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.
Highlights
In September 2009, the World Health Organization (WHO) recommended to include the 2009 pandemic influenza A(H1N1) virus as the H1N1 component of the trivalent, seasonal influenza vaccine for the 2010 influenza season in the southern hemisphere
In February 2010, the same recommendation was made for the 2010/2011 influenza season in the northern hemisphere. This indicates that the world-wide circulation the 2009 pandemic influenza A(H1N1) virus has not yet undergone significant antigenic and genetic changes
Elderly individuals were found to have pre-existing cross-reactive antibodies to the novel pandemic virus that were likely derived from previous infection with an antigenically related virus such as the Spanish influenza and its immediate descendant viruses that were circulating in the early decades of the 20th century [1,2]
Summary
In September 2009, the World Health Organization (WHO) recommended to include the 2009 pandemic influenza A(H1N1) virus as the H1N1 component of the trivalent, seasonal influenza vaccine for the 2010 influenza season in the southern hemisphere. In February 2010, the same recommendation was made for the 2010/2011 influenza season in the northern hemisphere This indicates that the world-wide circulation the 2009 pandemic influenza A(H1N1) virus has not yet undergone significant antigenic and genetic changes. This stability may be attributed to the lack of pre-existing immunity in large segments of the global human population. Elderly individuals were found to have pre-existing cross-reactive antibodies to the novel pandemic virus that were likely derived from previous infection with an antigenically related virus such as the Spanish influenza and its immediate descendant viruses that were circulating in the early decades of the 20th century [1,2]. 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
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