The purpose of this study is to investigate the presence of Epstein-Barr Virus (EBV) infection, phenotypical features and proliferative activity in Hodgkin's Disease (HD) for both the reactive and neoplastic cell populations. Sections from 4 lymphocyte predominance (LP), 13 nodular sclerosis (NS), 10 mixed cellularity (MC), total 27 HD tissue blocks were stained by avidin biotin complex method using primary antibodies against latent membrane protein-I (LMP-I), epithelial membran antigen (EMA), leukocyte common antigen (LCA), CD20, CD43, UCHL-1, S100, proliferating cell nuclear antigen (PCNA) and diaminobenzidine (DAB) was used as chromogen. Also double immunostaining was performed in 5 cases using avidin-biotin complex method and DAB chromogen for LMP-I and amino ethyl carbazole (AEC) chromogen for S 100 protein for identifying LMP-I expression by dendritic reticular cells. Number of PCNA positive HRS cells among 100 neoplastic cells and percentage of LCA, CD20, CD43, UCHL-1 positive reactive cells were compared for LP, NS, MC cases by Mann Whitney U Test. Also by the same method and for the described groups, LMP-1 positive and negative cases were compared. Of 27 HD cases 21 (77.77%) were positive by LMP-I, in the cytoplasm of Hodgkin-Reed Sternberg (HRS) cells. HRS cells were CD20 positive in one LPHD, while all HRS cells in this and other cases were negative for EMA, LCA, CD20, CD43, UCHL-1 and S 100. PCNA was positive in 79-100% of HRS cells, without significant difference for HD subtypes. Number of PCNA positive cells were more for LMP-1 positive cases. LMP-1 expression was not identified in dendritic-reticular cells. These findings provides additional data but phenotypical features of the disease are still controversial.

The purpose of this study is to investigate the presence of Epstein-Barr Virus (EBV) infection, phenotypical features and proliferative activity in Hodgkin's Disease (HD) for both the reactive and neoplastic cell populations. Sections from 4 lymphocyte predominance (LP), 13 nodular sclerosis (NS), 10 mixed cellularity (MC), total 27 HD tissue blocks were stained by avidin biotin complex method using primary antibodies against latent membrane protein-I (LMP-I), epithelial membran antigen (EMA), leukocyte common antigen (LCA), CD20, CD43, UCHL-1, S100, proliferating cell nuclear antigen (PCNA) and diaminobenzidine (DAB) was used as chromogen. Also double immunostaining was performed in 5 cases using avidin-biotin complex method and DAB chromogen for LMP-I and amino ethyl carbazole (AEC) chromogen for S 100 protein for identifying LMP-I expression by dendritic reticular cells. Number of PCNA positive HRS cells among 100 neoplastic cells and percentage of LCA, CD20, CD43, UCHL-1 positive reactive cells were compared for LP, NS, MC cases by Mann Whitney U Test. Also by the same method and for the described groups, LMP-1 positive and negative cases were compared. Of 27 HD cases 21 (77.77%) were positive by LMP-I, in the cytoplasm of Hodgkin-Reed Sternberg (HRS) cells. HRS cells were CD20 positive in one LPHD, while all HRS cells in this and other cases were negative for EMA, LCA, CD20, CD43, UCHL-1 and S 100. PCNA was positive in 79-100% of HRS cells, without significant difference for HD subtypes. Number of PCNA positive cells were more for LMP-1 positive cases. LMP-1 expression was not identified in dendritic-reticular cells. These findings provides additional data but phenotypical features of the disease are still controversial.