Molecular Epidemiology and Evolution of Influenza A(H1N1) pdm09 Virus in Kenya
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Date
2014-02-17
Authors
Maina, George Gachara
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Abstract
In April 2009, a novel influenza A virus was detected in Mexico and California. Thereafter, it
spread globally to cause the first influenza pandemic of the 21st century. The virus was found
to be antigenically unrelated to human seasonal influenza viruses but genetically related to
viruses known to circulate in pigs. In view of its likely swine origin, it was initially referred
to as ‘swine-origin influenza virus’ (S-OIV) A/H1N1, or pandemic influenza A (H1N1) 2009
virus but was later renamed by the World Health Organization as influenza A(H1N1)pdm09
virus. In its first year of circulation, the virus is estimated to have caused between 151,700
and 575,400 deaths globally. In Kenya, the virus was first detected in late June 2009 and in
the next one year was the dominant virus in circulation. However, no laboratory confirmed
deaths occurred in the country. The emergence and subsequent rapid global spread of this
influenza virus provided a unique opportunity to observe the evolutionary dynamics of a
pandemic influenza virus in Kenya, a tropical region where the virus circulates throughout
the year. Understanding the evolution of influenza A(H1N1)pdm09 virus within the
country is essential for studying global diversification, the emergence, spread and
resistance of the viruses circulating in this region of the world, as well as determining
the genetic relationships among the Kenyan strains and vaccine strains. The aim of this
study therefore was to reconstruct the evolutionary dynamics of the A(H1N1)pdm09
influenza virus in Kenya during its first year of circulation. To accomplish this, the study
undertook whole genome Sanger sequencing of 40 influenza A(H1N1)pdm09 virus isolates
sampled nationwide during the pandemic period. To understand the evolutionary dynamics of
the local A(H1N1)pdm09 viruses, the study employed the Bayesian evolutionary framework
to analyze the resulting 320 individual gene sequences and the 40 complete genomes and
compared them with sequences from two African countries, UK, USA and China isolated
during the same period. The phylogenetic analyses showed that all of the Kenyan sequences
sampled in the pandemic period grouped into at least four highly significant clusters and were
interspersed with isolates from other countries. Two global clades (2 and 7) were identifiable
within the first two weeks of the pandemic in Kenya, with clade 7 undergoing further
diversification while clade 2 was not detected beyond the introductory foci. The time of the
most recent common ancestor of the strains circulating in Kenya was estimated to be between
April and June 2009, two months before the first laboratory confirmed case. High
evolutionary rates and fast population growths was also observed. Progressive drift away
from the vaccine strain was observed at both the nucleotide and amino acid level, with 2010
strains clustering separate from 2009 strains. A few unique clusters of amino acid changes
were identified among all gene segments in the course of the pandemic, but no mutations
previously associated with increased virulence were detected. The local strains were shown to
be sensitive to neuraminidase inhibitors but resistant to adamantanes. Overall, results from
this study indicate that two clades of influenza A(H1N1)pdm09 virus were introduced in
Kenya and that the pandemic was sustained by multiple importations. They also indicate that
clade 7 viruses dominated local transmission with an efficient community spread that was
devoid of any spatial patterns but a progressive genetic drift was evident. In conclusion,
adaptive evolution and viral migration seem to play a vital role in shaping the evolutionary
dynamics of local A(H1N1)pdm09 viruses.
Description
Department of Medical Laboratory Sciences, 174p. 2013, RA 644 .V55M3