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Abstract
BackgroundIn early 2009, a novel influenza A(H1N1) virus that emerged in Mexico and United States rapidly disseminated worldwide. The spread of this virus caused considerable morbidity with over 18000 recorded deaths. The new virus was found to be a reassortant containing gene segments from human, avian and swine influenza viruses.Methods/ResultsThe first case of human infection with A(H1N1)pdm09 in Pakistan was detected on 18th June 2009. Since then, 262 laboratory-confirmed cases have been detected during various outbreaks with 29 deaths (as of 31st August 2010). The peak of the epidemic was observed in December with over 51% of total respiratory cases positive for influenza. Representative isolates from Pakistan viruses were sequenced and analyzed antigenically. Sequence analysis of genes coding for surface glycoproteins HA and NA showed high degree of high levels of sequence identity with corresponding genes of regional viruses circulating South East Asia. All tested viruses were sensitive to Oseltamivir in the Neuraminidase Inhibition assays.ConclusionsInfluenza A(H1N1)pdm09 viruses from Pakistan form a homogenous group of viruses. Their HA genes belong to clade 7 and show antigenic profile similar to the vaccine strain A/California/07/2009. These isolates do not show any amino acid changes indicative of high pathogenicity and virulence. It is imperative to continue monitoring of these viruses for identification of potential variants of high virulence or drug resistance.
Highlights
In April 2009, novel reassortant influenza A(H1N1) virus {A(H1N1)pdm09} emerged causing a pandemic that affected 214 countries and resulted in 18449 virologically confirmed deaths (WHO update on Pandemic H1N1 2009, 6th August 2010)
Influenza A(H1N1)pdm09 viruses from Pakistan form a homogenous group of viruses
Their HA genes belong to clade 7 and show antigenic profile similar to the vaccine strain A/California/07/2009
Summary
In April 2009, novel reassortant influenza A(H1N1) virus {A(H1N1)pdm09} emerged causing a pandemic that affected 214 countries and resulted in 18449 virologically confirmed deaths (WHO update on Pandemic H1N1 2009, 6th August 2010). Genetic analysis of the pandemic virus revealed a novel combination of genes from human, swine, and Eurasian avian viruses [2,3,4]. Molecular analysis showed that these viruses had diversified into at least seven distinct clades (clades 1–7) with well defined spatial distribution [4,6] These viruses lacked specific molecular determinants of adaptation to human hosts, thereby suggesting a role of as yet unknown/undocumented molecular markers associated with human transmission [6]. In early 2009, a novel influenza A(H1N1) virus that emerged in Mexico and United States rapidly disseminated worldwide. The spread of this virus caused considerable morbidity with over 18000 recorded deaths. The new virus was found to be a reassortant containing gene segments from human, avian and swine influenza viruses
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