Plasma Epstein-Barr virus and Hepatitis B virus in non-Hodgkin lymphomas: Two lymphotropic, potentially oncogenic, latently occurring DNA viruses.

CONTEXT: There is a need to study potential infective etiologies in lymphomas. Lymphocyte-transforming viruses can directly infect lymphocytes, disrupt normal cell functions, and promote cell division. Epstein-Barr virus (EBV) is known to be associated with several lymphomas, especially Hodgkin lymphomas (HLs). And recently, the lymphocyte-transforming role of hepatitis B virus (HBV) has been emphasized. AIMS: The aim of this study was to elucidate the association of two potentially oncogenic, widely prevalent latent DNA viruses, EBV and HBV, in non-HL (NHL). SETTINGS AND DESIGN: In this prospective study, we estimated plasma EBV and HBV DNA in NHL patients. MATERIALS AND METHODS: Peripheral blood was obtained from newly diagnosed, treatment na ïve, histologically confirmed NHL patients. Plasma EBV DNA was quantified by real-time polymerase chain reaction (PCR) targeting Epstein-Barr Nucleic acid 1 while the plasma HBV DNA was detected using nested PCR targeting HBX gene. In a small subset of patients, follow-up plasma samples post-anticancer chemotherapy were available and retested for viral DNA. RESULTS: Of the 110 NHL patients, ~79% were B-cell NHL and ~21% were T-cell NHL. Plasma EBV-DNA was detected in 10% NHLs with a higher EBV association in Burkitt lymphoma (33.3%) than other subtypes. Pretherapy HBV DNA was detected in 21% NHLs; most of them being diffuse large B-cell lymphoma (DLBCL). Moreover, 42% of DLBCL patients had HBV DNA in plasma. Since all patients were HBV surface antigen seronegative at diagnosis, baseline plasma HBV-DNAemia before chemotherapy was indicative of occult hepatitis B infection. CONCLUSIONS: Our findings indicate a significant association of HBV with newly diagnosed DLBCL.

Plasma Epstein Barr viral load in adult-onset Hodgkin lymphoma in South India.

OBJECTIVE/BACKGROUND: Epstein Barr Virus (EBV) DNA load is increasingly being used as a noninvasive biomarker for detecting EBV association in lymphomas. Since there is a need of data from India, we undertook to prospectively evaluate plasma EBV DNA load as a marker of EBV association in newly diagnosed adult-onset Hodgkin lymphoma (HL). METHODS: EBV DNA was quantified using real-time polymerase chain reaction. In a subset of patients, an assay was validated qualitatively with EBV latent membrane protein-1 (LMP1) immunohistochemistry (IHC). Wherever possible, follow-up plasma samples post three cycles of chemotherapy were obtained. RESULTS: Over a period of 10 months, 33 newly diagnosed adult-onset HL were enrolled in the study. Pretherapy plasma EBV DNA was detectable in ∼49% (16/33) patients (viral loads range, 1.0-51.2×10(3)copies/mL) and undetectable in 30 voluntary blood donors. LMP1 IHC was positive in 56% of cases tested (14/25). Sensitivity and specificity of plasma EBV DNA with respect to LMP1 IHC were 86% and 100%, respectively. Of the eight patients in whom follow-up plasma was available, in five EBV baseline-positive patients EBV load reverted to negative postchemotherapy and corroborated with clinical remission. CONCLUSION: Plasma EBV DNA load estimation may be useful in detecting EBV-association and possibly monitoring the response to therapy in EBV-related HL especially in our country where EBV association of HL is higher than in developed nations.

Distribution patterns of enamel fluorosis in permanent dentition.

PURPOSE: To describe the different patterns of the intraoral distribution of enamel fluorosis in permanent dentition. MATERIALS AND METHODS: This cross-sectional analysis was conducted in Nalgonda district of Andhra Pradesh, India. A group of 1000 school children aged 13-15 years were selected by stratified cluster sampling from four different areas with different levels of naturally occurring fluoride in the drinking water. Fluorosis was recorded using the Thylstrup and Fejerskov index (TFI). RESULTS: The prevalence of fluorosis (TFI score >=1) was 100% at all four fluoride levels. This study revealed two patterns of fluorotic enamel changes in dentition. In high fluoride areas, incisors exhibited lower TFI values than canines, premolars and molars, with the maximum affected being second molars followed by first molars. In low fluoride areas, a steeper profile of dental fluorosis, starting from incisors and first molars through canine and premolars to second molars, was noticed. CONCLUSION: With the exception of permanent second molars and permanent first molars in high fluoride communities, the intraoral distribution of different degrees of dental fluorosis was related to the completion of primary enamel formation.