Plasma interferon-gamma, interleukin-10 and soluble markers of immune activation in infants with primary adenovirus (ADV) and respiratory syncytial virus (RSV) infection.
Adenovirus (ADV) and respiratory syncytial virus (RSV) are etiological agents of acute respiratory tract infection in infants. Long-term prognosis of ADV infection includes severe lung damage, bronchiectasis and hyperlucent lung, while RSV infection is associated with development of recurrent wheezing and subsequent asthma. These differences may be related to differences in the primary immune responses elicited by these viruses. In this paper, we investigated the type of cytokine responses and the magnitude of immune activation in ADV and RSV infections in infants. We examined plasma concentrations of interferon-gamma (IFN-gamma), interleukin-10 (IL-10), soluble interleukin-2 receptor (sCD25) and soluble tumor necrosis factor receptor II (sTNFR-II) in previously healthy infants during the acute phase of primary ADV infection (n = 21) and RSV infection (n = 68), and in uninfected controls (n = 44). In ADV-infected infants, IFN-gamma plasma levels were significantly higher than those observed in RSV cases and the control group (p < 0.05). RSV cases did not show any differences in IFN-gamma plasma levels compared to the other groups. sCD25 levels were significantly higher in ADV- and RSV-infected infants than in controls (p < 0.0001), and higher in ADV than in RSV cases (p < 0.05). sTNFR-II levels were significantly higher in RSV- and ADV-infected infants than in controls (p < 0.0001, p < 0.05, respectively), and higher in RSV than in ADV infection (p < 0.05). No significant differences were observed in IL-10 plasma concentrations between the three groups. These results indicate that ADV and RSV infections in infants differ significantly with regard to the magnitude of production of interferon-gamma and soluble immune activation markers sCD25 and sTNFR-II. These immunological differences may be involved in the different clinical outcomes associated with these viral infections.
Fernández
J Alonso
JA
Developmental Immunobiology Laboratory, Anatomy and Developmental Biology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Independencia 1027, Clasificador 7, Correo 7, Santiago, Chile. jfernand@med.uchile.cl
Tapia
Lorena
L
Palomino
M Angélica
MA
Larrañaga
Carmen
C
Peña
Mónica
M
Jaramillo
Héctor
H
D000208:Acute Disease; D000257:Adenoviridae Infections / Q000276:immunology*; D015415:Biomarkers / Q000097:blood; D005260:Female; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007371:Interferon-gamma / Q000097:blood*; D016753:Interleukin-10 / Q000097:blood*; D008297:Male; D015375:Receptors, Interleukin-2 / Q000097:blood*; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000097:blood*; D018357:Respiratory Syncytial Virus Infections / Q000276:immunology*; D012141:Respiratory Tract Infections / Q000276:immunology / Q000821:virology; D012995:Solubility
D015415:Biomarkers; D015375:Receptors, Interleukin-2; D047889:Receptors, Tumor Necrosis Factor, Type II; D016753:Interleukin-10; D007371:Interferon-gamma