KSHV: pathways to tumorigenesis and persistent infection.

@article{Giffin2014KSHVPT,
  title={KSHV: pathways to tumorigenesis and persistent infection.},
  author={Louise C Giffin and B. Damania},
  journal={Advances in virus research},
  year={2014},
  volume={88},
  pages={
          111-59
        }
}
Kaposi's sarcoma-associated herpesvirus (KSHV; also known as human herpesvirus 8) is the etiologic agent of Kaposi's sarcoma, primary effusion lymphoma, and multicentric Castleman's disease. These cancers often occur in the context of immunosuppression, which has made KSHV-associated malignancies an increasing global health concern with the persistence of the AIDS epidemic. KSHV has also been linked to several acute inflammatory diseases. KSHV exists between a lytic and latent lifecycle, which… Expand
Regulation of Replication and Translation During KSHV Life Cycle
TLDR
A major latency associated protein, Latency Associated Nuclear Antigen (LANA) plays a significant role in maintaining the viral genome and regulating the growth of tumor cells and it was essential to study how LANA interacts with cellular proteins and facilitates DNA replication. Expand
Regulation of KSHV Latency and Lytic Reactivation
TLDR
This review presents the current understanding of how the transition between the phases of the K SHV life cycle is regulated, how the various phases contribute to KSHV pathogenesis, and how the viral life cycle can be exploited as a therapeutic target. Expand
Co-infections and Pathogenesis of KSHV-Associated Malignancies
TLDR
The roles of co-infection with HIV and other pathogens on KSHV infection and pathogenesis are discussed, with one of the most important co-factors, immune suppression, necessary for the progression of KSHv induced tumors, is immune suppression that frequently arises during co- infection withAIDS. Expand
Dynamics of KSHV gene expression during de novo infection and the role of LANA in immune modulation
TLDR
A comprehensive analysis of the viral transcriptome in the purified KSHV virions lays a foundation for future research targeting the viral genes whose expression may be critical for establishing a successful viral infection. Expand
A top-notch viral oncogene
TLDR
In the course of investigating the molecular mechanism of T-lymphoma development in this model, the authors discovered a new function for v-cyclin in controlling the Notch signal transduction pathway, providing strong evidence that v- cyclin can act as a true oncogene in the appropriate cellular context. Expand
Reactivation and Lytic Replication of Kaposi’s Sarcoma-Associated Herpesvirus: An Update
TLDR
Overall, extensive investigation of the initiation and regulation of KSHV reactivation and lytic replication has revealed a sophisticated regulation network that controls the important events in K SHV life cycle. Expand
KSHV and the Role of Notch Receptor Dysregulation in Disease Progression
TLDR
The current literature regarding Notch dysregulation by KSHV and its role in viral infection and cellular pathogenesis is reviewed. Expand
Towards Better Understanding of KSHV Life Cycle: from Transcription and Posttranscriptional Regulations to Pathogenesis
TLDR
The current research status on the biology of latent and lytic viral infection, the regulation of viral life cycles and the related pathogenesis is summarized. Expand
KSHV: Immune Modulation and Immunotherapy
TLDR
This review will focus on the mechanisms by which KSHV evades the immune system and the current immune-related clinical strategies to treat K SHV-associated disease. Expand
Kaposi’s Sarcoma-Associated Herpesvirus Infection Induces the Expression of Neuroendocrine Genes in Endothelial Cells
TLDR
Kaposi’s sarcoma-associated herpesvirus (KSHV) infection upregulates the expression of genes related to neuronal and neuroendocrine functions that are characteristic of NE tumors, both in vitro and in KS patient tissues and the heterogeneity of neuro endocrine receptors having opposing roles in KSHV-infected cell proliferation. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 329 REFERENCES
The Viral Interferon Regulatory Factors of KSHV: Immunosuppressors or Oncogenes?
Kaposi’s sarcoma-associated herpesvirus (KSHV) is a large double-stranded DNA gammaherpesvirus, and the etiological agent for three human malignancies: Kaposi’s sarcoma, primary effusion lymphoma,Expand
Toll-like receptor signaling controls reactivation of KSHV from latency
TLDR
This work demonstrates that secondary pathogen infection of latently infected cells can reactivate KSHV, and has broad implications for physiological triggers of latent viral infections, such as herpesviral reactivation and persistence in the host. Expand
p53 inhibition by the LANA protein of KSHV protects against cell death
TLDR
LANA interacts with the tumour suppressor protein p53 and represses its transcriptional activity, which contributes to viral persistence and oncogenesis in KS through its ability to promote cell survival by altering p53 function. Expand
Modulation of the immune system by Kaposi's sarcoma-associated herpesvirus.
TLDR
The genome of Kaposi's sarcoma-associated herpesvirus contains 86 genes, almost a quarter of which encode proteins with either demonstrated or potential immunoregulatory activity, including homologues of cellular proteins and unique KSHV proteins that can deregulate many aspects of the immune response. Expand
De Novo Infection and Serial Transmission of Kaposi's Sarcoma-Associated Herpesvirus in Cultured Endothelial Cells
TLDR
It is shown that human dermal microvascular endothelial cells immortalized by expression of telomerase can be readily infected by KSHV virions produced by PEL cells, and this behavior faithfully recapitulates the behavior of spindle cells explanted from primary KS biopsies, strongly supporting the biological relevance of this culture system. Expand
Activation of Plasmacytoid Dendritic Cells by Kaposi's Sarcoma-Associated Herpesvirus
TLDR
Evidence is reported that Kaposi's sarcoma-associated herpesvirus can infect human p DCs and that pDCs are activated upon KSHV infection, as measured by upregulation of CD83 and CD86 and by IFN-α secretion. Expand
The role of Kaposi's sarcoma-associated herpesvirus (KSHV/HHV-8) in lymphoproliferative diseases.
TLDR
The discovery of KSHV in a subset of malignant lymphomas has allowed the development of lymphoma cell lines which now serve as biological reagents for propagating the virus, as a substrate for serologic assays, and as a model system for pathobiologic studies. Expand
Latent Kaposi's Sarcoma-Associated Herpesvirus Infection of Monocytes Downregulates Expression of Adaptive Immune Response Costimulatory Receptors and Proinflammatory Cytokines
TLDR
KSHV minimizes its immunological signature by suppressing key immune response factors, enabling persistent infection and evasion from host detection. Expand
Inflammatory cytokines and the reactivation of Kaposi's sarcoma-associated herpesvirus lytic replication.
TLDR
It is shown for the first time that inflammatory cytokines can directly modulate KSHV replication and the identification of interferon-gamma as an activator and interfer on-alpha as an inhibitor of K SHV induction in vitro correlates well with in vivo observations and demonstrates for theFirst time thatinflammatory cytokinesCan directly modulates KSHv replication. Expand
Host and Viral Proteins in the Virion of Kaposi's Sarcoma-Associated Herpesvirus
TLDR
Immunoblotting of virus particles demonstrated that RTA, the lytic switch protein, and RAP, a viral protein that is a transcriptional and cell cycle modulator, were both incorporated into virus particles. Expand
...
1
2
3
4
5
...