. Oseltamivir-resistant influenza viruses circulating during the first year of the influenza A H1N1 pandemic in the Asia-Pacific region, March to March The pandemic influenza virus's ability to stick to the additional receptors may explain why the virus replicates and spreads between cells more quickly: if a flu virus can bind to more than one type of receptor, it can attach itself to a larger area of the respiratory tract, infecting more cells and causing a more serious infection.
Professor Ten Feizi, a corresponding author of today's paper from the Division of Medicine at Imperial College London, said: "Most people infected with swine-origin flu in the current pandemic have experienced relatively mild symptoms. However, some people have had more severe lung infections, which can be worse than those caused by seasonal flu. Our new research shows how the virus does this - by attaching to receptors mostly found on cells deep in the lungs.
This is something seasonal flu cannot do. The researchers found that pandemic H1N1 influenza bound more weakly to the receptors in the lungs than to those in the upper respiratory tract. This is why most people infected with the virus have experienced mild symptoms.
However, the researchers are concerned that the virus could mutate to bind more strongly to these receptors. We think scientists should be on the lookout for these kinds of changes in the virus so we can try to find ways of minimising the impact of such changes," added Professor Feizi.
The researchers compared the way seasonal and pandemic H1N1 flu viruses infect cells by identifying which receptors each virus binds to. To do this, the researchers used a glass surface with 86 different receptors attached to it, called a carbohydrate microarray.
When viruses were added to the glass surface, they stuck to their specific receptors and the corresponding areas on the plate 'lit up'.
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