scholarly journals Co-infection between the pandemic influenza virus A H1N1 and seasonal influenza A virus in a patient presenting severe acute respiratory disease

2010 ◽  
Vol 14 ◽  
pp. e103-e104
Author(s):  
A. Feltrin ◽  
K. Augusto ◽  
V. Isper ◽  
J. Delamain ◽  
B. Kemp ◽  
...  
Author(s):  
A. N. Shikov ◽  
E. I. Sergeeva ◽  
O. K. Demina ◽  
V. A. Ternovoy ◽  
V. V. Ryabinin ◽  
...  

Developed was the DNA-biochip to identify subtypes of influenza A virus, pathogenic for humans. Microchip was capable of detecting H1, H3, H5-subtypes of hemagglutinin (including H1-subtype of pandemic A/H1N1(2009) influenza virus ) and neuraminidase subtypes N1,N2 of influenza virus. This microchip was successfully tested on the strains of A/H5N1 highly pathogenic avian influenza virus, A/H1N1(2009) pandemic influenza virus, A/H1N1 and A/H3N2 seasonal influenza viruses.


2010 ◽  
Vol 202 (7) ◽  
pp. 1011-1020 ◽  
Author(s):  
Karen L. Laurie ◽  
Louise A. Carolan ◽  
Deborah Middleton ◽  
Sue Lowther ◽  
Anne Kelso ◽  
...  

2010 ◽  
Vol 17 (12) ◽  
pp. 1998-2006 ◽  
Author(s):  
Ali H. Ellebedy ◽  
Thomas P. Fabrizio ◽  
Ghazi Kayali ◽  
Thomas H. Oguin ◽  
Scott A. Brown ◽  
...  

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.


2011 ◽  
Vol 18 (9) ◽  
pp. 1401-1405 ◽  
Author(s):  
Elisabeth Huijskens ◽  
John Rossen ◽  
Paul Mulder ◽  
Ruud van Beek ◽  
Hennie van Vugt ◽  
...  

ABSTRACTThe emergence of a new influenza A virus (H1N1) variant in 2009 led to a worldwide vaccination program, which was prepared in a relatively short period of time. This study investigated the humoral immunity against this virus before and after vaccination with a 2009 influenza A virus (H1N1) monovalent MF59-adjuvanted vaccine, as well as the persistence of vaccine-induced antibodies. Our prospective longitudinal study included 498 health care workers (mean age, 43 years; median age, 44 years). Most (89%) had never or only occasionally received a seasonal influenza virus vaccine, and 11% were vaccinated annually (on average, for >10 years). Antibody titers were determined by a hemagglutination inhibition (HI) assay at baseline, 3 weeks after the first vaccination, and 5 weeks and 7 months after the second vaccination. Four hundred thirty-five persons received two doses of the 2009 vaccine. After the first dose, 79.5% developed a HI titer of ≥40. This percentage increased to 83.3% after the second dose. Persistent antibodies were found in 71.9% of the group that had not received annual vaccinations and in 43.8% of the group that had received annual vaccinations. The latter group tended to have lower HI titers (P=0.09). With increasing age, HI titers decreased significantly, by 2.4% per year. A single dose of the 2009 vaccine was immunogenic in almost 80% of the study population, whereas an additional dose resulted in significantly increased titers only in persons over 50. Finally, a reduced HI antibody response against the 2009 vaccine was found in adults who had previously received seasonal influenza virus vaccination. More studies on the effect of yearly seasonal influenza virus vaccination on the immune response are warranted.


2015 ◽  
Vol 89 (20) ◽  
pp. 10602-10611 ◽  
Author(s):  
Wei Wang ◽  
Christopher J. DeFeo ◽  
Esmeralda Alvarado-Facundo ◽  
Russell Vassell ◽  
Carol D. Weiss

ABSTRACTInfluenza virus hemagglutinin (HA) mediates virus entry by binding to cell surface receptors and fusing the viral and endosomal membranes following uptake by endocytosis. The acidic environment of endosomes triggers a large-scale conformational change in the transmembrane subunit of HA (HA2) involving a loop (B loop)-to-helix transition, which releases the fusion peptide at the HA2 N terminus from an interior pocket within the HA trimer. Subsequent insertion of the fusion peptide into the endosomal membrane initiates fusion. The acid stability of HA is influenced by residues in the fusion peptide, fusion peptide pocket, coiled-coil regions of HA2, and interactions between the surface (HA1) and HA2 subunits, but details are not fully understood and vary among strains. Current evidence suggests that the HA from the circulating pandemic 2009 H1N1 influenza A virus [A(H1N1)pdm09] is less stable than the HAs from other seasonal influenza virus strains. Here we show that residue 205 in HA1 and residue 399 in the B loop of HA2 (residue 72, HA2 numbering) in different monomers of the trimeric A(H1N1)pdm09 HA are involved in functionally important intermolecular interactions and that a conserved histidine in this pair helps regulate HA stability. An arginine-lysine pair at this location destabilizes HA at acidic pH and mediates fusion at a higher pH, while a glutamate-lysine pair enhances HA stability and requires a lower pH to induce fusion. Our findings identify key residues in HA1 and HA2 that interact to help regulate H1N1 HA stability and virus infectivity.IMPORTANCEInfluenza virus hemagglutinin (HA) is the principal antigen in inactivated influenza vaccines and the target of protective antibodies. However, the influenza A virus HA is highly variable, necessitating frequent vaccine changes to match circulating strains. Sequence changes in HA affect not only antigenicity but also HA stability, which has important implications for vaccine production, as well as viral adaptation to hosts. HA from the pandemic 2009 H1N1 influenza A virus is less stable than other recent seasonal influenza virus HAs, but the molecular interactions that contribute to HA stability are not fully understood. Here we identify molecular interactions between specific residues in the surface and transmembrane subunits of HA that help regulate the HA conformational changes needed for HA stability and virus entry. These findings contribute to our understanding of the molecular mechanisms controlling HA function and antigen stability.


