Genetic Diversity of the 2009 Pandemic Influenza A(H1N1) Viruses in Finland

Abstract

BackgroundIn Finland, the first infections caused by the 2009 pandemic influenza A(H1N1) virus were identified on May 10. During the next three months almost all infections were found from patients who had recently traveled abroad. In September 2009 the pandemic virus started to spread in the general population, leading to localized outbreaks and peak epidemic activity was reached during weeks 43–48.Methods/ResultsThe nucleotide sequences of the hemagglutinin (HA) and neuraminidase (NA) genes from viruses collected from 138 patients were determined. The analyzed viruses represented mild and severe infections and different geographic regions and time periods. Based on HA and NA gene sequences, the Finnish pandemic viruses clustered in four groups. Finnish epidemic viruses and A/California/07/2009 vaccine virus strain varied from 2–8 and 0–5 amino acids in HA and NA molecules, respectively, giving a respective maximal evolution speed of 1.4% and 1.1%. Most amino acid changes in HA and NA molecules accumulated on the surface of the molecule and were partly located in antigenic sites. Three severe infections were detected with a mutation at HA residue 222, in two viruses with a change D222G, and in one virus D222Y. Also viruses with change D222E were identified. All Finnish pandemic viruses were sensitive to oseltamivir having the amino acid histidine at residue 275 of the neuraminidase molecule.ConclusionsThe Finnish pandemic viruses were quite closely related to A/California/07/2009 vaccine virus. Neither in the HA nor in the NA were changes identified that may lead to the selection of a virus with increased epidemic potential or exceptionally high virulence. Continued laboratory-based surveillance of the 2009 pandemic influenza A(H1N1) is important in order to rapidly identify drug resistant viruses and/or virus variants with potential ability to cause severe forms of infection and an ability to circumvent vaccine-induced immunity.

Emergent 2009 influenza A(H1N1) viruses containing HA D222N mutation associated with severe clinical outcomes in the Americas

“…2 The cell tropisms and biochemical roles of 2009 A(H1N1) variants with changes in the receptor binding regions (e.g., D222G) have been linked to severe infections documented by several groups over the past two seasons. [3][4][5][6][7][8][9][10][11] Viruses carrying an asparagine (N) change at position 222 (D222N -H1 numbering) within the primary receptor-binding site were collected from two cases: one from Quito, Ecuador, in December 2010 and one from Washington, DC, USA, in March 2011. Both cases were complicated by acute respiratory distress, with the Ecuador case being fatal.…”

Extensive Geographical Mixing of 2009 Human H1N1 Influenza A Virus in a Single University Community

“…Unsurprisingly, there have been attempts to reconstruct the spread of H1N1/09 at both global (11,13,21) and national (8,9,14,15,19,24,26) scales. However, little is known about the patterns and dynamics of H1N1/09 spread at finer spatial scales.…”

Phylogenetic and nucleotide sequence analysis of influenza A (H1N1) HA and NA genes of strains isolated from Saudi Arabia

“…As none of the Saudi Arabian strains analyzed here displayed this mutation, or induced a fatal outcome, further study, especially in more serious cases, is warranted. Most of the Saudi isolates retained isoleucine (I) at position 321 of HA, but very few had the I321V mutation seen in certain European viruses [32]. In contrast to the HA D222G mutation [22], the effect of retaining isoleucine at this position on disease severity has not been clearly demonstrated.…”