Nuclear translocation and regulation of intranuclear distribution of cytoplasmic poly(A)-binding protein are distinct processes mediated by two Epstein Barr virus proteins.
Abstract: One ZEBRA mutant, Z(S186E), was deficient in translocation yet was capable of altering the intranuclear distribution of PABPC.
Result: 293 cells transfected with empty vector, or expression vectors for BGLF5, WT ZEBRA, Z(N182K), or Z(S186E) were analyzed for new protein synthesis.
Result: A ZEBRA mutant, Z(R183E), which induces nuclear aggregates and is concentrated in nuclear aggresomes, colocalized with PABPC within the nuclear aggregates and aggresomes when transfected in the absence of BGLF5
Uracil DNA glycosylase BKRF3 contributes to Epstein-Barr virus DNA replication through physical interactions with proteins in viral DNA replication complex.
Abstract: In complementation assays, the catalytic mutant BKRF3(Q90L,D91N) restored viral DNA replication, whereas the leucine loop mutant BKRF3(H213L) only partially rescued viral DNA replication, coupled with a reduced ability to interact with the viral DNA polymerase and Rta.
Essential role of Rta in lytic DNA replication of Epstein-Barr virus.
Abstract: Ectopic expression of the six components of the EBV lytic replication machinery failed to rescue replication by Z(S186A).
Abstract: However, addition of Rta to Z(S186A) and the mixture of replication factors activated viral replication and late gene expression.
Abstract: In addition, expression of Rta and Z(S186A) together, but not individually, activated synthesis of the BHLF1 transcript, a lytic transcript required for the process of viral DNA replication.
Abstract: We found that Z(S186A), a mutant of ZEBRA unable to a
Pin1 interacts with the Epstein-Barr virus DNA polymerase catalytic subunit and regulates viral DNA replication.
Abstract: Exogenous supply of wild-type BALF5 in HEK293 cells with knockout recombinant EBV allowed efficient synthesis of viral genome DNA, but BALF5 T178A could not provide support as efficiently as wild-type BALF5.
Abstract: Lambda protein phosphatase treatment abolished the binding of BALF5 to Pin1, and mutation analysis of BALF5 revealed that replacement of the Thr178 residue by Ala (BALF5 T178A) disrupted the interaction with Pin1.
The large groove found in the gH/gL structure is an important functional domain for Epstein-Barr virus fusion.
Abstract: We also observed that substitution of alanine for arginine 152, histidine 154, or threonine 174 reduces fusion with epithelial cells but not with B cells.
Abstract: We found that substitution of alanine for leucine 207 reduces both epithelial and B cell fusion and is accompanied by reduced gp42 binding.
Abstract: We found that the G49C mutant, predicted to bridge D-I and D-II with C153 of gH/gL, had normal B cell fusion activity but reduced epithelial cell fusion activity, which was partially restored by treatment with dithiothreitol.
Identification of a novel variant of LMP-1 of EBV in patients with endemic Burkitt lymphoma in western Kenya.
Abstract: However a novel LMP-1 variant was identified, called K for Kenya and for the G318K mutation that characterizes it.
Method: Plasmids containing cloned LMP-1 PCR products were sent to Genewiz (South Plainfield, NJ, USA) for sequencing using M13R universal primers.
Result: The G318K mutation was highly linked to the Q322E mutation, such that all 22 sequences observed containing G318K also contained Q322E.
Result: The atypical K variant containing H352R was found in 6 (16.2%) eBL sequences and 4 (16.7%) healthy controls (p=1.00, OR 0.97, 95% CI 0.24-3.87).
Result: This variant always differed
High molecular weight complex analysis of Epstein-Barr virus Latent Membrane Protein 1 (LMP-1): structural insights into LMP-1's homo-oligomerization and lipid raft association.
Abstract: LMP-1/C238A retains wild type LMP-1 NF-kappaB activity.
Method: The following cysteine substitution mutants are all constructed in the pCMV-LMP-1 background: pCMV-LMP-1/CsubA1 has an alanine codon in place of cysteine 78 (C78A); pCMV-LMP-1/CsubA1,2 has alanine codons in place of cysteines 78 and 84 (C78A; C84A); pCMV-LMP-1/CsubA3 has an alanine in place of cysteine 116 (C116A); pCMV-LMP-1/CsubA1-3 has alanine codons in place of cysteines 78, 84, and 116 (
Sequence analysis of Epstein-Barr virus EBNA-2 gene coding amino acid 148-487 in nasopharyngeal and gastric carcinomas.
Abstract: Three variations (g48991t, c48998a, t49613a) were detected in all of the samples (113/113, 100%).
Abstract: Variation analysis in EBNA-2 functional domains: the TAD residue (I438L) and the NLS residues (E476G, P484H and I486T) were only detected in NPC samples which located in the carboxyl terminus of EBNA-2 gene.
Result: Among the 20 loci with nucleotide changes, three nucleotide mutations (g48991t, c48998a and t49613a) were detected in all the
Genome-wide analysis of Epstein-Barr virus Rta DNA binding.
Abstract: Rta K156A failed to activate BALF5p, suggesting this promoter can be activated by an RRE-dependent mechanism.
Abstract: To assess whether BALF5 might be activated by an RRE-dependent mechanism, an Rta mutant (Rta K156A), deficient for DNA binding and RRE activation but competent for Zp/Rp activation, was used.
Genetic diversity of EBV-encoded LMP1 in the Swiss HIV Cohort Study and implication for NF-Kappab activation.
Abstract: F106Y was present in all LMP1 isolated in this study and its effect was variant dependent, suggesting that it was modulated by other polymorphisms.
Abstract: The two polymorphisms I124V and F144I were present in distinct phylogenetic groups and were linked with other specific polymorphisms nearby, I152L and D150A/L151I, respectively.
Abstract: The two sets of polymorphisms, I124V/I152L and F144I/D150A/L151I, which were markers of increased NF-kappaB activation in vitro, were not associated with EBV-associated
EBV mutation literature information.
PMID: 
2014
PloS one
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