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The role of Epstein-Barr virus in the pathogenesis of lymphocytic interstitial pneumonia

University of British Columbia

Epstein-Barr Virus (EBV) genome has been demonstrated in lung tissues of patients with lymphocytic interstitial pneumonia (LIP). Recent in vitro studies have shown that the EBV immortalizes and transforms cells by upregulation of the cellular proto-oncogene bcl-2 via the viral latent membrane protein LMP1. The purpose of the studies described in this thesis was to determine whether the presence of EBV LMP1 and over-expression of bcl-2 occurs in LIP. Immunohistochemistry was employed to detect EBV LMP1 and bcl-2 in formalin-fixed, paraffin-embedded lung sections from patients with LIP (n = 14), idiopathic pulmonary fibrosis (IPF, n = 9) and autopsy cases (AC, n = 9) without lung disease. EBV density, defined by the number of LMP1 positive cells per unit area of lung tissue, was used to estimate the level of LMP1 expression. The results showed increased LMP1 expression in lung tissue from patients with LIP (p<0.05). bcl-2 expression was assessed by a grading system based on cellularity (Grade 1, 2 and 3) and intensity of immunostaining (Grade 0, 1, 2, and 3). bcl-2 staining was greatest in LIP (p<0.05), and IPF showed more staining than AC (p<0.05). We conclude that EBV is more prevalent and LMP1 expression was increased in LIP associated with an upregulated bcl-2 expression. These results support the hypothesis that EBV infection is important in the pathogenesis of LIP and bcl-2 may play a role towards lymphomagenesis of LIP.

Thesis/Dissertation

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2009-01-26

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http://hdl.handle.net/2429/3907

Experimental Medicine

University of British Columbia

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