ELEVATION OF ANTIBODIES TO CYTOMEGALOVIRUS AND OTHER HERPES VIRUSES IN PULMONARY FIBROSIS

Citation
M. Yonemaru et al., ELEVATION OF ANTIBODIES TO CYTOMEGALOVIRUS AND OTHER HERPES VIRUSES IN PULMONARY FIBROSIS, The European respiratory journal, 10(9), 1997, pp. 2040-2045
Citations number
30
Categorie Soggetti
Respiratory System
ISSN journal
09031936
Volume
10
Issue
9
Year of publication
1997
Pages
2040 - 2045
Database
ISI
SICI code
0903-1936(1997)10:9<2040:EOATCA>2.0.ZU;2-I
Abstract
The aim of this study was to determine whether latent viral infection is associated with idiopathic pulmonary fibrosis (IPF), an interstitia l lung disease whose aetiology remains to be elucidated. Cytomegalovir us (CMV) immunoglobulin G (IgG) and complement fixation (CF), Epstein- Barr (EB) viral capsid antigen (VCA) IgG, herpes simplex virus (HSV) I gG, adenovirus CF, and parainfluenza 3 virus haemagglutinin inhibition (HI) titres were measured in the serum from patients with pulmonary d iseases. The study included five subject groups: 35 normal controls (a ged (mean+SD) 38 +/- 17 yrs); 43 IPF (63 +/- 10 yrs), seven collagen v ascular disease-related interstitial pneumonitis (CVD-IP) (62 +/- 12 y rs); 22 sarcoidosis (36 +/- 14 yrs); and 17 emphysema (66 +/- 11 yrs). Levels of CMV IgG in IPF (87.6 +/- 51.7) and CVD-IP (101.2 +/- 69.9) were significantly elevated compared to those in the control (30.9 +/- 24.1), sarcoidosis (34.4 +/- 38.3) and emphysema groups (40.3 +/- 24. 6), whereas CMV immunoglobulin M (IgM) was generally below the limit o f detection. Similarly, CMV CF titres in IPF and CVD-IP were elevated compared to those in other diseases. EB VCA IgG titres in IPF, CVD-IP and emphysema and HSV IgG in IPF were also elevated. In contrast, aden ovirus CF and parainfluenza 3 HI titres demonstrated no significant di fference among all of the groups investigated. Increases in cytomegalo virus immunoglobulin G and complement fixation titres with negative cy tomegalovirus immunoglobulin M suggest that latent cytomegalovirus inf ection may be more prominent in idiopathic pulmonary fibrosis or colla gen vascular disease-related interstitial pneumonitis. Together with t he elevation of Epstein-Barr virus viral capsid antigen and herpes sim plex virus immunoglobulin G in idiopathic pulmonary fibrosis and/or co llagen vascular disease-related interstitial pneumonitis, it is ration al to assume that these viruses may be implicated in the development o f pulmonary fibrosis. Further study is necessary to investigate the re lationship between latent viral infection and pulmonary fibrosis.