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https://www.readbyqxmd.com/read/28931678/ikk%C3%AE-mimetic-peptides-block-the-resistance-to-apoptosis-associated-with-kshv-infection
#1
Louise C Briggs, A W Edith Chan, Christopher A Davis, Nicholas Whitelock, Hajira A Hotiana, Mehdi Baratchian, Claire Bagnéris, David L Selwood, Mary K Collins, Tracey E Barrett
Primary effusion lymphoma (PEL) is a lymphogenic disorder associated with KSHV infection. Key to the survival and proliferation of PEL is the canonical NF-kB pathway that becomes constitutively activated following overexpression of the viral oncoprotein ks-vFLIP. This arises from its capacity to form a complex with the modulatory subunit of the IKK kinase, IKKγ (or NEMO) resulting in the overproduction of proteins that promote cellular survival and prevent apoptosis; both of which are important drivers of tumourigenesis...
September 20, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28922425/hypoxia-inducible-factor-1-alpha-as-a-therapeutic-target-for-primary-effusion-lymphoma
#2
Prabha Shrestha, David A Davis, Ravindra P Veeranna, Robert F Carey, Coralie Viollet, Robert Yarchoan
Primary effusion lymphoma (PEL) is an aggressive B-cell lymphoma with poor prognosis caused by Kaposi's sarcoma-associated herpesvirus (KSHV). Previous studies have revealed that HIF-1α, which mediates much of the cellular response to hypoxia, plays an important role in life cycle of KSHV. KSHV infection promotes HIF-1α activity, and several KSHV genes are in turn activated by HIF-1α. In this study, we investigated the effects of knocking down HIF-1α in PELs. We observed that HIF-1α knockdown in each of two PEL lines leads to a reduction in both aerobic and anaerobic glycolysis as well as lipid biogenesis, indicating that HIF-1α is necessary for maintaining a metabolic state optimal for growth of PEL...
September 18, 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28910389/cross-species-conservation-of-episome-maintenance-provides-a-basis-for-in-vivo-investigation-of-kaposi-s-sarcoma-herpesvirus-lana
#3
Aline C Habison, Marta Pires de Miranda, Chantal Beauchemin, Min Tan, Sofia A Cerqueira, Bruno Correia, Rajesh Ponnusamy, Edward J Usherwood, Colin E McVey, J Pedro Simas, Kenneth M Kaye
Many pathogens, including Kaposi's sarcoma herpesvirus (KSHV), lack tractable small animal models. KSHV persists as a multi-copy, nuclear episome in latently infected cells. KSHV latency-associated nuclear antigen (kLANA) binds viral terminal repeat (kTR) DNA to mediate episome persistence. Model pathogen murine gammaherpesvirus 68 (MHV68) mLANA acts analogously on mTR DNA. kLANA and mLANA differ substantially in size and kTR and mTR show little sequence conservation. Here, we find kLANA and mLANA act reciprocally to mediate episome persistence of TR DNA...
September 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28898712/inhibition-of-the-lytic-cycle-of-kaposi-s-sarcoma-associated-herpesvirus-by-cohesin-factors-following-de-novo-infection
#4
Zsolt Toth, Richard J Smindak, Bernadett Papp
Establishment of Kaposi's sarcoma-associated herpesvirus (KSHV) latency following infection is a multistep process, during which polycomb proteins are recruited onto the KSHV genome, which is crucial for the genome-wide repression of lytic genes during latency. Strikingly, only a subset of lytic genes are expressed transiently in the early phase of infection prior to the binding of polycomb proteins onto the KSHV genome, which raises the question what restricts lytic gene expression in the first hours of infection...
September 9, 2017: Virology
https://www.readbyqxmd.com/read/28893942/kaposi-sarcoma-herpesvirus-pathogenesis
#5
REVIEW
Giuseppe Mariggiò, Sandra Koch, Thomas F Schulz
Kaposi sarcoma herpesvirus (KSHV), taxonomical name human gammaherpesvirus 8, is a phylogenetically old human virus that co-evolved with human populations, but is now only common (seroprevalence greater than 10%) in sub-Saharan Africa, around the Mediterranean Sea, parts of South America and in a few ethnic communities. KSHV causes three human malignancies, Kaposi sarcoma, primary effusion lymphoma, and many cases of the plasmablastic form of multicentric Castleman's disease (MCD) as well as occasional cases of plasmablastic lymphoma arising from MCD; it has also been linked to rare cases of bone marrow failure and hepatitis...
