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
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.