Folia Microbiologica

, Volume 48, Issue 3, pp 291–318 | Cite as

Gamma herpesviruses: Pathogenesis of infection and cell signaling

  • J. Rajčáni
  • M. Kúdelová


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.


NASH Latent Membrane Protein Immediate Early Gamma Herpesvirus Lytic Virus Replication 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.



acquired immunodeficiency virus


adherent mononuclear (cells)


apoptosis receptor 1 (Fas receptor)


activator of replication and transcription


Burkitt’s lymphoma


BamHI R leftward fragment (EBV DNA)


BamHI Z leftward fragment (EBV DNA)


cluster of differentiation (leukocyte marker)


cyclin-dependent kinases


cellular ju-nana (japanese expression for 17 sarcoma virus)




centraf nervous system


(cAMP-response element)-binding protein


C-terminal activator regions


death domain


death effector domain


dyad symmetry (EBV DNA region)


Epstein—Barr encoded nonpolyadenylated RNA


Epstein—Barr nuclear antigen


Epstein—Barr virus


Fas receptor-associated death domain


FS-7 associated cell surface (protein)


N-formylglycinamide ribotide aminotransferase


FADD-like interleukin converting enzyme inhibitor protein (vFLIP)


family of repeats


gamma-activated sequence


G-protein coupled receptor


HS-1 associated protein X-1


human herpesvirus


human immunodeficiency virus


Hodgkin’s lymphoma


human leukocyte antigen


hemopoetic specific protein 1


herpes simplex virus 1


herpesvirus saimiri


interleukin-1β converting enzyme


immediate early proteins




inactivator kinases




infectious mononucleosis


IFN regulating factor




immunoreceptor tyrosine-based activator motif


KSHV analogue of the EBV-specified Zta


kinase inhibitor protein/cyclin inhibitor protein


Kaposi’s sarcoma


Kaposi’s sarcoma (associated) herpesvirus


latent nuclear antigen


lymphoblastoid cell lines


latent membrane protein


lymphoproliferative disorders


large tegument protein


mitogen activated protein kinase


mitogen activated kinase/kinase cascade


multicentric Castleman disease


monocyte chemoattractant proteins


murine herpesvirus


nuclear factor activator of T cells


nuclear factor κB


NF-κB inducing kinase


nasopharyngeal carcinoma


ori-binding protein


polyadenylated nuclear RNA species


primary effusion lymphoma


retinoblastoma (proteins)


ribonucleotide reductase (genes)


Reed—Sternberg (cells)


R transactivator protein (R fragment encoded)


son of sevenless (protein)


signaling transduction and transcription


thymidine kinase


tumor necrosis factor


TNF receptor


4β,9α,12β,13α,20-pentahydroxytiglia-1,6-dien-3-one 12β-myristate 13α-acetate (‘12-O-tetradecanoylphorbol 13-acetate’)


TNFR-associated death domain


TNFR-associated factor


viral cyclin


vascular endothelial growth factor


viral FLICE (caspase 1) inhibitor protein


viral G-protein coupled receptor


viral macrophage inflammatory protein


varicella zoster virus


Z (‘Zebra’) transactivator protein (Z fragment encoded)


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© Institute of Microbiology, Academy of Sciences of the Czech Republic 2003

Authors and Affiliations

  1. 1.Institute of Microbiology and ImmunologyJessenius Medical FacultyMartinSlovakia
  2. 2.Institute of VirologySlovak Academy of SciencesBratislavaSlovakia

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