scholarly journals Evidence of Cross-Reactive Immunity to 2009 Pandemic Influenza A Virus in Workers Seropositive to Swine H1N1 Influenza Viruses Circulating in Italy

PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e57576 ◽  
Author(s):  
Maria A. De Marco ◽  
Stefano Porru ◽  
Paolo Cordioli ◽  
Bruno M. Cesana ◽  
Ana Moreno ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Pandemic Influenza ◽  
Influenza A ◽  
H1n1 Influenza ◽  
Influenza Viruses

scholarly journals Contemporary Seasonal Influenza A (H1N1) Virus Infection Primes for a More Robust Response To Split Inactivated Pandemic Influenza A (H1N1) Virus Vaccination in Ferrets

2010 ◽  
Vol 17 (12) ◽  
pp. 1998-2006 ◽  
Author(s):  
Ali H. Ellebedy ◽  
Thomas P. Fabrizio ◽  
Ghazi Kayali ◽  
Thomas H. Oguin ◽  
Scott A. Brown ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Pandemic Influenza ◽  
Influenza A ◽  
Seasonal Influenza ◽  
H1n1 Virus ◽  
H1n1 Influenza ◽  
Influenza Viruses ◽  
Inactivated Vaccine ◽  
H1n1 Influenza Virus ◽  
Influenza A H1n1

ABSTRACT Human influenza pandemics occur when influenza viruses to which the population has little or no immunity emerge and acquire the ability to achieve human-to-human transmission. In April 2009, cases of a novel H1N1 influenza virus in children in the southwestern United States were reported. It was retrospectively shown that these cases represented the spread of this virus from an ongoing outbreak in Mexico. The emergence of the pandemic led to a number of national vaccination programs. Surprisingly, early human clinical trial data have shown that a single dose of nonadjuvanted pandemic influenza A (H1N1) 2009 monovalent inactivated vaccine (pMIV) has led to a seroprotective response in a majority of individuals, despite earlier studies showing a lack of cross-reactivity between seasonal and pandemic H1N1 viruses. Here we show that previous exposure to a contemporary seasonal H1N1 influenza virus and to a lesser degree a seasonal influenza virus trivalent inactivated vaccine is able to prime for a higher antibody response after a subsequent dose of pMIV in ferrets. The more protective response was partially dependent on the presence of CD8+ cells. Two doses of pMIV were also able to induce a detectable antibody response that provided protection from subsequent challenge. These data show that previous infection with seasonal H1N1 influenza viruses likely explains the requirement for only a single dose of pMIV in adults and that vaccination campaigns with the current pandemic influenza vaccines should reduce viral burden and disease severity in humans.

scholarly journals Reassortants of pandemic influenza A virus H1N1/2009 and endemic porcine HxN2 viruses emerge in swine populations in Germany

2012 ◽  
Vol 93 (8) ◽  
pp. 1658-1663 ◽  
Author(s):  
Elke Starick ◽  
Elke Lange ◽  
Christian Grund ◽  
Elisabeth grosse Beilage ◽  
Stefanie Döhring ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Pandemic Influenza ◽  
Influenza A ◽  
Swine Influenza ◽  
Biological Properties ◽  
Influenza Viruses ◽  
West Germany ◽  
Virus H1n1 ◽  
North West ◽  
Synonymous Mutations

The incursion of the human pandemic influenza A virus H1N1 (2009) (H1N1 pdm) into pig populations and its ongoing co-circulation with endemic swine influenza viruses (SIVs) has yielded distinct human–porcine reassortant virus lineages. The haemagglutinin (HA) gene of H1N1 pdm was detected in 41 influenza virus-positive samples from seven swine herds in north-west Germany in 2011. Eight of these samples yielded virus that carried SIV-derived neuraminidase N2 of three different porcine lineages in an H1N1 pdm backbone. The HA sequences of these viruses clustered in two distinct groups and were distinguishable from human and other porcine H1 pdm by a unique set of eight non-synonymous mutations. In contrast to the human population, where H1N1 pdm replaced seasonal H1N1, this virus seems to co-circulate and interact more intensely with endemic SIV lineages, giving rise to reassortants with as-yet-unknown biological properties and undetermined risks for public health.

scholarly journals Epidemiological Surveillance of Influenza Virus Matrix Gene in Pigs, in Lagos, Nigeria, 2015-2016