October 19, 2017: Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences
https://www.readbyqxmd.com/read/28881567/restoration-of-immune-surface-molecules-in-kaposi-sarcoma-associated-herpes-virus-infected-cells-by-lenalidomide-and-pomalidomide
#6
David A Davis, Suraj Mishra, Holda A Anagho, Ashley I Aisabor, Prabha Shrestha, Victoria Wang, Yuki Takamatsu, Kenji Maeda, Hiroaki Mitsuya, Jerome B Zeldis, Robert Yarchoan
Kaposi sarcoma-associated herpesvirus (KSHV) is the cause of several tumors, including Kaposi sarcoma and primary effusion lymphoma (PEL). Most viruses have evolved means of escaping immune recognition. KSHV downregulates MHC-I expression during lytic infection, and expression of ICAM-1 and B7-2 (CD86) during latent infection, allowing evasion of T cell and natural killer immunity respectively. These effects are largely mediated by two KSHV-encoded proteins, K3 and K5. We show here that lenalidomide (Len) and pomalidomide (Pom) prevent down-regulation of MHC-I during lytic activation, and restore ICAM-1 and B7-2 surface expression in latently infected PEL cells...
August 1, 2017: Oncotarget
https://www.readbyqxmd.com/read/28872106/an-in-vitro-model-for-studying-cellular-transformation-by-kaposi-sarcoma-herpesvirus
#7
Shane C McAllister, Ryan L Hanson, Kyleen N Grissom, Sara Botto, Ashlee V Moses
Kaposi sarcoma (KS) is an unusual tumor composed of proliferating spindle cells that is initiated by infection of endothelial cells (EC) with KSHV, and develops most often in the setting of immunosuppression. Despite decades of research, optimal treatment of KS remains poorly defined and clinical outcomes are especially unfavorable in resource-limited settings. KS lesions are driven by pathological angiogenesis, chronic inflammation, and oncogenesis, and various in vitro cell culture models have been developed to study these processes...
August 25, 2017: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/28855246/localisation-of-double-strand-break-repair-proteins-to-viral-replication-compartments-following-lytic-reactivation-of-kshv
#8
Robert Hollingworth, Richard D Horniblow, Calum Forrest, Grant S Stewart, Roger J Grand
Double-strand breaks (DSBs) in DNA are recognised by the Ku70/80 heterodimer and the MRE11-RAD50-NBS1 (MRN) complex and result in activation of the DNA-PK and ATM kinases that play key roles in regulating the cellular DNA damage response (DDR). DNA tumour viruses such as Kaposi's sarcoma-associated herpesvirus (KSHV) are known to interact extensively with the DDR during the course of their replicative cycles. Here we show that during lytic amplification of KSHV DNA, the Ku70/80 heterodimer and the MRN complex consistently co-localise with viral genomes in replication compartments (RCs) whereas other DSB repair proteins form foci outside of RCs...
August 30, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28854249/deregulation-of-kshv-latency-conformation-by-er-stress-and-caspase-dependent-rad21-cleavage
#9
Alessandra De Leo, Horng-Shen Chen, Chih-Chi Andrew Hu, Paul M Lieberman
Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is a human gammaherpesvirus recognized as the principal causative agent of KS and primary effusion lymphoma (PEL). KSHV establishes persistent latent infection in B lymphocytes where viral gene expression is restricted, in part, by a cohesin-dependent chromosome conformation. Here, we show that endoplasmic reticulum (ER) stress induces a rapid, caspase-dependent cleavage of cohesin subunit RAD21. ER stress-induced cleavage of RAD21 correlated with a rapid and strong viral lytic transcriptional activation...
August 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28845155/corrigendum-clinical-manifestations-of-kaposi-sarcoma-herpesvirus-lytic-activation-multicentric-castleman-disease-kshv-mcd-and-the-kshv-inflammatory-cytokine-syndrome
#10
Mark N Polizzotto, Thomas S Uldrick, Duosha Hu, Robert Yarchoan
[This corrects the article on p. 73 in vol. 3, PMID: 22403576.].
