Epstein-Barr virus: clinical and epidemiological revisits and genetic basis of oncogenesis

Epstein-Barr virus (EBV) is classified as a member in the order herpesvirales, family herpesviridae, subfamily gammaherpesvirinae and the genus lymphocytovirus. The virus is an exclusively human pathogen and thus also termed as human herpesvirus 4 (HHV4). It was the first oncogenic virus recognized and has been incriminated in the causation of tumors of both lymphatic and epithelial nature. It was reported in some previous studies that 95% of the population worldwide are serologically positive to the virus. Clinically, EBV primary infection is almost silent, persisting as a life-long asymptomatic latent infection in B cells although it may be responsible for a transient clinical syndrome called infectious mononucleosis. Following reactivation of the virus from latency due to immunocompromised status, EBV was found to be associated with several tumors. EBV linked to oncogenesis as detected in lymphoid tumors such as Burkitt's lymphoma (BL), Hodgkin's disease (HD), post-transplant lymphoproliferative disorders (PTLD) and T-cell lymphomas (e.g. Peripheral T-cell lymphomas; PTCL and Anaplastic large cell lymphomas; ALCL). It is also linked to epithelial tumors such as nasopharyngeal carcinoma (NPC), gastric carcinomas and oral hairy leukoplakia (OHL). In vitro, EBV many studies have demonstrated its ability to transform B cells into lymphoblastoid cell lines (LCLs). Despite these malignancies showing different clinical and epidemiological patterns when studied, genetic studies have suggested that these EBV- associated transformations were characterized generally by low level of virus gene expression with only the latent virus proteins (LVPs) upregulated in both tumors and LCLs. In this review, we summarize some clinical and epidemiological features of EBV- associated tumors. We also discuss how EBV latent genes may lead to oncogenesis in the different clinical malignancie

Cognitive neuropsychology of alexithymia: Implications for personality typology

Introduction: We examine the cognitive neuroscience of the five components of the alexithymia syndrome, and propose a classification of alexithymia types based on psychobiological traits. Method: Literature review. Results: The following neural structures have been shown to be prominent in emotional function: right and left hemisphere, corpus callosum, anterior commissure, anterior cingulate, prefrontal cortex, amygdala, and insular cortex. The specific relevance of these structures to alexithymia is discussed. Conclusions: The following conclusions and/or propositions are presented: The right hemisphere produces a global, nonverbal overview of emotional information; the left hemisphere seems dedicated to analysing emotions and higher explicit emotional cognitions. Both orbitoprefrontal cortices are important in affective aspects of alexithymia, while right temporal cortex is involved in cognitive aspects. Two subparts of anterior cingulate fulfil functions in the affective and cognitive dimensions of alexithymia. The amygdalae are involved in both cognitive and affective aspects. All structures mentioned can modulate one another. The role of interhemispheric information transfer via the corpus callosum and the anterior commissure is also discussed. The evidence that that cognitive processing of emotional information inhibits affective processing of such information is discussed in terms of its implications for a theory of alexithymia subtypes