2017 ◽  
Vol 2 (1) ◽  
pp. 1-7
Author(s):  
Abdul-Azeez A. Anjorin ◽  
Olumuyiwa B. Salu ◽  
Akeeb O.B. Oyefolu ◽  
Bamidele O. Oke ◽  
James B. Ayorinde ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Influenza A Virus ◽  
Pandemic Influenza ◽  
Influenza A ◽  
Virus Disease ◽  
Influenza Viruses ◽  
Epidemiological Surveillance ◽  
Viral Gene ◽  
Cross Sectional ◽  
Matrix Gene

AbstractThe co-infection of different influenza A virus enable viral gene re-assortments especially in pigs that serve as mixing vessel with the possibility of emergence of novel subtypes. Such re-assortants pose serious public health threat, as epitomised by the emergence of pandemic influenza in 2009. In Nigeria, there is mixture of animal species and highly populated densities that can increase the risk of influenza virus endemicity, genetic reshuffling and emergence of future pandemic influenza viruses. Thus, this study was aimed at determining influenza virus disease burden in pigs. This study was a cross sectional molecular surveillance of influenza virus. A total of 194 pig nasal samples from reported cases and randomly sampled were collected from pig farms in Ojo and Ikorodu in Lagos State between October, 2015 and April, 2016. The samples were investigated for the presence of influenza virus matrix gene by Reverse Transcriptase Polymerase Chain Reaction and detected by gel electrophoresis. P-values were calculated using Chi-square and Fisher’s exact tests. The result showed that 25 (12.9%) samples were positive for influenza A virus, out of which, 20 (80%) were samples from Ojo while 5 (20%) were samples from Ikorodu. Epidemiological parameters for the sampled locations, methods either as reported case or randomised, and sex compared were significant at 95% confidence interval. This study determined influenza viral burden in pigs with a molecular prevalence of 12.9% to influenza A. It further confirmed the sub-clinical and clinical circulation of Influenza A virus in pigs in Ojo and Ikorodu in Lagos. Therefore, the detection of influenza A virus in commercial pigs in Nigeria accentuates the importance of continuous surveillance and monitoring of the virus in order to prevent the advent of virulent strains that may spread to Pig-handlers and the community at large.

scholarly journals The PB2-E627K Mutation Attenuates Viruses Containing the 2009 H1N1 Influenza Pandemic Polymerase

mBio ◽  
2010 ◽  
Vol 1 (1) ◽  
Author(s):  
Brett W. Jagger ◽  
Matthew J. Memoli ◽  
Zong-Mei Sheng ◽  
Li Qi ◽  
Rachel J. Hrabal ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
H1n1 Virus ◽  
Influenza Pandemic ◽  
Influenza Infection ◽  
H1n1 Influenza ◽  
Influenza Viruses ◽  
Pandemic Virus ◽  
2009 H1n1 ◽  
Animal Reservoirs

ABSTRACTThe swine-origin H1N1 influenza A virus emerged in early 2009 and caused the first influenza pandemic in 41 years. The virus has spread efficiently to both the Northern and the Southern Hemispheres and has been associated with over 16,000 deaths. Given the virus’s recent zoonotic origin, there is concern that the virus could acquire signature mutations associated with the enhanced pathogenicity of previous pandemic viruses or H5N1 viruses with pandemic potential. We tested the hypothesis that mutations in the polymerase PB2 gene at residues 627 and 701 would enhance virulence but found that influenza viruses containing these mutations in the context of the pandemic virus polymerase complex are attenuated in cell culture and mice.IMPORTANCEInfluenza A virus (IAV) evolution is characterized by host-specific lineages, and IAVs derived in whole or in part from animal reservoirs have caused pandemics in humans. Because IAVs are known to acquire host-adaptive genome mutations, and since the PB2 gene of the 2009 H1N1 virus is of recent avian derivation, there exists concern that the pathogenicity of the 2009 H1N1 influenza A pandemic virus could be potentiated by acquisition of the host-adaptive PB2-E627K or -D701N mutations, which have been shown to enhance the virulence of other influenza viruses. We present data from a mouse model of influenza infection showing that such mutations do not increase the virulence of viruses containing the 2009 H1N1 viral polymerase.

