Temporal distribution and genetic variants in influenza A(H1N1)pdm09 virus circulating in Mexico, seasons 2012 and 2013

Abstract

The 2012 and 2013 annual influenza epidemics in Mexico were characterized by presenting different seasonal patterns. In 2012 the A(H1N1)pdm09 virus caused a high incidence of influenza infections after a two-year period of low circulation; whereas the 2013 epidemic presented circulation of the A(H1N1)pdm09 virus throughout the year. We have characterized the molecular composition of the Hemagglutinin (HA) and Neuraminidase (NA) genes of the A(H1N1)pdm09 virus from both epidemic seasons, emphasizing the genetic characteristics of viruses isolated from Yucatan in Southern Mexico. The molecular analysis of viruses from the 2012 revealed that all viruses from Mexico were predominantly grouped in clade 7. Strikingly, the molecular characterization of viruses from 2013 revealed that viruses circulating in Yucatan were genetically different to viruses from other regions of Mexico. In fact, we identified the occurrence of two genetic variants containing relevant mutations at both the HA and NA surface antigens. There was a difference on the temporal circulation of each genetic variant, viruses containing the mutations HA-A141T / NA-N341S were detected in May, June and July; whereas viruses containing the mutations HA-S162I / NA-L206S circulated in August and September. We discuss the significance of these novel genetic changes.

Molecular characterization of the influenza A(H1N1)pdm09 isolates collected in the 2015‐2016 season and comparison of HA mutations detected in Turkey since 2009

“…T72A was recognized in four isolates collected from Finnish patients in the period of 2009 to 2013 . N260D was identified in 12 Mexican isolates of 2012, in 11 Vietnamese isolates during 2011–2013 period, in 5 German isolates in the 2011‐2012 season, in 39 Mexican, and 43 North American isolates in 2012 . L314M was also detected in 10 Japanese isolates of 2009 .…”

“…Influenza A(H1N1)pdm09 viruses were initially susceptible to oseltamivir and zanamivir but resistance to oseltamivir has emerged during the outbreak possibly as a result of increased clinical use of this drug . To date, the vast majority of influenza A(H1N1)pdm09 isolates remained largely oseltamivir sensitive, however, sporadic cases caused by oseltamivir‐resistant variants also continued to be reported from many countries . Oseltamivir‐resistant influenza A(H1N1)pdm09 viruses have been shown to carry several NA mutations associated with reduced inhibition by NAIs but only the most common NA‐H275Y mutation that confers highly reduced inhibition by oseltamivir was examined in our study.…”

“…Vietnamese isolates during 2011-2013 period, 37 American isolates in 2012. 39 L314M was also detected in 10…”

“…46 To date, the vast majority of influenza A (H1N1)pdm09 isolates remained largely oseltamivir sensitive, 20,47 however, sporadic cases caused by oseltamivir-resistant variants also continued to be reported from many countries. 28,37,39,48,49 Oseltamivir-resistant influenza A(H1N1)pdm09 viruses have been shown to carry several NA mutations associated with reduced inhibition by NAIs 10,47,50-52 but only the most common NA-H275Y mutation that confers highly reduced inhibition by oseltamivir was examined in our study. As with the previous reports from the Turkish Public Health General Directorate, 11,12 the influenza A(H1N1)pdm09 isolates of 2015-2016 season did not carry H275Y mutation.…”

Clinical characteristics and viral analysis of severe influenza A [H1N1]pdm09 in Guangzhou, 2019

“…Influenza virus was isolated and cultured in MDCK cells, and RNA was extracted, transcribed, and amplified according to the kit provided by Takara Bao Biological Engineering (Dalian) Co., Ltd. The primers 1 F1/R1, F2/R2, F3/R3, F5/R5 used by Jose Reyes Canche‐Pech in the 2013 literature were used for amplification. According to the HA sequence of influenza A [H1N1]pdm09 virus in GenBank (GenBank sequence: MK898455.1), the primer F4Unix R4 was designed (shown in Table 1).…”