Genetic characterization of circulating seasonal Influenza A viruses (2005–2009) revealed introduction of oseltamivir resistant H1N1 strains during 2009 in eastern India

Agrawal, Anurodh Shankar; Sarkar, Mehuli; Ghosh, Swati; Roy, Tapasi; Chakrabarti, Sekhar; Lal, Renu; Mishra, Akhilesh C.; Chadha, Mandeep S.; Chawla‐Sarkar, Mamta

doi:10.1016/j.meegid.2010.07.019

Cited by 19 publications

(22 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In the northeast, on the other hand, the climate is usually semi-humid and dry with generally little rainfall compared to other regions. In the neighboring countries and other countries in tropical climate zones, influenza activity has been reported to peak in the rainy season [21][22][23][24]. Also, in this study, the peak of influenza activity was usually observed during and immediately after the rainy season, which might have had a direct or indirect effect on influenza seasonality.…”

Section: Discussionmentioning

confidence: 46%

Epidemiology of seasonal influenza in Bangkok between 2009 and 2012

Prachayangprecha

Makkoch

Suwannakarn

et al. 2013

J Infect Dev Ctries

View full text Add to dashboard Cite

Introduction: This study investigated influenza activity in Bangkok, Thailand between June 2009 and July 2012. Methodology: Real-time reverse transcription polymerase chain reaction (RT-PCR) was performed to detect influenza viruses among patients with influenza-like illnesses. Results: Of the 6417 patients tested, influenza virus infection was detected in 42% (n = 2697) of the specimens. Influenza A pH1N1 viruses comprised the predominant strain between 2009 and 2010, and seasonal influenza (H3) had a high prevalence in 2011. Laboratory data showed a prevalence and seasonal pattern of influenza viruses. In 2009, influenza activity peaked in July, the rainy season. In 2010, influenza activity happened in two phases, with the initial one at the beginning of the year and another peak between June and August 2010, which again corresponded to the rainy period. Influenza activity was low for several consecutive weeks at the beginning of 2011, and high H3N2 activity was recorded during the rainy season between July and September 2011. However, from the beginning of 2012 through July 2012, pH1N1, influenza H3N2, and influenza B viruses continuously circulated at a very low level. Conclusion: The seasonal pattern of influenza activity in Thailand tended to peak during rainy season between July and September.

show abstract

Section: Discussionmentioning

confidence: 46%

Epidemiology of seasonal influenza in Bangkok between 2009 and 2012

Prachayangprecha

Makkoch

Suwannakarn

et al. 2013

J Infect Dev Ctries

View full text Add to dashboard Cite

show abstract

“…The visionary work by M.A Rameix-Welti et al (68), for the first time, revealed the distinct level of NA enzyme affinity and distinct cluster patterns of NA and HA genes of wild-type and H275Y mutant viruses among the older and new isolates of seasonal H1N1 viruses. In line with this study, subsequently, some phylogeny studies classified the specific cluster patterns of the NA and HA genes as different clades and showed the same trends that vast majority of H275Y mutant H1N1 viruses, especially the naturally resistant ones, commonly belonged to the Clade 2B (62)(63)(64)(65)(66). Further studies have associated the higher enzyme affinity in some Clade 2B viruses to certain NA amino acid substitutions (63;69) and one study confirmed the role of NA D344N substitution in NA enzyme affinity (70).…”

Section: Discussionsupporting

confidence: 79%

“…This study also showed that all the tested naturally resistant H275Y mutant viruses belonged to the high NA affinity group which genetically clustered together in the same group. This particular cluster was recognized as Clade 2B later and was consistently showed as a common feature for the naturally resistant H1N1 viruses characterized in different studies (62)(63)(64)(65)(66). Further studies have associated the high enzyme affinity in some viruses to certain NA amino acid substitutions (63;69) and one study confirmed the role of D344N substitution in increasing enzyme affinity (70).…”

Section: Na Inhibitor Resistance In Human Seasonal Influenza a Virusesmentioning

confidence: 80%

“…Surveillance studies provided informative clues for this question by examining the genetic changes in the H275Y mutant H1N1 viruses. The phylogenetic analyses by different groups using various circulating H1N1 viruses collected from respective regions showed two common features of these viruses (62)(63)(64)(65)(66). First, the NA and HA genes of seasonal H1N1 viruses exhibited same cluster patterns, which were classified as Clade 1, Clade 2A, 2B, 2C, represented by H1N1 vaccine strains New Caledonia/20/1999 virus, Solomon Island/23/2006 virus, Brisbane/59/2007 virus respectively (though no vaccine strain representing the Clade 2C); second, the vast majority of the naturally resistant viruses belonged to the Clade 2B in the phylogeny.…”

Section: Na Inhibitor Resistance In Human Seasonal Influenza a Virusesmentioning

confidence: 99%

See 1 more Smart Citation

The Molecular Basis of Fitness and Transmissibility of Neuraminidase Inhibitor Resistant Influenza A Viruses