scholarly journals Adaptation of Pandemic H1N1 Influenza Viruses in Mice

2010 ◽  
Vol 84 (17) ◽  
pp. 8607-8616 ◽  
Author(s):  
Natalia A. Ilyushina ◽  
Alexey M. Khalenkov ◽  
Jon P. Seiler ◽  
Heather L. Forrest ◽  
Nicolai V. Bovin ◽  
...  
Keyword(s):  
Amino Acid ◽  
Pandemic Influenza ◽  
Influenza A ◽  
H1n1 Influenza ◽  
Influenza Viruses ◽  
Mouse Lung ◽  
Mammalian Host ◽  
Influenza A Viruses ◽  
Receptor Specificity ◽  
Viral Receptor

ABSTRACT The molecular mechanism by which pandemic 2009 influenza A viruses were able to sufficiently adapt to humans is largely unknown. Subsequent human infections with novel H1N1 influenza viruses prompted an investigation of the molecular determinants of the host range and pathogenicity of pandemic influenza viruses in mammals. To address this problem, we assessed the genetic basis for increased virulence of A/CA/04/09 (H1N1) and A/TN/1-560/09 (H1N1) isolates, which are not lethal for mice, in a new mammalian host by promoting their mouse adaptation. The resulting mouse lung-adapted variants showed significantly enhanced growth characteristics in eggs, extended extrapulmonary tissue tropism, and pathogenicity in mice. All mouse-adapted viruses except A/TN/1-560/09-MA2 grew faster and to higher titers in cells than the original strains. We found that 10 amino acid changes in the ribonucleoprotein (RNP) complex (PB2 E158G/A, PA L295P, NP D101G, and NP H289Y) and hemagglutinin (HA) glycoprotein (K119N, G155E, S183P, R221K, and D222G) controlled enhanced mouse virulence of pandemic isolates. HA mutations acquired during adaptation affected viral receptor specificity by enhancing binding to α2,3 together with decreasing binding to α2,6 sialyl receptors. PB2 E158G/A and PA L295P amino acid substitutions were responsible for the significant enhancement of transcription and replication activity of the mouse-adapted H1N1 variants. Taken together, our findings suggest that changes optimizing receptor specificity and interaction of viral polymerase components with host cellular factors are the major mechanisms that contribute to the optimal competitive advantage of pandemic influenza viruses in mice. These modulators of virulence, therefore, may have been the driving components of early evolution, which paved the way for novel 2009 viruses in mammals.

scholarly journals Infrarenal Aorta Thrombosis Associated with H1N1 Influenza A Virus Infection

2016 ◽  
Vol 2016 ◽  
pp. 1-3 ◽  
Author(s):  
Can Hüzmeli ◽  
Mustafa Saglam ◽  
Ali Arıkan ◽  
Barıs Doner ◽  
Gulay Akıncı ◽  
...  
Keyword(s):  
Virus Infection ◽  
Influenza A Virus ◽  
Influenza A ◽  
H1n1 Virus ◽  
H1n1 Influenza ◽  
Influenza Viruses ◽  
Infrarenal Aorta ◽  
Influenza A H1n1 ◽  
Polymerase Chain ◽  
Influenza A Virus Infection

Influenza viruses are members of the Orthomyxoviridae family, of which influenza A, B, and C viruses constitute three separate genera. Arterial thrombosis associated with H1N1 influenza A virus infection has rarely been reported. A Turkish man aged 28 years was admitted to our emergency department with dyspnea, bilateral lower extremity insensitivity, and cold. He reported symptoms of fever, myalgia, and cough, which he had had for fifteen days before being admitted to our hospital. The patient was tested for pandemic influenza A (H1N1) virus using polymerase chain reaction (PCR) tests, which were positive. Abdominal computerized tomography with contrast revealed a large occlusive thrombus within the infrarenal aorta.

scholarly journals Epidemiological Features of Pandemic Influenza in Kyrgyzstan due to Influenza A(H1N1)pdm

2016 ◽  
Vol 15 (5) ◽  
pp. 30-37
Author(s):  
K. T. Kasymbekova ◽  
Z. S. Nurmatov ◽  
A. B. Komissarov ◽  
A. V. Fadeev ◽  
D. V. Pereyaslov ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Pandemic Influenza ◽  
Influenza A ◽  
Molecular Genetic ◽  
Influenza Viruses ◽  
Kyrgyz Republic ◽  
Genetic Characteristics ◽  
Influenza A H1n1 ◽  
The Republic ◽  
Reference Strains

