Evolution of the neuraminidase gene of seasonal influenza A and B viruses in Thailand between 2010 and 2015

Tewawong, Nipaporn; Vichiwattana, Preeyaporn; Korkong, Sumeth; Klinfueng, Sirapa; Suntronwong, Nungruthai; Thongmee, Thanunrat; Theamboonlers, Apiradee; Vongpunsawad, Sompong; Poovorawan, Yong

doi:10.1371/journal.pone.0175655

Cited by 23 publications

(23 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…From the study performed in US community cluster, Australia, Japan, Brazil the same observations found. However presence of N386K mutation was not found in Australia and Japan and its role in viral fitness is still controversial …”

Section: Discussionmentioning

confidence: 99%

Oseltamivir‐resistant influenza A(H1N1)pdm09 virus associated with high case fatality, India 2015

Tandel

Sharma

Dash

et al. 2018

Journal of Medical Virology

View full text Add to dashboard Cite

Influenza A viruses has been associated with severe global pandemics of high morbidity and mortality with devastating impact on human health and global economy. India witnessed a major outbreak of influenza A(H1N1)pdm09 in 2015. This study comprises detailed investigation of cases died of influenza A(H1N1)pdm09 virus infection during explosive outbreak of 2015, in central part of India. To find out presence of drug resistant virus among patients who died of influenza A(H1N1)pdm09 virus infection and to find out presence of other mutations contributing to the morbidity and mortality. Twenty-two patients having confirmed influenza A(H1N1)pdm09 infection and subsequently died of this infection along with 20 non fatal cases with influenza A(H1N1)pdm09 infection were included in the study. Samples were investigated through RT-PCR/RFLP analysis, followed by nucleotide cycle sequencing of whole NA gene for detection of H275Y amino acid substitution in NA gene responsible for oseltamivir drug resistance. Out of 22 fatal cases, 6 (27.27%) were found to harbor oseltamivir resistant virus strains, whereas the H275Y mutation was not observed among the 20 non fatal cases. Amino acid substitution analysis of complete NA gene revealed V241I, N369K, N386K substitution in all strains playing synergistic role in oseltamivir drug resistance. High morbidity and mortality associated with influenza A(H1N1)pdm09 viruses can be explained by presence of drug resistant strains circulating in this outbreak. Presence of Oseltamivir resistant influenza A(H1N1)pdm09 viruses is a cause of great concern and warrants continuous screening for the circulation of drug resistant strains.

show abstract

Section: Discussionmentioning

confidence: 99%

Oseltamivir‐resistant influenza A(H1N1)pdm09 virus associated with high case fatality, India 2015

Tandel

Sharma

Dash

et al. 2018

Journal of Medical Virology

View full text Add to dashboard Cite

show abstract

“…Presently, A (H1N1) pdm09 has become endemic in humans, co-circulating with A/H3N2 and B as seasonal influenza viruses [1,2,5,11]. Influenza virus hemagglutinin (HA) protein is the prime target of host's neutralizing antibodies [12][13][14][15]. It is typically cleaved by host cells proteases into HA1 and HA2 domains [16].…”

Section: Introductionmentioning

confidence: 99%

Assessing antigenic drift and phylogeny of influenza A (H1N1) pdm09 virus in Kenya using HA1 sub-unit of the hemagglutinin gene

et al. 2020

View full text Add to dashboard Cite

Influenza A (H1N1) pdm09 virus emerged in North America in 2009 and has been established as a seasonal strain in humans. After an antigenic stasis of about six years, new antigenically distinct variants of the virus emerged globally in 2016 necessitating a change in the vaccine formulation for the first time in 2017. Herein, we analyzed thirty-eight HA sequences of influenza A (H1N1) pdm09 strains isolated in Kenya during 2015-2018 seasons, to evaluate their antigenic and molecular properties based on the HA1 sub-unit. Our analyses revealed that the A (H1N1) pdm09 strains that circulated in Kenya during this period belonged to genetic clade 6B, subclade 6B.1 and 6B.2. The Kenyan 2015 and 2016 isolates differed from the vaccine strain A/California/07/2009 at nine and fourteen antigenic sites in the HA1 respectively. Further, those isolated in 2017 and 2018 correspondingly varied from A/Michigan/45/2015 vaccine strain at three and fifteen antigenic sites. The predicted vaccine efficacy of A/California/07/2009 against Kenyan 2015/2016 was estimated to be 32.4% while A/Michigan/45/2015 showed estimated vaccine efficacies of 39.6% -41.8% and 32.4% -42.1% against Kenyan 2017 and 2018 strains, respectively. Hemagglutinationinhibition (HAI) assay using ferret post-infection reference antiserum showed that the titers for the Kenyan 2015/2016 isolates were 2-8-fold lower compared to the vaccine strain. Overall, our results suggest the A (H1N1) pdm09 viruses that circulated in Kenya during 2015/2016 influenza seasons were antigenic variants of the recommended vaccine strains, denoting sub-optimal vaccine efficacy. Additionally, data generated point to a swiftly evolving influenza A (H1N1) pdm09 virus in recent post pandemic era, underscoring the need for sustained surveillance coupled with molecular and antigenic analyses, to inform appropriate and timely influenza vaccine update.

