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J Virol, August 1998, p. 6884-6887, Vol. 72, No. 8
Department of Microbiology and Immunology,
Received 18 March 1998/Accepted 24 April 1998
The influence of diabetes on susceptibility to influenza virus
infection was examined in a mouse model in which RIP-Kb
transgenic mice and their nontransgenic littermates were used as the
diabetic and nondiabetic hosts, respectively. Influenza virus A/Phil/82
(H3N2) grew to significantly higher titers in the lungs of diabetic
than nondiabetic mice. The extent of viral replication in the lungs was
proportional to blood glucose levels in the mice at the time of
infection, and the enhanced susceptibility of diabetic mice was
reversed with insulin. Growth of A/HKx31 (H3N2) virus was also enhanced
in diabetic mice, whereas the highly virulent strain A/PR/8/34 (H1N1)
showed no difference in virus yields in diabetic and nondiabetic mice,
even with low inocula. A/Phil/82 and A/HKx31 are sensitive to
neutralization in vitro by the pulmonary collectin surfactant protein D
(SP-D), whereas A/PR/8/34 is essentially resistant. Glucose is a ligand
for SP-D, and neutralization of A/Phil/82 virus by SP-D was abolished
in the presence of glucose at levels commonly found in diabetic mice. These findings suggest that in mice, and perhaps in humans, diabetes predisposes to influenza virus infection through compromise of collectin-mediated host defense of the lung by glucose.
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Increased Susceptibility of Diabetic Mice to
Influenza Virus Infection: Compromise of Collectin-Mediated Host
Defense of the Lung by Glucose?
*
Corresponding author. Mailing address: Dept. of
Microbiology and Immunology, University of Melbourne, Grattan St.,
Parkville, Victoria 3052, Australia. Phone: 61 3 9344 5702. Fax: 61 3 9347 1540. E-mail:
m.anders{at}microbiology.unimelb.edu.au.
J Virol, August 1998, p. 6884-6887, Vol. 72, No. 8
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
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