Journal of Virology, September 1999, p. 7099-7107, Vol. 73, No. 9
Division of Viral and Rickettsial Diseases,
National Center of Infectious Diseases, Centers for Disease Control
and Prevention, Atlanta, Georgia 30333,1
and Departments of Pediatrics and Microbiology, University
of Alabama School of Medicine, Birmingham, Alabama
352332
Received 1 March 1999/Accepted 12 May 1999
BALB/c mice sensitized to vaccinia virus expressed G protein of
respiratory syncytial virus (RSV) develop a Th2-type cytokine response
and pulmonary eosinophilia when challenged with live RSV. In this
study, BALB/c mice were immunized or challenged with an RSV mutant
lacking the G and SH proteins or with DNA vaccines coding for RSV G or
F protein. F or G protein DNA vaccines were capable of sensitizing for
pulmonary eosinophilia. The absence of the G and/or SH protein in the
infecting virus resulted in a consistent increase both in pulmonary
natural killer cells and in gamma interferon and tumor necrosis factor
expression, as well as, with primary infection, a variable increase in
neutrophils and CD11b+ cells. The development of pulmonary
eosinophilia in formalin-inactivated RSV-vaccinated mice required the
presence of the G and/or SH protein in the challenge virus. These data
show that G and/or SH protein has a marked impact on the inflammatory
and innate immune response to RSV infection.
0022-538X/99/$04.00+0
Respiratory Syncytial Virus G and/or SH Protein Alters Th1
Cytokines, Natural Killer Cells, and Neutrophils Responding to
Pulmonary Infection in BALB/c Mice
*
Corresponding author. Mailing address: Centers for
Disease Control and Prevention, 1600 Clifton Rd., MS G-09, Atlanta, GA 30333. Phone: (404) 639-3427. Fax: (404) 639-1307. E-mail:
rgt3{at}cdc.gov.
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