Moderate local and systemic respiratory syncytial virus-specific T-cell responses upon mild or subclinical RSV infection
✍ Scribed by L. de Waal; L.P. Koopman; I.J. van Benten; A.H. Brandenburg; P.G.H. Mulder; R.L. de Swart; W.J. Fokkens; H.J. Neijens; A.D.M.E. Osterhaus
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 142 KB
- Volume
- 70
- Category
- Article
- ISSN
- 0146-6615
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✦ Synopsis
Abstract
Respiratory syncytial virus (RSV) infections are a major cause of severe respiratory disease in infants. It has been shown that there is an increased frequency of childhood wheezing in ex‐bronchiolitic preteen children. This was postulated to be mediated by a vigorous virus‐specific Th2 response influencing the further development of the immune system. Little is known about the possible role of the immune response to clinically mild RSV infections in this respect. We have studied the RSV‐specific cellular immune response in infants with a laboratory‐confirmed RSV upper respiratory tract infection (URTI; n = 13, mean age 12 months, range 2–22 months) in comparison with infants with non‐RSV mediated URTI (n = 9, mean age 9.3 months, range 4–18 months) or infants with severe RSV bronchiolitis (n = 11, mean age 2.3 months, range 1–6 months). RSV‐specific cytokine‐producing cells were enumerated using the ELISPOT method in peripheral blood mononuclear cells and nasal brush T‐cells, collected during the acute and convalescent phase of the infection. Mixed Th1 (IFN‐γ) and Th2 (IL‐4 and IL‐13) responses were detected in all three groups. Frequencies of RSV‐specific T‐cells were lower in both URTI groups than in the RSV bronchiolitis group, and not significantly different between the RSV URTI and the non‐RSV URTI group. The absence of vigorous virus‐specific Th2 responses upon mild RSV infection does not support the hypothesis that these infections influence the development of the immune system and that they predispose for the development of atopic disease. J. Med. Virol. 70: 309–318, 2003. © 2003 Wiley‐Liss, Inc.