当前位置： SCI文献检索 > FOLIA MICROBIOLOGICA期刊下所有文献 > Gamma herpesviruses: pathogenesis of infection and cell signaling.

Gamma herpesviruses: pathogenesis of infection and cell signaling.

Abstract：

:Altered cell signaling is the molecular basis for cell proliferation occurring in association with several gamma herpesvirus infections. Three gamma herpesviruses, namely EBV/HHV-4, KSHV/HHV-8 and the MHV-68 (and/or MHV-72) and their unusual cell-pirated gene products are discussed in this respect. The EBV, KSHV as well as the MHV DNA may persist lifelong in an episomal form in the host carrier cells (mainly in lymphocytes but also in macrophages, in non-hornifying squamous epithelium and/or in blood vessel endothelial cells). Under conditions of extremely limited transcription, the EBV-infected cells express EBNA1 (EB nuclear antigen 1), the KSHV infected cells express LANA1 (latent nuclear antigen 1), while the MHV DNA carrier cells express the latency-associated protein M2. With the full set of latency-associated proteins expressed, EBV carrier cells synthesize additional EBNAs and at least one LMP (latent membrane protein 1). The latent KSHV carrier cells, in addition to LANA1, may express a viral cyclin, a viral Fas-DD-like ICE inhibitor protein (vFLIP) and a virus-specific transformation protein called kaposin (K12). In MHV latency with a wide expression of latency-associated proteins, the carrier cells express a LANA analogue (ORF73), the M3 protein, the K3/IE (immediate early) proteins and M11/bcl-2 homologue proteins. During the period of limited gene expression, the latency-associated proteins serve mainly for the maintenance of the latent episomal DNA (a typical example is EBNA1). In contrast, during latency with a broader spectrum gene expression, the virus-encoded products activate transcription of otherwise silenced cellular genes, which leads to the synthesis of enzymes capable of promoting not only viral but also cellular DNA replication. Thus, the latency-associated proteins block apoptosis and drive host cells towards division and immortalization. Proliferation of hemopoetic cells, which had become gamma herpesvirus DNA carriers, can be initiated and strongly enhanced in the presence of inflammatory cytokines and by virus-encoded analogues of interleukins, chemokines and IFN regulator proteins. At early stages of tumor formation, many proliferating hemopoetic and/or endothelium cells, which had became transcriptionally active under the influence of chemokines and cytokines, may not yet be infected. In contrast, at later stages of oncogenesis, the virus-encoded proteins, inducing false signaling and activating the proliferation pathways, bring the previously infected cells into full transformation burst.

journal_name

Folia Microbiol (Praha)

journal_title

Folia microbiologica

authors

Rajcáni J,Kúdelová M

doi

10.1007/BF02931360

keywords:

subject

Has Abstract

pub_date

2003-01-01 00:00:00

pages

291-318

issue

eissn

0015-5632

issn

1874-9356

journal_volume

pub_type

杂志文章,评审

在线工具

Gamma herpesviruses: pathogenesis of infection and cell signaling.