2017: Frontiers in Microbiology
https://www.readbyqxmd.com/read/28841715/nuclease-escape-elements-protect-messenger-rna-against-cleavage-by-multiple-viral-endonucleases
#11
Mandy Muller, Britt A Glaunsinger
During lytic Kaposi's sarcoma-associated herpesvirus (KSHV) infection, the viral endonu- clease SOX promotes widespread degradation of cytoplasmic messenger RNA (mRNA). However, select mRNAs, including the transcript encoding interleukin-6 (IL-6), escape SOX-induced cleavage. IL-6 escape is mediated through a 3' UTR RNA regulatory element that overrides the SOX targeting mechanism. Here, we reveal that this protective RNA element functions to broadly restrict cleavage by a range of homologous and non-homologous viral endonucleases...
August 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28837697/herpesviruses-shape-tumour-microenvironment-through-exosomal-transfer-of-viral-micrornas
#12
Ohad Yogev, Stephen Henderson, Matthew John Hayes, Sara Sofia Marelli, Yifat Ofir-Birin, Neta Regev-Rudzki, Javier Herrero, Tariq Enver
Metabolic changes within the cell and its niche affect cell fate and are involved in many diseases and disorders including cancer and viral infections. Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiological agent of Kaposi's sarcoma (KS). KSHV latently infected cells express only a subset of viral genes, mainly located within the latency-associated region, among them 12 microRNAs. Notably, these miRNAs are responsible for inducing the Warburg effect in infected cells. Here we identify a novel mechanism enabling KSHV to manipulate the metabolic nature of the tumour microenvironment...
August 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28836703/anoikis-resistance-and-oncoviruses
#13
Ehsan Kakavandi, Ramin Shahbahrami, Hossein Goudarzi, Gita Eslami, Ebrahim Faghihloo
Anoikis is known as a special type of programmed cell death which occurs in response to loss of correct cell-extracellular matrix (ECM) connections. This process could be as pivotal event in normal development and tissue homeostasis and found as important mechanism in cancer invasiveness and metastasis. The persistent infection with oncoviruses including EBV (Epstein Bar virus), HPV (Human Papillomaviruses), HBV (Hepatitis B virus), KSHV (Human herpesvirus 8), HTLV-1 (Human T-lymphotropic virus-1), and HCV (Hepatitis C virus) accounted as one of main risk factor for cancer progression...
August 24, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28835496/expression-and-subcellular-localization-of-the-kshv-k15p-protein-during-latency-and-lytic-reactivation-in-primary-effusion-lymphoma-cells
#14
Caitlin G Smith, Himanshu Kharkwal, Duncan W Wilson
The K15P membrane protein of Kaposi's sarcoma-associated herpesvirus (KSHV) interacts with multiple cellular signaling pathways, and is thought to play key roles in KSHV-associated endothelial cell angiogenesis, regulation of B-cell receptor (BCR) signaling and the survival, activation and proliferation of BCR-negative primary effusion lymphoma (PEL) cells. Although full-length K15P is ∼45kDa in size, numerous lower molecular weight forms of the protein exist as a result of differential splicing and poorly characterized post-translational processing...
August 23, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28835494/zic2-is-essential-for-maintenance-of-latency-and-is-a-target-of-an-immediate-early-protein-during-kshv-lytic-reactivation
#15
Yuanzhi Lyu, Kazushi Nakano, Ryan R Davis, Clifford G Tepper, Mel Campbell, Yoshihiro Izumiya
Bivalent histone modifications are defined as repressive and activating epigenetic marks that simultaneously decorate the same genomic region. The H3K27me3 mark silences gene expression while H3K4me3 mark prevents the region from becoming permanently silenced and prepares the domain for activation when needed. Specific regions of Kaposi's sarcoma-associated herpesvirus (KSHV) latent episomes are "poised" to be activated by the KSHV replication and transcription activator (K-Rta). How KSHV episomes are prepared such that they maintain latent infection and switch to lytic replication by K-Rta remains unclear...
