Second Stage of Swine Flu - Autumn Pandemic

http://www.recombinomics.com/News/05030901/Swine_H1N1_H2S.html

Swine H1N1 Transmission From Human to Swine

Recombinomics Commentary Dr. Henry Nieman May 3, 2009

The pigs in Alberta were thought to be infected by a farm worker who returned from Mexico on April 12 and began working on the farm two days later. Officials noticed the pigs had flu-like symptoms April 24, Evans said.

Approximately 10 percent of the 2,200 pigs on the farm have been infected, Evans said.

The above comments describe the transmission of the H1N1 swine flu from an infected farm worker to swine in Alberta, Canada. This efficient transmission from human to swine suggests that much of the speculation in the past week is overly optimistic.

The virus is swine, WHO newspeak notwithstanding, and contains six swine gene segments as well as a human PB1 and an avian PB2 that have been in swine for more than a decade. Therefore, although swine to swine transmission is not unexpected, the trans mission from human to swine is striking. The H1N1 is called swine H1N1 for scientific reason. It is not a "nickname" as some media accounts mis-report, but a descriptive name that defines its normal host. The species differences in sequence are easily determined, and species jumps are rare, but can be deadly. Usually the virus replicates most effectively in is host species.

The jump to humans is cause for concern. The last time as swine flu jumped to human and was efficiently spread in the new host was in 1918.

The fact that the virus can jump from human to swine as well as swine to humans suggests this virus is not going to fade away. It has already moved into the southern hemisphere. Suspect cases have been reported in Brazil, Australia, and New Zealand, where the seasonal flu season is just beginning.

Co-circulation of human and swine H1N1 provide significant opportunities for adaptation to the human host via recombination. Two polymorphisms are already fixed in seasonal flu, H274Y for Tamiflu resistance, and E627K in PB2 which allows the virus to more efficiently replicate at lower temperatures.

These changes can lead to adaptation in humans, as well antiviral resistance. Therefore, the evolution of the H1N1 over the summer will be closely monitored. The current H1N1 has already acquired tandem human H1N1 polymorphism in HA, which may have led to the species jump from swine to human.

Thus, the efficient transmission from swine to human and vice verse, raises concerns that further adaptation to humans can lead to a fall pandemic similar to 1918. The species jump indicates the virus can adapt to a new host, and additional acquisitions over the summer continue to be a cause for concern.