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Y Cui

Publications and source records attributed to Y Cui.

At least 145 records · Page 8Linked to original sources
PubMed1999

Thrombotic microangiopathy in the HIV-2-infected macaque.

Thrombotic microangiopathy (TMA) has been increasingly reported in human immunodeficiency virus (HIV)-infected humans over the past decade. The pathogenesis is unknown. We prospectively analyzed the renal pathology and function of 27 pigtailed macaques (Macaca nemestrina), infected intravenously with a virulent HIV-2 strain, HIV-2(287), in addition to that of four uninfected control macaques. Necropsies were performed between 12 hours and 28 days after infection. HIV-2 antigen was detectable in peripheral blood mononuclear cell (PBMC) cocultures in all animals after 10 days of HIV-2 infection; a rapid decline in CD4(+) PBMC (<350/microliter) was seen in five of six animals 21 days and 28 days after infection. No macaque developed features of clinical AIDS. Typical lesions of human HIV-associated nephropathy were undetectable. Six of the 27 HIV-2-infected macaques demonstrated both histological TMA lesions (thrombi in glomerular capillary loops and small arteries, mesangiolysis) and ultrastructural lesions (mesangiolysis, subendothelial lucency, platelet thrombi in glomerular capillary lumina). Extrarenal thrombi were detected in the gastrointestinal and adrenal microvasculature of macaques that had developed renal TMA. None of the control animals demonstrated features of renal TMA at necropsy. In a retrospective analysis of kidneys obtained from 39 additional macaques infected with HIV-2(287), seven cases demonstrated TMA. In situ hybridization showed no detectable HIV-2 RNA in kidney sections of 65/66 HIV-2-infected macaques, including all 13 TMA cases. Expression of the chemokine receptor CXCR4, the putative coreceptor for HIV-2(287), was absent in intrinsic renal cells in all HIV-2-infected macaques. The HIV-2-infected macaque may be a useful model of human HIV-associated TMA. Our data do not support a role of direct HIV-2 infection of intrinsic renal cells as an underlying mechanism.

Animals↗
PubMed1999

Increased serum mitogenic activity for arterial smooth muscle cells associated with relaxation and low educational level in human subjects with high but not low hostility traits: implications for atherogenesis.

Proliferation of arterial smooth muscle cells (aSMC) is a key component of atherogenesis. A sample of 225 volunteers, aged 21-65 years, was exposed to "frustration," "harassment," or "relaxation," after completing the 50-item Hostility subscale of the Minnesota Multiphasic Personality Inventory (MMPI). Whole blood was measured before and after exposure for platelet-derived growth factor (PDGF), and sera were evaluated for total and HDL cholesterol concentrations and PDGF-independent mitogenic activity (SMA). Blood pressure and pulse rate were also evaluated. Analyses of SMA (i.e., serum independent of PDGF) revealed an increase in mitogenic effect for cultured human aSMC when hostility was treated as a dichotomous modifier. Among high-hostility subjects, surprisingly, those in the relaxed group and those with a lower educational level were found to have a significant mitogen response; no significant effects were observed for the low-hostility groups. The data suggest that endogenous stresses may occur in high-hostility individuals when "relaxed," to influence proliferation of arterial smooth muscle cells, as a contribution to atherogenesis. In individuals with lower educational levels and higher hostility scores, lifestyle changes may play a role.

Adult↗
PubMed1999

Export pumps for anionic conjugates encoded by MRP genes.

Several members of the multidrug resistance protein (MRP) family mediate the ATP-dependent transport of amphiphilic anions across membranes. The substrate specificity of recombinant human MRP1 has been most extensively defined by use of inside-out membrane vesicles. Substrates include the glutathione S-conjugate leukotriene C4, 17 beta-glucuronosyl estradiol, glucuronosyl bilirubin, glutathione disulfide, in addition to the fluorescent lipophilic anion Fluo-3. These substances are also substrates for the apical isoform MRP2, also termed canalicular multispecific organic anion transporter, cMOAT, which shares only 49% amino acid sequence identity with MRP1. The K(m) of leukotriene C4 for MRP2 is 10-fold higher than for MRP1, and the K(m) of 17 beta-glucuronosyl estradiol is 4.8-fold higher for MRP2 than for recombinant human MRP1. Human as well as rat MRP2 confer multidrug resistance to polarized MDCKII cells permanently expressing the recombinant glycoprotein in their apical plasma membrane. Resistance of cells transfected with human and rat MRP2 to etoposide was enhanced 5-fold and 3.8-fold, and resistance to vincristine was enhanced 2.3-fold and 6.0-fold, respectively. Conjugate-transporting members of the MRP family with a related sequence and a similar function have been detected recently. In addition to several MRP isoforms (MRP1-6) and orthologs in mammals (human, rat, rabbit, mouse), MRP family members have been identified in the nematode Caenorhabditis elegans, in the yeast Saccharomyces cerevisiae, and in the plant Arabidopsis thaliana. These conjugate export pumps of the MRP family play a widespread role in detoxification, drug resistance, and, because of the role in the export of glutathione disulfide by MRP1 and MRP2, in the defense against oxidative stress.