August 23, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28811348/a-critical-role-of-glutamine-and-asparagine-%C3%AE-nitrogen-in-nucleotide-biosynthesis-in-cancer-cells-hijacked-by-an-oncogenic-virus
#16
Ying Zhu, Tingting Li, Suzane Ramos da Silva, Jae-Jin Lee, Chun Lu, Hyungjin Eoh, Jae U Jung, Shou-Jiang Gao
While glutamine is a nonessential amino acid that can be synthesized from glucose, some cancer cells primarily depend on glutamine for their growth, proliferation, and survival. Numerous types of cancer also depend on asparagine for cell proliferation. The underlying mechanisms of the glutamine and asparagine requirement in cancer cells in different contexts remain unclear. In this study, we show that the oncogenic virus Kaposi's sarcoma-associated herpesvirus (KSHV) accelerates the glutamine metabolism of glucose-independent proliferation of cancer cells by upregulating the expression of numerous critical enzymes, including glutaminase 2 (GLS2), glutamate dehydrogenase 1 (GLUD1), and glutamic-oxaloacetic transaminase 2 (GOT2), to support cell proliferation...
August 15, 2017: MBio
https://www.readbyqxmd.com/read/28808378/rutamarin-an-active-constituent-from-ruta-angustifolia-pers-induced-apoptotic-cell-death-in-the-ht29-colon-adenocarcinoma-cell-line
#17
Shafinah Ahmad Suhaimi, Sok Lai Hong, Sri Nurestri Abdul Malek
BACKGROUND: Ruta angustifolia Pers. is a perennial herb that is cultivated worldwide, including Southeast Asia, for the treatment of various diseases as traditional medicine. OBJECTIVE: The purpose of the study was to identify an active principle of R. angustifolia and to investigate its effect on the HT29 cell death. MATERIALS AND METHODS: The methanol and fractionated extracts (hexane, chloroform, ethyl acetate, and water) of R. angustifolia Pers...
July 2017: Pharmacognosy Magazine
https://www.readbyqxmd.com/read/28802146/epigenetic-manipulation-of-host-chromatin-by-kaposi-sarcoma-associated-herpesvirus-a-tumor-promoting-factor
#18
REVIEW
Thomas Günther, Adam Grundhoff
Molecular and epidemiological evidence links Kaposi sarcoma-associated herpesvirus (KSHV) to a number of malignancies of endothelial or B cell origin. As for most virus-associated cancers, however, the tumor initiating and promoting events remain poorly understood. Given the emerging role of epigenetic alterations as drivers of human cancers, an interesting (and as of yet under-explored) hypothesis is that viral manipulation of host cell chromatin may contribute to the pathogenesis of KSHV-associated tumors...
August 9, 2017: Current Opinion in Virology
https://www.readbyqxmd.com/read/28801242/oxidant-species-are-involved-in-t-b-mediated-erk1-2-phosphorylation-that-activates-p53-p21-axis-to-promote-kshv-lytic-cycle-in-pel-cells
#19
Roberta Gonnella, Shivangi Yadav, Maria Saveria Gilardini Montani, Marisa Granato, Roberta Santarelli, Alessia Garufi, Gabriella D'Orazi, Alberto Faggioni, Mara Cirone
KSHV is a gammaherpesvirus strongly associated to human cancers such as Primary Effusion Lymphoma (PEL) and Kaposi's Sarcoma. The naturally virus-infected tumor cells usually display latent infection since a minority of cells undergoes spontaneous viral replication. The lytic cycle can be induced in vitro upon appropriate stimuli such as TPA (T), alone or in combination with butyrate (B), (T/B). In previous studies, Protein Kinase C (PKC) δ, Extracellular Signal-regulated Kinase1/2 (ERK1/2) and p53-p21 axis have been separately reported to play a role in KSHV reactivation from latency...
August 8, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28777778/kshv-and-the-role-of-notch-receptor-dysregulation-in-disease-progression
#20
REVIEW
Jennifer L DeCotiis, David M Lukac
Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of two human cancers, Kaposi's Sarcoma (KS) and primary effusion lymphoma (PEL), and a lymphoproliferation, Multicentric Castleman's Disease (MCD). Progression to tumor development in KS is dependent upon the reactivation of the virus from its latent state. We, and others, have shown that the Replication and transcriptional activator (Rta) protein is the only viral gene product that is necessary and sufficient for viral reactivation. To induce the reactivation and transcription of viral genes, Rta forms a complex with the cellular DNA binding component of the canonical Notch signaling pathway, recombination signal binding protein for Jk (RBP-Jk)...
August 4, 2017: Pathogens
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