1998 Fiscal Year Final Research Report Summary
The study Epstein-Barr virus on the disease progression in patients with idiopathic interstitial pneumonia.
| Project/Area Number |
09670605
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine |
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Principal Investigator |
CHIBA Kingo Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Assistant Professor, 医学部附属病院, 講師 (40197611)
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| Project Period (FY) |
1997 – 1998
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| Keywords | idiopathic interstitial pneumonia / Epstein-Barr virus |
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| Research Abstract |
The relevance of Epstein-Barr virus (EBV) for idiopathic pulmonary fibrosis (LPF) is controversial in recent literatures. Our aims in this study are to elucidate the existence of the virus as well as to clarify the influences of EBV to the clinical features of IPF.Twenty-time lung specimens from IPF patients and 5 from systemic sclerosis patients with puImonary fibrosis (SSc) and 15 from normal controls (NC) were prepared. Detection of EBV DNA and EBV latent membrane protein-1 (LMP1) were analyzed using two-step PCR methods and immunohistry. respectively. The detection ratio was significantly higher in the lungs with IPF patients than in those with NC by two-step PCR methods (96% in IPF vs 71% in NC_4 P<0.05). ImmunohistochemieaI analysis reveded taht cuboidai epithelial cells were positively stained with and-LMP1 andbody in 9 of 29 lungs front IPF patients. In contrast, none of the SSc patients and NC showed positive staining, It was significant that LMP I -positive IPF patients had more freqnency in "disease progression", defined as if PaO2 decreased snore than 15 torr during foIIow up periods, titan LMP1 -negative paIienis : 5 of 7 LMPI-positive vs 1 of 13 LN'IP1-negative patients ; p<0.01. We concluded that EBV was involved in the progression of the lung fibosis by expressing LMP1, at least, in some of the parients with IPF.
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