I have seen this posted and do not know how to upload but thought many might be interested.
http://www.sciencemag.org/cgi/rapidpdf/1176225v1.pdf
Since its identification in April 2009 an A(H1N1) virus
containing a unique combination of gene segments from
both North American and Eurasian swine lineages has
continued to circulate in humans. The lack of similarity
between the 2009 A(H1N1) virus and its nearest relatives
indicates that its gene segments have been circulating
undetected for an extended period. Its low genetic
diversity suggests the introduction into humans was a
single event or multiple events of similar viruses.
Molecular markers predictive of adaptation to humans
are not currently present in 2009 A(H1N1) viruses,
suggesting previously unrecognized molecular
determinants could be responsible for the transmission
among humans. Antigenically the viruses are
homogeneous and similar to North American swine
A(H1N1) viruses but distinct from seasonal human
A(H1N1).
Influenza pandemics occur when an influenza virus with a
hemagglutinin (HA), against which there is little or no
existing immunity, emerges in the human population and
efficiently transmits from human-to-human. The genomes of
the last three pandemic influenza viruses (1918 H1N1, 1957
H2N2 and 1968 H3N2) all originated in whole or in part from
non-human reservoirs, and the HA genes of all of the
pandemic viruses ultimately originated from avian influenza
viruses.
A(H1N1) influenza viruses were first isolated from swine
in 1930 (1) and have been shown to be antigenically highly
similar to a recently reconstructed human 1918 A(H1N1)
virus (2), and likely share a common ancestor (3, 4). From
1930 to the late 1990s these "classical swine influenza"
viruses circulated in swine and remained relatively
antigenically stable (5, 6).
In, or just before, 1998 the classical swine influenza
viruses reassorted with a contemporary human A(H3N2)
influenza virus and an American lineage avian influenza virus
of an unknown subtype resulting in the emergence of a triple
reassortant H3N2 (rH3N2) swine virus in swine populations
throughout North America (7?9). Shortly after the initial
detection of the rH3N2 virus, subsequent reassortment
between the rH3N2 virus and classical H1N1 swine virus is
http://www.sciencemag.org/cgi/rapidpdf/1176225v1.pdf
Since its identification in April 2009 an A(H1N1) virus
containing a unique combination of gene segments from
both North American and Eurasian swine lineages has
continued to circulate in humans. The lack of similarity
between the 2009 A(H1N1) virus and its nearest relatives
indicates that its gene segments have been circulating
undetected for an extended period. Its low genetic
diversity suggests the introduction into humans was a
single event or multiple events of similar viruses.
Molecular markers predictive of adaptation to humans
are not currently present in 2009 A(H1N1) viruses,
suggesting previously unrecognized molecular
determinants could be responsible for the transmission
among humans. Antigenically the viruses are
homogeneous and similar to North American swine
A(H1N1) viruses but distinct from seasonal human
A(H1N1).
Influenza pandemics occur when an influenza virus with a
hemagglutinin (HA), against which there is little or no
existing immunity, emerges in the human population and
efficiently transmits from human-to-human. The genomes of
the last three pandemic influenza viruses (1918 H1N1, 1957
H2N2 and 1968 H3N2) all originated in whole or in part from
non-human reservoirs, and the HA genes of all of the
pandemic viruses ultimately originated from avian influenza
viruses.
A(H1N1) influenza viruses were first isolated from swine
in 1930 (1) and have been shown to be antigenically highly
similar to a recently reconstructed human 1918 A(H1N1)
virus (2), and likely share a common ancestor (3, 4). From
1930 to the late 1990s these "classical swine influenza"
viruses circulated in swine and remained relatively
antigenically stable (5, 6).
In, or just before, 1998 the classical swine influenza
viruses reassorted with a contemporary human A(H3N2)
influenza virus and an American lineage avian influenza virus
of an unknown subtype resulting in the emergence of a triple
reassortant H3N2 (rH3N2) swine virus in swine populations
throughout North America (7?9). Shortly after the initial
detection of the rH3N2 virus, subsequent reassortment
between the rH3N2 virus and classical H1N1 swine virus is
