Abstract
As we enter the year of 2011, the 2009 H1N1 pandemic influenza virus is in the news again. At least 20 people have died of this virus in China since the beginning of 2011 and it is now the predominant flu strain in the country. Although this novel virus was quite stable during its run in the flu season of 2009-2010, a genetic variant of this virus was found in Singapore in early 2010, and then in Australia and New Zealand during their 2010 winter influenza season. Several critical mutations in the HA protein of this variant were uncovered in the strains collected from January 2010 to April 2010. Moreover, a structural homology model of HA from the A/Brisbane/10/2010(H1N1) strain was made based on the structure of A/California/04/2009 (H1N1). The purpose of this study was to investigate mutations in the HA protein of 2009 H1N1 from sequence data collected worldwide from May 2010 to February 2011. A fundamental problem in bioinformatics and biology is to find the similar gene sequences for a given gene sequence of interest. Here we proposed the inverse problem, i.e., finding the exemplars from a group of related gene sequences. With a clustering algorithm affinity propagation, six exemplars of the HA sequences were identified to represent six clusters. One of the clusters contained strain A/Brisbane/12/2010(H1N1) that only differed from A/Brisbane/10/2010 in the HA sequence at position 449. Based on the sequence identity of the six exemplars, nine mutations in HA were located that could be used to distinguish these six clusters. Finally, we discovered the change of correlation patterns for the HA and NA of 2009 H1N1 as a result of the HA receptor binding specificity switch, revealing the balanced interplay between these two surface proteins of the virus.
Highlights
A report on February 10, 2011 indicated that 2009 H1N1 has become the predominant strain of influenza virus in China and caused at least twenty deaths in the country since the beginning of 2011 [1]
We discovered the change of correlation patterns for the HA and NA of 2009 H1N1 as a result of the HA receptor binding specificity switch, revealing the balanced interplay between these two surface proteins of the virus
One of them happened to be N125D (Figure 1), a mutation found in the genetic variant of 2009 H1N1 in Singapore, Australia and New Zealand [2]
Summary
A report on February 10, 2011 indicated that 2009 H1N1 has become the predominant strain of influenza virus in China and caused at least twenty deaths in the country since the beginning of 2011 [1]. As the 20102011 flu season continues, this virus remains a public health concern This novel swine-origin virus maintained its genetic stability during its run in the 2009-2010 flu season for the most part. Several vaccine breakthroughs and fatal cases might be linked to this variant [2]. These new developments call for a continued surveillance of its circulation and evolution, even though extensive research on 2009 H1N1 has been conducted including a series of studies in [3,4,5,6,7,8,9,10,11,12,13]
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