BACKGROUND: Cryptogenic fibrosing alveolitis (CFA) is a well defined clinical entity of unknown aetiology. An association between CFA and the presence of protein indicating Epstein-Barr virus (EBV) replication within epithelial cells of the respiratory tract has recently been suggested, leading to speculation for a role for EBV in the pathogenesis of CFA. METHODS: Lung tissue was obtained from patients in three groups: those with cryptogenic fibrosing alveolitis, either lone or associated with systemic sclerosis; patients with other pulmonary disorders; and patients with normal lung. Paraffin blocks were stained using three antibodies raised against well defined EBV antigens. In addition, EBER-1 and EBER-2 anti-sense nucleotide probes were used in an attempt to identify EBV RNA. DNA was also extracted from the tissue sections and evaluated for evidence of EBV DNA using the polymerase chain reaction. RESULTS: Immunohistochemistry showed inconsistent focal positive staining with anti-EBV antibodies in all three groups, but there was no evidence of EBV RNA using in situ hybridisation. None of the samples from patients with pulmonary fibrotic disorders was found to contain EBV DNA following gene amplification. CONCLUSION: Contrary to an earlier report, these results do not support the hypothesis that EBV has a role in the pathogenesis of CFA.
BACKGROUND: Cryptogenic fibrosing alveolitis (CFA) is a well defined clinical entity of unknown aetiology. An association between CFA and the presence of protein indicating Epstein-Barr virus (EBV) replication within epithelial cells of the respiratory tract has recently been suggested, leading to speculation for a role for EBV in the pathogenesis of CFA. METHODS: Lung tissue was obtained from patients in three groups: those with cryptogenic fibrosing alveolitis, either lone or associated with systemic sclerosis; patients with other pulmonary disorders; and patients with normal lung. Paraffin blocks were stained using three antibodies raised against well defined EBV antigens. In addition, EBER-1 and EBER-2 anti-sense nucleotide probes were used in an attempt to identify EBV RNA. DNA was also extracted from the tissue sections and evaluated for evidence of EBV DNA using the polymerase chain reaction. RESULTS: Immunohistochemistry showed inconsistent focal positive staining with anti-EBV antibodies in all three groups, but there was no evidence of EBV RNA using in situ hybridisation. None of the samples from patients with pulmonary fibrotic disorders was found to contain EBV DNA following gene amplification. CONCLUSION: Contrary to an earlier report, these results do not support the hypothesis that EBV has a role in the pathogenesis of CFA.
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