scholarly journals Epidemic mechanisms of Type A influenza

1979 ◽  
Vol 83 (1) ◽  
pp. 11-26 ◽  
Author(s):  
R. E. Hope-simpson
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Latent Virus ◽  
Antigenic Drift ◽  
Specific Immunity ◽  
Free Interval ◽  
Serial Interval ◽  
Minor Variant ◽  
Tentative Hypothesis ◽  
H3n2 Influenza

SUMMARYThe antigenic varieties of influenza A virus isolated from 1968 to 1976 in a surveillance of a small, rather remote population were similar to those from England and Wales as a whole, despite frequent antigenic changes during the period. Household studies in the first two H3N2 influenza A epidemics found low attack rates within households, a high proportion (70%) of affected households with only one case of influenza, similar distributions of affected households in the two epidemics by the number of cases of influenza and similar distributions of the influenza cases by the day of their onset in the household outbreak. No serial interval could be demonstrated by cumulating household outbreaks. More than one minor variant was causing influenza contemporaneously in the same villages in several seasons, and different variants were on one occasion found on successive days in bedfellows. The regular occurrence of epidemics in winter was often accompanied by the disappearance of the epidemic variants and their replacement, after a virus-free interval, by new variants.These epidemiological findings seem best interpreted on the following tentative hypothesis. Influenza A sufferers do not transmit the virus during their illness; instead it rapidly becomes latent in their tissues so that they become symptomless carrier-hosts and develop specific immunity. Next season an extraneous seasonally mediated stimulus reactivates the latent virus residues so that the carrier-host becomes briefly infectious, though symptomless. Antigenic drift occurs because particles reconstituted to be identical with the progenitor virus cannot escape the specific immunity it has provoked in the carrier host. He can shed only mutants also determined by the progenitor virus. From the assortment of mutants shed by the carrier-host, his non-immune companions select that (those) which is best fitted to survive, and it rapidly causes influenzal illness. Epidemics consist largely or entirely of such persons sick with influenza caused by reactivated virus caught from symptomless carrier-hosts.

scholarly journals Unseasonal Transmission of H3N2 Influenza A Virus During the Swine-Origin H1N1 Pandemic

2010 ◽  
Vol 84 (11) ◽  
pp. 5715-5718 ◽  
Author(s):  
Elodie Ghedin ◽  
David E. Wentworth ◽  
Rebecca A. Halpin ◽  
Xudong Lin ◽  
Jayati Bera ◽  
...  
Keyword(s):  
New York ◽  
Influenza A Virus ◽  
Influenza A ◽  
New York State ◽  
The United States ◽  
Influenza Viruses ◽  
Influenza A Viruses ◽  
York State ◽  
Low Incidence ◽  
H3n2 Influenza

ABSTRACT The initial wave of swine-origin influenza A virus (pandemic H1N1/09) in the United States during the spring and summer of 2009 also resulted in an increased vigilance and sampling of seasonal influenza viruses (H1N1 and H3N2), even though they are normally characterized by very low incidence outside of the winter months. To explore the nature of virus evolution during this influenza “off-season,” we conducted a phylogenetic analysis of H1N1 and H3N2 sequences sampled during April to June 2009 in New York State. Our analysis revealed that multiple lineages of both viruses were introduced and cocirculated during this time, as is typical of influenza virus during the winter. Strikingly, however, we also found strong evidence for the presence of a large transmission chain of H3N2 viruses centered on the south-east of New York State and which continued until at least 1 June 2009. These results suggest that the unseasonal transmission of influenza A viruses may be more widespread than is usually supposed.

scholarly journals octoFLU: Automated Classification for the Evolutionary Origin of Influenza A Virus Gene Sequences Detected in U.S. Swine

2019 ◽  
Vol 8 (32) ◽  
Author(s):  
Jennifer Chang ◽  
Tavis K. Anderson ◽  
Michael A. Zeller ◽  
Phillip C. Gauger ◽  
Amy L. Vincent
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Antigenic Drift ◽  
Evolutionary Origin ◽  
Automated Classification ◽  
Gene Sequences ◽  
Influenza A Viruses ◽  
Query Gene ◽  
Data Set ◽  
Virus Gene

The diversity of the 8 genes of influenza A viruses (IAV) in swine reflects introductions from nonswine hosts and subsequent antigenic drift and shift. Here, we curated a data set and present a pipeline that assigns evolutionary lineage and genetic clade to query gene segments.

scholarly journals Targeting Hemagglutinin: Approaches for Broad Protection against the Influenza A Virus

Viruses ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 405 ◽  
Author(s):  
Zhang ◽  
Xu ◽  
Zhang ◽  
Liu ◽  
Xue ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Protective Efficacy ◽  
Structure And Function ◽  
Antigenic Drift ◽  
Influenza A Viruses ◽  
Universal Vaccine ◽  
Vaccine Candidates ◽  
And Function ◽  
Ha Protein

Influenza A viruses are dynamically epidemic and genetically diverse. Due to the antigenic drift and shift of the virus, seasonal vaccines are required to be reformulated annually to match with current circulating strains. However, the mismatch between vaccinal strains and circulating strains occurs frequently, resulting in the low efficacy of seasonal vaccines. Therefore, several “universal” vaccine candidates based on the structure and function of the hemagglutinin (HA) protein have been developed to meet the requirement of a broad protection against homo-/heterosubtypic challenges. Here, we review recent novel constructs and discuss several important findings regarding the broad protective efficacy of HA-based universal vaccines.

scholarly journals Population-Based Hospitalization Burden of Influenza A Virus Subtypes and Antigenic Drift Variants in Children in Hong Kong (2004–2011)

PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e92914 ◽  
Author(s):  
Susan S. Chiu ◽  
Janice Y. C. Lo ◽  
Kwok-Hung Chan ◽  
Eunice L. Y. Chan ◽  
Lok-Yee So ◽  
...  
Keyword(s):  
Hong Kong ◽  
Influenza A Virus ◽  
Influenza A ◽  
Population Based ◽  
Antigenic Drift

Interaction network linking the human H3N2 influenza A virus genomic RNA segments

Vaccine ◽  
2012 ◽  
Vol 30 (51) ◽  
pp. 7359-7367 ◽  
Author(s):  
Emilie Fournier ◽  
Vincent Moules ◽  
Boris Essere ◽  
Jean-Christophe Paillart ◽  
Jean-Daniel Sirbat ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Interaction Network ◽  
Genomic Rna ◽  
H3n2 Influenza

scholarly journals Measuring site-specific glycosylation similarity between influenza A virus variants with statistical certainty

2020 ◽  
Author(s):  
Deborah Chang ◽  
William E. Hackett ◽  
Lei Zhong ◽  
Xiu-Feng Wan ◽  
Joseph Zaia
Keyword(s):  
Influenza A Virus ◽  
Protein Sequence ◽  
Influenza A ◽  
Viral Fitness ◽  
Antigenic Drift ◽  
Viral Escape ◽  
Strain Selection ◽  
Expression Vectors ◽  
Site Specific ◽  
Measuring Site

AbstractInfluenza A virus (IAV) mutates rapidly, resulting in antigenic drift and poor year-to-year vaccine effectiveness. One challenge in designing effective vaccines is that genetic mutations frequently cause amino acid variations in IAV envelope protein hemagglutinin (HA) that create new N-glycosylation sequons; resulting N-glycans cause antigenic shielding, allowing viral escape from adaptive immune responses. Vaccine candidate strain selection currently involves correlating antigenicity with HA protein sequence among circulating strains, but quantitative comparison of site-specific glycosylation information may likely improve the ability to design vaccines with broader effectiveness against evolving strains. However, there is poor understanding of the influence of glycosylation on immunodominance, antigenicity, and immunogenicity of HA, and there are no well-tested methods for comparing glycosylation similarity among virus samples. Here, we present a method for statistically rigorous quantification of similarity between two related virus strains that considers the presence and abundance of glycopeptide glycoforms. We demonstrate the strength of our approach by determining that there was a quantifiable difference in glycosylation at the protein level between wild-type IAV HA from A/Switzerland/9715293/2013 (SWZ13) and a mutant strain of SWZ13, even though no N-glycosylation sequons were changed. We determined site-specifically that WT and mutant HA have varying similarity at the glycosylation sites of the head domain, reflecting competing pressures to evade host immune response while retaining viral fitness. To our knowledge, our results are the first to quantify changes in glycosylation state that occur in related proteins of considerable glycan heterogeneity. Our results provide a method for understanding how changes in glycosylation state are correlated with variations in protein sequence, which is necessary for improving IAV vaccine strain selection. Understanding glycosylation will be especially important as we find new expression vectors for vaccine production, as glycosylation state depends greatly on the host species.

scholarly journals Measuring Site-specific Glycosylation Similarity between Influenza a Virus Variants with Statistical Certainty

2020 ◽  
Vol 19 (9) ◽  
pp. 1533-1545
Author(s):  
Deborah Chang ◽  
William E. Hackett ◽  
Lei Zhong ◽  
Xiu-Feng Wan ◽  
Joseph Zaia
Keyword(s):  
Influenza A Virus ◽  
Protein Sequence ◽  
Influenza A ◽  
Viral Fitness ◽  
Antigenic Drift ◽  
Viral Escape ◽  
Strain Selection ◽  
Expression Vectors ◽  
Site Specific ◽  
Measuring Site

Influenza A virus (IAV) mutates rapidly, resulting in antigenic drift and poor year-to-year vaccine effectiveness. One challenge in designing effective vaccines is that genetic mutations frequently cause amino acid variations in IAV envelope protein hemagglutinin (HA) that create new N-glycosylation sequons; resulting N-glycans cause antigenic shielding, allowing viral escape from adaptive immune responses. Vaccine candidate strain selection currently involves correlating antigenicity with HA protein sequence among circulating strains, but quantitative comparison of site-specific glycosylation information may likely improve the ability to design vaccines with broader effectiveness against evolving strains. However, there is poor understanding of the influence of glycosylation on immunodominance, antigenicity, and immunogenicity of HA, and there are no well-tested methods for comparing glycosylation similarity among virus samples. Here, we present a method for statistically rigorous quantification of similarity between two related virus strains that considers the presence and abundance of glycopeptide glycoforms. We demonstrate the strength of our approach by determining that there was a quantifiable difference in glycosylation at the protein level between WT IAV HA from A/Switzerland/9715293/2013 (SWZ13) and a mutant strain of SWZ13, even though no N-glycosylation sequons were changed. We determined site-specifically that WT and mutant HA have varying similarity at the glycosylation sites of the head domain, reflecting competing pressures to evade host immune response while retaining viral fitness. To our knowledge, our results are the first to quantify changes in glycosylation state that occur in related proteins of considerable glycan heterogeneity. Our results provide a method for understanding how changes in glycosylation state are correlated with variations in protein sequence, which is necessary for improving IAV vaccine strain selection. Understanding glycosylation will be especially important as we find new expression vectors for vaccine production, as glycosylation state depends greatly on the host species.

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