Trans-regulation of the Early MS Gene of EBV and Its Dependence on the Host Cell

Marschall, Manfred; Schwarzmann, Fritz; Alliger, Peter; Wolf, Hans

doi:10.1007/978-1-4612-0405-3_17

Cited by 1 publication

(1 citation statement)

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“…For the BSLF2/BMLF1 regulatory up stream region, a silencing function was de tected in latently infected B-lymphocytes which was shown to be inefficient in EBVnegative lymphoid and epithelial cells [Marschall et al, 1990]. Using teratocarcinoma cells as an in vitro differentiation model, the down-regulation of EBV promoter activi ty was demonstrated for unstimulated imma ture cells, whereas specific transcriptional re sponses became obvious during proceed- ing cell differentiation , In view of biology, the activation of the lyt ic cycle only in differentiated cells, as in the salivary ducts of the parotid gland [Wolf et al, 1984], a proven site of lifelong EBV replica tion in the presence of an efficient immune control, limits viral production to very few privileged sites without causing any lesions.…”

Section: How Does Ebv Enter Its Host and Its Host Cells?mentioning

confidence: 99%

Epstein-Barr Virus and Its Interaction with the Host

1993

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Epstein-Barr virus (EBV) as a member of the herpesvirus family persists lifelong in the human body and causes diseases associated with virus replication (infectious mononucleosis, oral hairy leukoplakia) as well as neoplastic conditions such as nasopharyngeal carcinoma, B-cell lymphoma, Hodgkin’s disease associated with viral latency. This complex biology relates to a highly regulated control of the persisting virus. Still, EBV is lytically produced in certain compartments of the human body. Epithelial cells were found to be of key importance for this. Various routes (cell fusion, IgA receptor-mediated uptake) were described for EBV to enter epithelial cells in the absence of CR2 receptor. Viral entry into cells, however, via CR2 receptor fusion or IgA mediated was not found to be sufficient for viral production. The molecular mechanisms for the lack of viral production in most target cells are primarily the presence of silencer activities and the early elimination of cells entering the lytic cycle. Only terminally differentiated epithelial cells are capable of supporting an efficient lytic cycle of EBV replication. EBV-mediated suppression of apoptosis as well as down-regulation of cellular and viral gene products, such as HLA molecules, which mediate recognition by the immune system, are important contributing factors to the development of these neoplasias where viral genes, possibly via interaction with anti-oncogenes, such as p53, in context with genetic and environmental factors play a key role. Novel diagnostic tools and a vaccine have been developed which could help to control EBV-related diseases.

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Section: How Does Ebv Enter Its Host and Its Host Cells?mentioning

confidence: 99%