Epstein-Barr Virus (EBV) Gene Expression in Interstitial Pneumonitis in Brazilian Human Immunodeficiency Virus-1-Infected Children: Is EBV Associated or Not?

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Toro, Adyleia A. D. C.
Altemani, Albina M. A.
Da Silva, Marcos T. N.
Morcillo, Andre M.
Vilela, Maria Marluce S.
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To gain further knowledge on the subject we evaluated Epstein-Barr virus (EBV) gene expression and TCD4+, TCD8+, and B lymphocyte counts in lung tissue samples from 20 human immunodeficiency virus (HIV)-infected children with chronic lung disease. Twenty HIV-1 infected children with chronic pulmonary disease underwent open lung biopsy to define the diagnosis. Histological section of this material was submitted to nonisotopic in situ hybridization (ISH) using EBV-encoded RNA (EBER) 1/2 probes and TCD4+, TCD8+, and CD20+ B-cell counts by immunohistochemistry. the histology of 16 out of the 20 children (median age 53.5 months) proved to be examples of pulmonary lymphoid hyperplasia/lymphoid interstitial pneumonitis (PLH/LIP) complex, 13 of which were EBER positive, but no significant association was found (Fisher exact test P = 0.439). Four patients had non-LIP diseases (3, nonspecific interstitial pneumonia; 1, diffuse advanced alveolar damage), two being EBER negative. Nineteen children showed a predominant T-CD8+ cell response (CD4+/CD8+ <1) in lung tissue. the mean TCD4+ and theTCD4/TCD8 ratio in lung tissue were significantly higher in the sections with PLH/LIP complex, but without significant difference between EBER positive and EBER negative samples. EBV gene expression was detected in the majority of the lung samples but without significant association with PLH/LIP complex or with TCD4+, TCD8+, B cells and the TCD4+/TCD8+ ratio. Regarding the pattern of lung disease in HIV-1 infected children, associated or not to EBV, the findings are of importance concerning the possible role of EBV in the pathogenesis of PLH/LIP.
Pediatric and Developmental Pathology. Lawrence: Alliance Communications Group Division Allen Press, v. 13, n. 3, p. 184-191, 2010.