ATP-Binding Cassette Transporters↗
PubMed1999

Neuroprotective effect of mild hypothermia cannot be explained in terms of a reduction of glutamate release during ischemia.

An exogenous glutamate injection into the hypothermic hippocampal CA1 during 5-min ischemia produced the same extent of extracellular glutamate levels as observed in the normothermic CA1 during 5-min ischemia; however, neuronal death was not induced in the hypothermic CA1. Glutamate is released excessively into the extracellular space during ischemia, and is thought to induce brain injury by its neurotoxicity. It has been reported that the massive glutamate release is reduced by mild hypothermia, and it has been proposed that the reduction of ischemia-induced glutamate release exerts the neuroprotective effect on postischemic neuronal death. In the present study, to determine whether the neuroprotective effect of mild hypothermia on postischemic hippocampal CA1 neuronal death is due to the reduction of ischemia-induced glutamate release, gerbils were subjected to 5-min ischemia under hypothermic condition at 31 degrees C and were simultaneously injected exogenously with L-glutamate, so that the hypothermic CA1 around a microdialysis probe was exposed to the same extracellular glutamate levels as seen during normothermic ischemia, and the histological outcome was examined. An injection with 1 mM L-glutamate into the hypothermic CA1 during 5-min ischemia produced a similar extent of increased glutamate (17-fold increase) to that observed in the normothermic CA1 during 5-min ischemia (16-fold increase). However, neuronal death was not induced in the hypothermic CA1. This result indicates that the neuroprotective effect of mild hypothermia cannot be explained in terms of a reduction of glutamate release during ischemia.

Animals↗
PubMed1999

Mutations in the MOF2/SUI1 gene affect both translation and nonsense-mediated mRNA decay.

Recent studies have demonstrated that cells have evolved elaborate mechanisms to rid themselves of aberrant proteins and transcripts. The nonsense-mediated mRNA decay pathway (NMD) is an example of a pathway that eliminates aberrant mRNAs. In yeast, a transcript is recognized as aberrant and is rapidly degraded if a specific sequence, called the DSE, is present 3' of a premature termination codon. Results presented here show that strains harboring the mof2-1, mof4-1, mof5-1, and mof8-1 alleles, previously demonstrated to increase the efficiency of programmed -1 ribosomal frameshifting, decrease the activity of the NMD pathway. The effect of the mof2-1 allele on NMD was characterized in more detail. Previous results demonstrated that the wild-type MOF2 gene is identical to the SUI1 gene. Studies on the mof2-1 allele of the SUI1 gene indicate that in addition to its role in recognition of the AUG codon during translation initiation and maintenance of the appropriate reading frame during translation elongation, the Mof2 protein plays a role in the NMD pathway. The Mof2p/Sui1 p is conserved throughout nature and the human homolog of the Mof2p/Sui1p functions in yeast cells to activate NMD. These results suggest that factors involved in NMD are general modulators that act in several aspects of translation and mRNA turnover.

Alleles↗
PubMed1999

Cloning and tissue expressional characterization of a full-length cDNA encoding human neuronal protein P17.3.

A full-length cDNA of 595 bp was isolated from a human fetal brain cDNA library. It contains an open reading frame encoding 153 amino acids, with an 18-bp 5'UTR and a 118-bp 3'UTR in which there is an atypical polyadenylation signal (ATTAAA). The calculated molecular weight of the deduced protein is 17.3 kU. The predicted isoelectric point is 4.89. On account of its high homology to mouse neuronal protein NP15.6 (81.2% identity), the deduced protein was named neuronal protein 17.3 (NP17.3). When its secondary structure was examined by the GGBSM program of PCGENE software, it was found that 32.6 and 15.0% of its amino acids are involved in forming alpha-helices and beta-sheets, respectively. Examined with the PESTFIND program, a typical PEST region found in rapidly degraded proteins was found between residue 48 and residue 68.

5' Untranslated Regions↗
PubMed1999

Efficacy and safety analyses of a recombinant human immunodeficiency virus type 1 derived vector system.