Duan¹

View full text Add to dashboard Cite

DEDICATIONThis dissertation is dedicated to my parents and my own family who have been always giving me unconditional love, indissoluble strength, endless inspiration. iv ACKNOWLEDGEMENTSAll of this would not have been possible had Dr. Robert G. Webster not taken me as his graduate student. I will always remember my first conversation with Dr. Webster about my rotating his lab and the first conversation with Dr. Webster at the day I officially joined the lab: "Work hard, young people." I have been doing nothing but following this simple instruction through all my studies during these years. I will be eternally grateful for Dr. Webster for having faith in me to take me as his student and mentoring my Ph.D study. I thank Dr. Webster for being my mentor in every way, for always giving me the biggest vision about the research and career, for teaching me to start strong and end strong a scientific story, for enlightening me with the most important and critical questions for now and for future in the world of influenza virology.This dissertation would not have been completed in its present way without Dr. Elena G. Govorkova's supervision. The greatest appreciation is to Elena as my supervisor in all kinds of trainings: from introducing me the knowledge of the antiviral field, to helping me experiments in person, to supporting me to develop different projects, to teaching me to write manuscripts, to educating me to be a philosopher, and always reminding me to look pretty as a woman. I will always value all these precious training and experience.Special deep thanks to Dr. Richard J. Webby for providing me different training opportunities in other aspects of influenza virology, for giving me different visions to see different questions. Especially many thanks for his biggest push to greatly move forward the second study in this thesis by adding new angles and much more depth.Special thanks to my committee members, Dr. Paul Thomas, Dr. Michael Whitt and Dr. Tony Marion for giving me different perspectives to look the virology field, for always teaching me to think questions harder, deeper and more precisely.Special thanks to Scott Krauss for his general support for all studies.Special thanks to Dr. Subrata Barman and Dr. Charles Russell for kindly providing related experimental materials and working instructions.Many thanks to a former postdoctor fellow in our lab, Dr. David Boltz, for being a good teacher and good friend to me, for introducing me the influenza genome analysis, for helping me to develop the methodology project and for giving me encouragement to through the ups and downs of the studies. Many thanks to another former postdoctor fellow, Dr. Hui-ling Yen, for also being a great teacher and friend to me, for her unique comments and inspiring discussion on many influenza questions and for her dear encouragement for me all the time. Many thanks to other current and former postdoctor fellows in our flu group for helping me with their respective expertise and those include Dr. Hassan, Zarakat, Dr. Henju Marjuki, D...

show abstract

“…Seasonal human influenza A virus continuously evolves by undergoing mutations, thus altering the antigenic sites of the surface antigens in hemagglutinin (HA) and neuraminidase (NA) (1,4,29,31). Current subcutaneous human influenza vaccines induce neutralizing IgG antibody responses to the highly variable influenza HA protein; therefore, the immunization protects against homologous but not antigenically distinct viruses, including drift variants and different viral subtypes.…”

Section: Discussionmentioning

confidence: 99%

Intranasal Immunization with a Formalin-Inactivated Human Influenza A Virus Whole-Virion Vaccine Alone and Intranasal Immunization with a Split-Virion Vaccine with Mucosal Adjuvants Show Similar Levels of Cross-Protection

Okamoto

Matsuoka

Takenaka

et al. 2012

Clin. Vaccine Immunol.

View full text Add to dashboard Cite

ABSTRACTThe antigenicity of seasonal human influenza virus changes continuously; thus, a cross-protective influenza vaccine design needs to be established. Intranasal immunization with an influenza split-virion (SV) vaccine and a mucosal adjuvant induces cross-protection; however, no mucosal adjuvant has been assessed clinically. Formalin-inactivated intact human and avian viruses alone (without adjuvant) induce cross-protection against the highly pathogenic H5N1 avian influenza virus. However, it is unknown whether seasonal human influenza formalin-inactivated whole-virion (WV) vaccine alone induces cross-protection against strains within a subtype or in a different subtype of human influenza virus. Furthermore, there are few reports comparing the cross-protective efficacy of the WV vaccine and SV vaccine-mucosal adjuvant mixtures. Here, we found that the intranasal human influenza WV vaccine alone induced both the innate immune response and acquired immune response, resulting in cross-protection against drift variants within a subtype of human influenza virus. The cross-protective efficacy conferred by the WV vaccine in intranasally immunized mice was almost the same as that conferred by a mixture of SV vaccine and adjuvants. The level of cross-protective efficacy was correlated with the cross-reactive neutralizing antibody titer in the nasal wash and bronchoalveolar fluids. However, neither the SV vaccine with adjuvant nor the WV vaccine induced cross-reactive virus-specific cytotoxic T-lymphocyte activity. These results suggest that the intranasal human WV vaccine injection alone is effective against variants within a virus subtype, mainly through a humoral immune response, and that the cross-protection elicited by the WV vaccine and the SV vaccine plus mucosal adjuvants is similar.

show abstract

Genetic characterization of circulating seasonal Influenza A viruses (2005–2009) revealed introduction of oseltamivir resistant H1N1 strains during 2009 in eastern India

Cited by 19 publications

References 28 publications

Epidemiology of seasonal influenza in Bangkok between 2009 and 2012

Epidemiology of seasonal influenza in Bangkok between 2009 and 2012

The Molecular Basis of Fitness and Transmissibility of Neuraminidase Inhibitor Resistant Influenza A Viruses

Intranasal Immunization with a Formalin-Inactivated Human Influenza A Virus Whole-Virion Vaccine Alone and Intranasal Immunization with a Split-Virion Vaccine with Mucosal Adjuvants Show Similar Levels of Cross-Protection

Contact Info

Product

Resources

About