Relevance. Virological laboratory of the Department of prevention of diseases and Sanitary Inspection Healthcare Ministry f of the Kyrgyz Republic is nominated as the National Centre for Influenza Surveillance and accreditated by WHO, and in 2009 is included into a global network of influenza Goal. The purpose of this study - Assessment of epidemic features of manifestations of pandemic influenza A (H1N1) pdm09 in 2009 on the territory of the Kyrgyz Republic, as a comparative study of the molecular and genetic characteristics of influenza A virus (H1N1) pdm09, circulating on the territory of the Republic and the influenza virus reference strains recommended WHO for inclusion in the vaccine for the northern hemisphere. Materials and methods. On the basis of long-term retrospective analysis of the incidence of influenza and severe acute respiratory infections (SARI), and sentinel epidemiological surveillance (SS) data studied pandemic especially in Kyrgyzstan due to influenza A(H1N1)pdm09. Comparative molecular genetic characteristics of influenza viruses A(H1N1)pdm09 allocated in Kyrgyzstan, with reference strains recommended by the World Health Organization (WHO) for inclusion in the vaccine. Results. Overall, the analysis of the results of laboratory tests carried out as part of the routine and sentinel surveillance showed that from January 2009 to March 2010 at 38.8% of those surveyed from among, influenza viruses (at 655 out of 1687) were found. From January to April 2009 in the main circulating influenza A virus (H3N2), which accounted for 55.9 - 77.9% of the number of positive findings. Seasonal influenza A virus (H1N1) was detected in January - February (35.3 and 13.4%, respectively). The share of the flu virus in January accounted for 8%, in March-April - 25%. Not typeable influenza A virus was detected in February in 8.7% of cases. Conclusions. The results of the molecular genetic and virological studies have shown that the influenza pandemic in 2009 in the Republic was due to the spread of pandemic influenza virus A (H1N1) pdm09.

Influenza Virus-Containing Immune Complexes Activate Platelets Through FcγRIIa Resulting In Bioactive Lipid Synthesis and Microparticle Release

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 1056-1056
Author(s):  
Eric Boilard ◽  
Guillaume Pare ◽  
Cloutier Nathalie ◽  
Isabelle Dubuc ◽  
Matthieu Rousseau ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Influenza Virus ◽  
Influenza A Virus ◽  
Platelet Activation ◽  
Immune Complexes ◽  
Influenza A ◽  
H1n1 Influenza ◽  
Human Platelets ◽  
Influenza Viruses ◽  
Potent Inducer

Abstract After red blood cells, platelets represent the most abundant cell lineage in blood, where they sentinel the vasculature and play crucial functions in haemostasis and the prevention of bleedings. Platelets also express a vast array of immune mediators and receptors, suggesting that they can also be regarded as tiny immune cells capable of the recognition of pathogens. Indeed, platelets express functional Toll-like receptors and are thought to actively participate to innate immunity. During severe cases of H1N1 influenza A virus infection, circulating platelets display markers of activation. The specific platelet activation triggers during Influenza infection remain however unknown. In this study, we incubated human platelets with H1N1 influenza A virus (IAV) and monitored platelet activation. We found that IAV is a highly potent inducer of de novo lipid mediators production and a trigger for the release of microparticles from platelets. This activation process takes place independently of the Toll-like receptor 4 and requires the presence of serum, pointing to the contribution of soluble factor(s) present in blood. We observed that the virus scaffolds with immunoglobulin G to form large immune-complexes (∼1micron in size) that activate platelets through the engagement of FcgRIIA. Accordingly, the serum of naïve mice housed in a pathogen-free facility is ineffective at initiating human platelet activation when incubated in the presence of IAV. Intrigued by the fact that all the tested human sera were capable of forming immune complexes with IAV, we hypothesized that significant antibody cross-reactivity between different influenza viruses was sufficient to promote the formation of virus-containing immune complexes. Using in vivo approaches, we found that the antibodies from H3N2 influenza virus-immunized mice generate immune complexes when put in presence of H1N1, activating human platelets and transgenic mouse platelets that express FcgRIIA. Taken together, our observations demonstrate that beyond their activities in haemostasis and innate immunity, platelets can also play a role during the active stage of adaptive immune responses against pathogens through FcγRIIa activation. Disclosures: No relevant conflicts of interest to declare.

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