Gert van der Hoek
In Memoriam - Editor, Senior Moderator
google translated from French
Influenza A (H1N1): whence its virulence?
The interaction with receptors of lung and immune factors seem to explain the
virulence of influenza A (H1N1) in some people.
Jean-Jacques Perrier
The new influenza virus A (H1N1) is it more dangerous than seasonal virus?
The death in mid - September, two French apparently healthy, aged 26 and 29 years, is a
question that hangs from the beginning of the pandemic. Both died of pneumonia
followed by a syndrome of acute respiratory distress (ARDS), one so explosive, the other after
several weeks of hospitalization in Greece.
Gold Team Ten Feizi, Imperial College London, has highlighted a
mechanism that explains why the virus causes more severe symptoms of the virus
seasonal in some people. All influenza viruses infect cells of the device
breathing by binding to receptors. These receptors are molecules of sialic acid linked
to galactose by links called alpha-2, 6 and alpha-2, 3. Now, explain T. Feizi and
colleagues, while the seasonal virus attaches to receptors alpha-2, 6 present in the cells
of the upper respiratory tract, influenza A (H1N1) has the particularity to bind to receptors also
alpha-2, 3 lining the lower respiratory tract, causing injury and infection more
serious.
This conclusion corroborates the results obtained in July in mice, ferrets and macaques
by the team of Ron Fouchier of Erasmus Center Rotterdam, and several Japanese teams
coordinated by Yoshihiro Kawaoka, University of Kobe, they showed that the new virus
settles in the lungs and that causes damage bronchial and lung
sharper than the seasonal virus (see photo).
According to Antoine Flahault, professor of epidemiology at the Graduate School of Public Health,
Data from Mauritius and New Caledonia indicate that mortality "direct"
virus 2009, by ARDS is much higher than the seasonal virus: approximately 1 in 10
000, against 1 per million.
Mexican data published August 13 do not
overall statistics, but confirmed that at least seven young subjects in good health
died from the flu between March 24 and April 24, 2009, about 18 cases of pneumonia due to
virus.
According to a Spanish publication of the September 15, of 32 adults admitted to intensive care
for viral pneumonia between June 23 and July 31, 2009, only 16 were suffering from a pathology
preexisting.
These facts suggest that individual factors are involved: the individual characteristics of
viral receptors could be included, but also variations in the quality of responses
Immunity.
A study team of Beatrice Riteau at INRA in Jouy-en-Josas, and shows
various strains of influenza virus A trigger in the cells of the alveoli
pulmonary production of HLA-G, known to inhibit immune responses.
By making these molecules, cells infected with H1N1 are not recognized by the
immune system and are not destroyed, allowing the virus to proliferate in
body. The HLA-G is synthesized mainly during pregnancy, this
discovery could also explain the greater vulnerability of pregnant women vis-?-vis
influenza A (H1N1). Indeed, by producing large quantities of HLA-G, their
immune system is inhibited even before influenza infection occurs.
http://www.pourlascience.fr/ewb_pages/a/actualite-virus-a-h1n1-d-ou-vient-sa-virulencea-23413.php
Influenza A (H1N1): whence its virulence?
The interaction with receptors of lung and immune factors seem to explain the
virulence of influenza A (H1N1) in some people.
Jean-Jacques Perrier
The new influenza virus A (H1N1) is it more dangerous than seasonal virus?
The death in mid - September, two French apparently healthy, aged 26 and 29 years, is a
question that hangs from the beginning of the pandemic. Both died of pneumonia
followed by a syndrome of acute respiratory distress (ARDS), one so explosive, the other after
several weeks of hospitalization in Greece.
Gold Team Ten Feizi, Imperial College London, has highlighted a
mechanism that explains why the virus causes more severe symptoms of the virus
seasonal in some people. All influenza viruses infect cells of the device
breathing by binding to receptors. These receptors are molecules of sialic acid linked
to galactose by links called alpha-2, 6 and alpha-2, 3. Now, explain T. Feizi and
colleagues, while the seasonal virus attaches to receptors alpha-2, 6 present in the cells
of the upper respiratory tract, influenza A (H1N1) has the particularity to bind to receptors also
alpha-2, 3 lining the lower respiratory tract, causing injury and infection more
serious.
This conclusion corroborates the results obtained in July in mice, ferrets and macaques
by the team of Ron Fouchier of Erasmus Center Rotterdam, and several Japanese teams
coordinated by Yoshihiro Kawaoka, University of Kobe, they showed that the new virus
settles in the lungs and that causes damage bronchial and lung
sharper than the seasonal virus (see photo).
According to Antoine Flahault, professor of epidemiology at the Graduate School of Public Health,
Data from Mauritius and New Caledonia indicate that mortality "direct"
virus 2009, by ARDS is much higher than the seasonal virus: approximately 1 in 10
000, against 1 per million.
Mexican data published August 13 do not
overall statistics, but confirmed that at least seven young subjects in good health
died from the flu between March 24 and April 24, 2009, about 18 cases of pneumonia due to
virus.
According to a Spanish publication of the September 15, of 32 adults admitted to intensive care
for viral pneumonia between June 23 and July 31, 2009, only 16 were suffering from a pathology
preexisting.
These facts suggest that individual factors are involved: the individual characteristics of
viral receptors could be included, but also variations in the quality of responses
Immunity.
A study team of Beatrice Riteau at INRA in Jouy-en-Josas, and shows
various strains of influenza virus A trigger in the cells of the alveoli
pulmonary production of HLA-G, known to inhibit immune responses.
By making these molecules, cells infected with H1N1 are not recognized by the
immune system and are not destroyed, allowing the virus to proliferate in
body. The HLA-G is synthesized mainly during pregnancy, this
discovery could also explain the greater vulnerability of pregnant women vis-?-vis
influenza A (H1N1). Indeed, by producing large quantities of HLA-G, their
immune system is inhibited even before influenza infection occurs.
http://www.pourlascience.fr/ewb_pages/a/actualite-virus-a-h1n1-d-ou-vient-sa-virulencea-23413.php