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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; Arlene Stecenko, MD
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*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@vanderbilt.edu



Chest. 2001;120(1_suppl):S74-S75. doi:10.1378/chest.120.1_suppl.S74
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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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