2022 ◽  
Author(s):  
J. Brian Kimble ◽  
Meghan Wymore Brand ◽  
Bryan S. Kaplan ◽  
Phillip Gauger ◽  
Elizabeth M. Coyle ◽  
...  

Influenza A virus (IAV) causes respiratory disease in swine and humans. Vaccines are used to prevent influenza illness in both populations but must be frequently updated due to rapidly evolving strains. Mismatch between the circulating strains and strains contained in vaccines may cause loss in efficacy. Whole inactivated virus (WIV) vaccines with adjuvant utilized by the swine industry are effective against antigenically similar viruses; however, vaccine-associated enhanced respiratory disease (VAERD) may happen when the WIV is antigenically mismatched with the infecting virus. VAERD is a repeatable model in pigs, but had yet to be experimentally demonstrated in other mammalian species. We recapitulated VAERD in ferrets, a standard benchmark animal model for studying human influenza infection, in a direct comparison to VAERD in pigs. Both species were vaccinated with WIV with oil in water adjuvant containing a δ-1 H1N2 (1B.2.2) derived from the pre-2009 human seasonal lineage, then challenged with a 2009 pandemic H1N1 (H1N1pdm09, 1A.3.3.2) five weeks after vaccination. Nonvaccinated and challenged groups showed typical signs of influenza disease, but the mismatched vaccinated and challenged pigs and ferrets showed elevated clinical signs, despite similar viral loads. VAERD affected pigs exhibited a 2-fold increase in lung lesions, while VAERD affected ferrets showed a 4-fold increase. Similar to pigs, antibodies from VAERD affected ferrets preferentially bound to the HA2 domain of the H1N1pdm09 challenge strain. These results indicate VAERD is not limited to pigs, as demonstrated here in ferrets, and the need to consider VAERD when evaluating new vaccine platforms and strategies. Importance We demonstrated the susceptibility of ferrets, a laboratory model species for human influenza A virus research, to vaccine associated enhanced respiratory disease (VAERD) using an experimental model previously demonstrated in pigs. Ferrets developed clinical characteristics of VAERD very similar to that in pigs. The hemagglutinin (HA) stalk is a potential vaccine target to develop more efficacious, broadly reactive influenza vaccine platforms and strategies. However, non-neutralizing antibodies directed towards a conserved epitope on the HA stalk induced by an oil-in-water adjuvanted whole influenza virus vaccine were previously shown in VAERD-affected pigs and were also identified here in VAERD-affected ferrets. The induction of VAERD in ferrets highlights the potential risk of mismatched influenza vaccines to humans and the need to consider VAERD when designing and evaluating vaccine strategies.


2010 ◽  
Vol 84 (7) ◽  
pp. 3312-3319 ◽  
Author(s):  
Xinhui Ge ◽  
Venus Tan ◽  
Paul L. Bollyky ◽  
Nathan E. Standifer ◽  
Eddie A. James ◽  
...  

ABSTRACT Very limited evidence has been reported to show human adaptive immune responses to the 2009 pandemic H1N1 swine-origin influenza A virus (S-OIV). We studied 17 S-OIV peptides homologous to immunodominant CD4 T epitopes from hemagglutinin (HA), neuraminidase (NA), nuclear protein (NP), M1 matrix protein (MP), and PB1 of a seasonal H1N1 strain. We concluded that 15 of these 17 S-OIV peptides would induce responses of seasonal influenza virus-specific T cells. Of these, seven S-OIV sequences were identical to seasonal influenza virus sequences, while eight had at least one amino acid that was not conserved. T cells recognizing epitopes derived from these S-OIV antigens could be detected ex vivo. Most of these T cells expressed memory markers, although none of the donors had been exposed to S-OIV. Functional analysis revealed that specific amino acid differences in the sequences of these S-OIV peptides would not affect or partially affect memory T-cell responses. These findings suggest that without protective antibody responses, individuals vaccinated against seasonal influenza A may still benefit from preexisting cross-reactive memory CD4 T cells reducing their susceptibility to S-OIV infection.


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 ◽  
...  

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.


Sign in / Sign up

Export Citation Format

Share Document