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(Chest. 2001;120:S74-S75.)
© 2001 American College of Chest Physicians

Increased Detection of Herpesvirus DNA in Idiopathic Pulmonary Fibrosis*

Yi-Wei Tang, MD, PhD; Joyce Johnson, MD; Roberto Cruz-Gervis, MD; Barney Graham, MD, PhD; Kenneth Brigham, MD; John Oates, MD; James Loyd, MD and Arlene Stecenko, MD

* From the Departments of Medicine (Drs. Tang, Cruz-Gervis, Loyd, Brigham, and Stecenko), Pathology (Dr. Johnson), Microbiology and Immunology (Dr. Graham), and Pharmacology (Dr. Oates), Vanderbilt University School of Medicine, Nashville, TN.

Correspondence to: Yi-Wei Tang, MD, PhD, A3310 MCN, Division of Infectious Diseases, Vanderbilt University Medical Center, Nashville, TN 37232-2605; e-mail: yiwei.tang{at}vanderbilt.edu

Inflammation and fibrogenesis are both hallmarks of idiopathic pulmonary fibrosis (IPF). The stimulus for inflammation is unknown, but its nature suggests that a microbial pathogen could be responsible. A 1999 study1 reported increased detection of Epstein-Barr virus DNA in lung tissue of IPF patients compared to control subjects. We speculated that latent infection with herpesviruses could act as a stimulus for inflammation in IPF and therefore tested lung specimens from IPF patients for the presence of eight herpesviruses (herpes simplex virus-1, herpes simplex virus-2, cytomegalovirus, Epstein-Barr virus, varicella-zoster virus, and human herpesvirus [HHV]-6, HHV-7, and HHV-8) using an organism-specific colorimetric microtiter plate polymerase chain reaction technique.2 We studied lung tissue from 23 IPF patients (6 familial and 17 sporadic). Tissue was obtained at autopsy (n = 7), open-lung biopsy prior to starting any treatment (n = 3), or at lung transplant (n = 13). Histology was reviewed and pathologic classification was usual interstitial pneumonia (n = 18), nonspecific interstitial pneumonia (n = 2), and others (n = 3). Eleven normal lung tissues (n = 6, unused donor lungs, n = 5, lobectomy for pulmonary nodule) were selected as control lungs. As shown in Table 1 , one or more herpesviruses was detected in 22 of 23 IPF patients and in only 1 of 11 normal control subjects (p < 0.01). Of interest was the high rate of detection of HHV-8 (43%), which is usually found only in patients with HIV or Kaposi’s sarcoma. In addition, there was a high rate of coinfection with two or more herpesviruses in IPF subjects: two or more herpesviruses were detected in 14 IPF lungs (61%) and in 1 normal control lung (9%; Table 1 ). Since many of the IPF subjects were critically ill with end-stage lung disease, specimens from eight disease control patients with end-stage disease (n = 4 cystic fibrosis, n = 3 pulmonary hypertension, and n = 1 sarcoidosis) were also evaluated. One herpesvirus was found in three control patients, but none of them had more than one herpesvirus (Table 1) . These data support the hypothesis that herpesvirus infections could play a role in stimulating lung inflammation in patients with IPF.


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  		Table 1. Herpesvirus Detection by Polymerase Chain Reaction in Lung Tissues*

 

Footnotes

Abbreviations: HHV = human herpesvirus; IPF = idiopathic pulmonary fibrosis

References

  1. Stewart, JP, Egan, JJ, Ross, AJ, et al (1999) The detection of Epstein-Barr virus DNA in lung tissue from patients with idiopathic pulmonary fibrosis. Am J Respir Crit Care Med 159(4 Pt 1),1336-1341
  2. Tang, YW, Rys, PN, Rutledge, BJ, et al (1998) Comparative evaluation of colorimetric microtiter plate systems for detection of herpes simplex virus in cerebrospinal fluid. J Clin Microbiol 36,2714-2717




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