Re: A report on Global Spreading of 1957 1968 pandemic and 2009 novel strain
Pandemic H1N1/09 Virus Generation
Based on genomic analysis results, it appears that the
pandemic H1N1/09 virus first evolved around September
2008 and circulated in the human population for several
months before the first cases were detected. It emerged
from a triple-reassortant swine influenza A (H1N1) virus
that developed and became enzootic in pigs in North
America at the end of the 1990s [15?17]. This triple-reassortant
swine influenza A virus contains genes from
avian, human, and swine influenza viruses. Its spread to
humans was detected sporadically, but all patients recovered.
Severe illnesses of the lower respiratory tract and
unusual influenza symptoms, such as diarrhea, were reported
[16]. The triple-reassortant swine influenza A
(H1N1) virus contains classic swine RNA segments of
North American lineage (hemagglutinin [H], nucleoprotein
[NP], non-structural proteins [NS], neuraminidase
[N], matrix proteins [M]), avian influenza RNA segments
of North American lineage (polymerase basic protein 2
[PB2], polymerase acidic protein [PA]), and PB1 of human
seasonal H3N2 viruses [15, 16]. In the pandemic
H1N1/09 virus, the N and M segments of triple-reassortant
swine influenza A (H1N1) were replaced by N and M
from the Eurasian influenza A (H1N1) swine lineage [15,
16]. Therefore, in contrast to the 1918 pandemic for which
the zoonotic sources of the introduced viral gene segments
remain to this day ambiguous [14], it is known that pandemic
H1N1/09 virus probably emerged from swine into
humans. However, there were no confirmed influenza
virus outbreaks in Central American pigs before the reported
H1N1/09 infections in humans. The asymptomatic
infection of H1N1/09 in specific pathogen-free miniature
pigs (swine influenza model), despite efficient virus replication,
may explain the lack of reports on H1N1/09
outbreaks in pigs prior to its transmission to humans [18].
This lack of similarity between the pandemic H1N1/
09 virus and its nearest relatives indicates that its gene
segments have already circulated for years [17, 19]. The
genetic diversity of pandemic H1N1/09 virus is low, suggesting
that its transmission to humans results from a
single event or that very similar viruses were transmitted.
The pandemic H1N1/09 virus lacks molecular markers
thought to be associated with the adaptation of influenza
A viruses to humans [19]. Consequently, pandemic
H1N1/09 virus spread in humans appears to result from
unidentified molecular events that warrant further studying.
Moreover, the results of evolutionary analysis aimed
at estimating the timescale of the origins and the early
development of pandemic H1N1/09 virus epidemic revealed
that the initial transmission to humans occurred
several months before the recognition of the outbreak
[17]. The multiple genetic ancestry of pandemic H1N1/09
virus suggests that the pandemic H1N1/09 virus has
developed naturally, and no indications of artificial origin
were found [17]. The pandemic H1N1/09 virus pandemic
clearly proves that the mixing of genetic elements from
different influenza A viruses in pigs can result in pandemic
viruses and that the surveillance of influenza viruses
in pigs is warranted.
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