Scientific News Health care Preventive maintenance of diseases INFLUENZA INFECTION ATTRACTS PNEUMONIA BACTERIA
INFLUENZA
INFECTION ATTRACTS PNEUMONIA BACTERIA
Lung cells infected with the influenza A virus
are more likely to bind with bacteria that cause pneumonia than uninfected
cells, but this phenomenon can be reversed with antiviral treatment. Researchers
from the University of Kansas Medical Center present their findings today at the
102nd General Meeting of the American Society for Microbiology. “Bacterial
pneumonia caused by Streptococcus pneumoniae can occur secondary to viral
infections such as influenza. Previous studies have shown that by treating the
influenza virus with Tamiflu, a neuraminidase inhibitor that attacks the
influenza virus at the cellular level, secondary complications such as pneumonia
can be reduced,” says Dr. Rebecca Horvat, one of the researchers on the study.
Dr. Horvat and her colleagues examined the
relationship between the binding of S. pneumoniae bacteria to a lung epithelial
cell line (the cells that line the respiratory system) with and without
influenza A infection. Preliminary studies showed that after 24, 48 or 72 hours
of viral infection, the bacteria bound to the influenza-infected cells 4 to 10
times higher than uninfected cells. When the flu virus was treated with Tamiflu,
the increased binding was reversed.
“An influenza-infected lung epithelial cell
will bind more S. pneumoniae bacteria than uninfected cells. Treatment with
Tamiflu at doses used to treat influenza infections can prevent this increased
bacterial binding, and perhaps prevent post-influenza complications, such as
pneumonia,” says Dr. Horvat.
S. pneumoniae continues to be the leading cause
of community-acquired pneumonia worldwide. Although the ability of bacteria to
bind to host cells is the first step in the process of infection, few studies
have correlated S. pneumoniae cell binding with the severity of lower
respiratory tract infections. Dr. Horvat notes that this study has implications
only for influenza A infections and additional research must be done on
influenza B infection.
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The study was funded by F. Hoffmann-La Roche.
This release is a summary of a presentation from
the 102nd General Meeting of the American Society for Microbiology, May 19-23,
2002, in Salt Lake City, Utah. Additional information on these and other
presentations at the 102nd ASM General Meeting can be found online at http://www.asmusa.org/pcsrc/gm2002/presskit.htm
or by contacting Jim Sliwa (jsliwa@asmusa.org)
in the ASM Office of Communications. The phone number for the General Meeting
Press Room is (801) 534-4720 and will be active from 10:00 a.m. MDT, May 19
until 12:00 noon MDT, May 23.
Contact: Jim Sliwa, jsliwa@asmusa.org,
202-942-9297, American Society for Microbiology
Source of the given news and the copyrights
belong to a American
Society for Microbiology
Publishing date: May 28, 2002
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