- Hello Jeff - Remember this? Scientists isolate genes
that made the 1918 flu lethal. This was dated Dec. 29, 2008. It hasn't
been very long since this discovery was made then the new strain variant
showed up in Mexico and the US, not very long, indeed.
- "The 1918 virus replicates in the upper respiratory
tract, but also in the lungs, causing primary pneumonia among its victims."
- I think it is pretty obvious that the Mexican variant
also replicates in upper respiratory tract and also in the lungs causing
primary pneumonia. I think we are seeing this in the Mexican cases. Coincidence?
Or, is the Mexican virus a lab developed copy of the Spanish Flu.
- "For the most part, substituting single genes from
the 1918 virus onto the template of a much more benign contemporary virus
yielded agents that could only replicate in the upper respiratory tract.
One exception, however, included a complex of three genes that, acting
in concert with another key gene, allowed the virus to efficiently colonize
lung cells and make RNA polymerase, a protein necessary for the virus to
- Scientists Isolate Genes That Made 1918 Flu Lethal
- By Terry Devitt
- By mixing and matching a contemporary flu virus with
the "Spanish flu" - a virus that killed between 20 and 50 million
people 90 years ago in history's most devastating outbreak of infectious
disease - researchers have identified a set of three genes that helped
underpin the extraordinary virulence of the 1918 virus.
- Writing today (Dec. 29) in the Proceedings of the National
Academy of Sciences, a team led by University of Wisconsin-Madison virologists
Yoshihiro Kawaoka and Tokiko Watanabe identifies genes that gave the 1918
virus the capacity to reproduce in lung tissue, a hallmark of the pathogen
that claimed more lives than all the battles of World War I combined.
- "Conventional flu viruses replicate mainly in the
upper respiratory tract: the mouth, nose and throat. The 1918 virus replicates
in the upper respiratory tract, but also in the lungs," causing primary
pneumonia among its victims, says Kawaoka, an internationally recognized
expert on influenza and a professor of pathobiological sciences in the
UW-Madison School of Veterinary Medicine. "We wanted to know why the
1918 flu caused severe pneumonia."
- Autopsies of 1918 flu victims often revealed fluid-filled
lungs severely damaged by massive hemorrhaging. Scientists assumed that
the ability of the virus to take over the lungs is associated with the
pathogen's high level of virulence, but the genes that conferred that ability
- Discovery of the complex and its role in orchestrating
infection in the lungs is important because it could provide a way to quickly
identify the potential virulence factors in new pandemic strains of influenza,
Kawaoka says. The complex could also become a target for a new class of
antiviral drugs, which is urgently needed as vaccines are unlikely to be
produced fast enough at the outset of a pandemic to blunt its spread.
- To find the gene or genes that enabled the virus to invade
the lungs, Kawaoka and his group blended genetic elements from the 1918
flu virus with those of a currently circulating avian influenza virus and
tested the variants on ferrets, an animal that mimics human flu infection.
- For the most part, substituting single genes from the
1918 virus onto the template of a much more benign contemporary virus yielded
agents that could only replicate in the upper respiratory tract. One exception,
however, included a complex of three genes that, acting in concert with
another key gene, allowed the virus to efficiently colonize lung cells
and make RNA polymerase, a protein necessary for the virus to reproduce.
- "The RNA polymerase is used to make new copies of
the virus," Kawaoka explains. Without the protein, the virus is unable
to make new virus particles and spread infection to nearby cells.
- In the late 1990s, scientists were able to recover genes
from the 1918 virus by looking in the preserved lung tissue of some of
the pandemic's victims. Using the relic genes, Kawaoka's group was able
to generate viruses that carry different combinations of the 1918 virus
and modern seasonal influenza virus.
- When tested, most of the hybrid viruses only infected
the nasal passages of ferrets and didn't cause pneumonia. But one did infect
the lungs, and it carried the RNA polymerase genes from the 1918 virus
that allowed the virus to make the key step of synthesizing its proteins.
- In 2004, Kawaoka and his team identified another key
gene from the 1918 virus that enhanced the pathogen's virulence in mice.
That gene makes hemagglutinin, a protein found on the surface of the virus
and that confers on viral particles the ability to attach to host cells.
- "Here, I think we are talking about another mechanism,"
Kawaoka says. The RNA polymerase is used to make copies of the virus once
it has entered a host cell. The role of hemagglutinin is to help the virus
gain access to cells.
- In addition to the study's lead authors, Watanabe and
Kawaoka, co-authors of the new PNAS paper are Shinji Watanabe, Jin Hyun
Kim and Masato Hatta, also of UW-Madison; and Kyoko Shinya of Kobe University.
The work was funded by the Japanese Ministry of Education, Culture, Sports,
Science and Technology and by grants-in-aid from the Ministry of Health,
Labor and Welfare of Japan.
- Patricia A. Doyle DVM, PhD Bus Admin, Tropical Agricultural
Economics Univ of West Indies Please visit my "Emerging Diseases"
message board at: http://www.emergingdisease.org/phpbb/index.php Also my
new website: http://drpdoyle.tripod.com/ Zhan le Devlesa tai sastimasa
Go with God and in Good Health