Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 200, Issue 3, Pages 439-447Publisher
OXFORD UNIV PRESS INC
DOI: 10.1086/600108
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Funding
- Oak Ridge Institute for Science and Education (ORISE)
- National Institutes of Health [5R01AI06275-03]
- Georgia Research Alliance
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Because the G protein of respiratory syncytial virus (RSV) has a CX3C chemokine motif that has been associated with the ability of RSV G protein to modulate the virus-induced host immune response, we examined whether therapeutic treatment with an anti-RSV G monoclonal antibody (mAb), 131-2G, that blocks the CX3C-associated activity of RSV G protein might decrease the pulmonary inflammation associated with infection in BALB/c mice. The results show that treatment with mAb 131-2G on day 3 after RSV infection reduces both inflammation and RSV titer in the lungs. Later administration of anti-RSV G mAb (day 5 after RSV infection) effectively reduced the viral titer but had a minimal effect on pulmonary inflammation. This study suggests that an anti-RSV G mAb might be an effective antiviral, either alone or in combination with anti-RSV F protein neutralizing antibodies, for decreasing the virus-induced host response to infection and improve treatment outcome.
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