show abstract

“…The influenza virus mutates its genes to obtain the ability to adapt to its host, while the high mutation rate for the virus provides a feasible condition for the process [7][8][9]. Regarding the H5N2 subtype avian influenza virus, HA generated a Q234L mutation after many generations in the lungs of mice, which helped to the virus obtain the ability to infect mammals [7].…”

Section: Introductionmentioning

confidence: 99%

Effect of the Selection Pressure of Vaccine Antibodies on Evolution of H9N2 Avian Influenza Virus in Chickens

Zhao

Zheng

et al. 2020

Preprint

View full text Add to dashboard Cite

H9N2 avian influenza virus has spread worldwide, and vaccination with an inactivated virus is currently the major prevention method in China. To further understand the effect of the selection pressure from antibodies on the evolution of H9N2 avian influenza virus, F/98 (A/Chicken/Shanghai/F/98), which is the vaccine representative of H9N2 avian influenza virus in East China, was used for serial passaging for 20 generations in chickens with and without vaccination. After plaque purification from trachea and lung tissues, 390 quasispecies were obtained. The second-generation quasispecies under the selection pressure of vaccine antibodies had undergone 100% antigen variation, while after passaging to the fifth generation, only 30-40% of the quasispecies displayed antigen variation when there was no selection pressure of vaccine antibodies, implying that the selection pressure of vaccine antibodies promotes the antigen variation of F/98. We found for the first time that there were three mutation hotspots in the HA genes of the quasispecies under the selection pressure of vaccine antibodies, which were K131R, A168T, and N201D. Moreover, under the selection pressure of vaccine antibodies, 10 amino acids (67-76) of the NA protein of all quasispecies were deleted, and PB2 of the quasispecies had undergone a high-frequency R355K mutation. However, without selection pressure of vaccine antibodies, NP had undergone two high-frequency mutations, namely, V186I and L466I, and a high-frequency mutation of L77I appeared in the NS gene. This result shows that the vaccine antibody selection pressure could control and regulate gene variation of the F/98 virus. Compared to that of the parental virus F/98, the EID 50 of the twentieth passaged virus under the selection pressure of vaccine antibodies did not change, while the EID 50 of the twentieth passaged virus without selection pressure of vaccine antibodies was significantly enhanced by 794 times. Furthermore, the twentieth passaged virus with selection pressure from vaccine antibodies lost its lethal ability in embryonated chicken eggs, whereas the EID 50 of the twentieth passaged virus without selection pressure of vaccine antibodies increased to 6.3 times that of the F/98 strain. All the above results show that the selection pressure of vaccine antibodies promotes the antigen variation of H9N2 avian influenza virus and plays a role in regulating and controlling gene mutation of H9N2 avian influenza virus.

show abstract

Evolution of the neuraminidase gene of seasonal influenza A and B viruses in Thailand between 2010 and 2015

Cited by 23 publications

References 59 publications

Oseltamivir‐resistant influenza A(H1N1)pdm09 virus associated with high case fatality, India 2015

Oseltamivir‐resistant influenza A(H1N1)pdm09 virus associated with high case fatality, India 2015

Assessing antigenic drift and phylogeny of influenza A (H1N1) pdm09 virus in Kenya using HA1 sub-unit of the hemagglutinin gene

Effect of the Selection Pressure of Vaccine Antibodies on Evolution of H9N2 Avian Influenza Virus in Chickens

Contact Info

Product

Resources

About