Lentiviruses infect both dividing and nondividing cells. In this study we characterized a lentiviral vector system consisting of a packaging vector (pHP) and a transducing vector (pTV) derived from a recombinant human immunodeficiency virus type 1 (HIV-1). In pHP, the long terminal repeats (LTRs), the 5' untranslated leader and portions of the env and nef genes were deleted. The leader sequence of pHP was substituted with a modified Rous sarcoma virus (RSV) 59 bp leader containing a mutated RSV gag AUG and a functional 5' splice site. The pHP construct was found to direct Gag-Pol synthesis as efficiently as wild-type HIV-1. The pTV construct contains sequences required for RNA packaging, reverse transcription and integration, but lacks viral genes. Co-transfection of pHP, pTV and a vesicular stomatitis virus G (VSV-G) envelope plasmid produced vectors at titers of 10(5)-10(6) transducing units per milliliter in 48 h. Replication-competent virus (RCV) was not detected when deletions were made in the env gene in pHP. The ability of this vector system to transduce dividing and nondividing cell in vitro and in vivo was also demonstrated. Compared with a Moloney murine leukemia virus (MLV) vector, the HP/TV vectors transduced human muscle-, kidney-, liver-derived cell lines and CD34+ primary hematopoietic progenitor cells more efficiently. Although the levels of the pTV transgene expression were high soon after transduction, the expression tended to decrease with time due either to the loss of proviral DNA or to the inactivation of promoter activity, which was found to be cell type-dependent. Analyses of extrachromosomal DNA showed that the unintegrated proviral DNA of lentiviral vectors survived much longer than that of the retroviral vectors. We demonstrate that the HP/TV vector is capable of high efficiency transduction and that long-term expression of lentiviral vectors is dependent on target cell type, the internal promoter and the transgene itself in the transducing vector.

Animals↗
PubMed1999

Esophagogastric anastomotic wound healing in rats.

Esophagectomy with esophagogastric anastomosis is commonly complicated by anastomotic dehiscence. Although this is a major problem in clinical esophageal surgery, laboratory investigation of esophagogastric anastomotic wound healing has been hampered by the lack of a practical rodent model. Problems with aspiration pneumonia and anastomotic strictures hindered our previous studies in the rat. Other researchers have turned to large animal experiments, or used various upper gastrointestinal pseudoanastomotic techniques in rodents. None of these approaches has proved satisfactory. We developed a technique of side-to-side esophagogastric anastomosis in the rat, and then studied normal esophagogastric anastomotic healing in this model. Anastomoses were performed in 24 rats. Anastomotic breaking strength and hydroxyproline concentration were measured 1 and 2 weeks after surgery. Anastomotic breaking strength was 3.78 +/- 1.18 N at 1 week and 4.83 +/- 0.91 N after 2 weeks (p < 0.03). Anastomotic tissue hydroxyproline concentration was 370.6 +/- 31.2 nmol/mg at 1 week and 462.1 +/- 69.7 nmol/mg after 2 weeks (p < 0.001). Many of the problems encountered in esophagogastric anastomotic studies in the rat have been overcome using this new model.

Anastomosis, Surgical↗
PubMed1999

CNS-specific prostacyclin ligands as neuronal survival-promoting factors in the brain.

Prostacyclin (PGI2) is a critical regulator of the cardiovascular system, via dilatation of vascular smooth muscle and inhibition of platelet aggregation (Moncada, S. 1982, Br. J. Pharmacol., 76, 3). Our previous studies demonstrated that a novel subtype of PGI2 receptor, which is clearly distinct from a peripheral subtype in terms of ligand specificity, is expressed in the rostral region of the brain, e.g. cerebral cortex, hippocampus, thalamus and striatum, and that (15R)-16-m-17,18,19,20-tetranorisocarbacyclin (15R-TIC) and 15-deoxy-16-m-17,18,19,20-tetranorisocarbacyclin (15-deoxy-TIC) specifically bind to the central nervous system (CNS)-specific PGI2 receptor. Here, we report that these CNS-specific PGI2 receptor ligands, including PGI2 itself, prevented the neuronal death. They prevented apoptotic cell death of hippocampal neurons induced by high (50%) oxygen atmosphere, xanthine + xanthine oxidase, and serum deprivation. IC50s for neuronal death were approximately 30 and 300 nM for 15-deoxy-TIC and 15R-TIC, respectively, which well correlated with the binding potency for the CNS-specific PGI2 receptor. 6-Keto-PGF1alpha (a stable metabolite of PGI2), peripheral nervous system-specific PGI2 ligands and other prostaglandins (PGs) than PGI2 did not show such neuroprotective effects. In vivo, 15R-TIC protected CA1 pyramidal neurons against ischaemic damage in gerbils. These results indicate that CNS-specific PGI2 ligands have neuronal survival-promoting activity both in vitro and in vivo, and may represent a new type of therapeutic drug for neurodegeneration.

Animals↗
PubMed1999

Localization of fibroblast growth factor-2 (basic FGF) and FGF receptor-1 in adult human kidney.

BACKGROUND: The expression pattern of fibroblast growth factor-2 (FGF-2; basic FGF), a pleiotrophic growth factor, as well as one of its receptors (FGFR1), in the kidney is highly controversial. METHODS: Using an approach that combines multiple antibodies for immunohistochemistry and correlative in situ hybridization, we assessed the intrarenal expression of both FGF-2 and FGFR1 in 13 specimens of adult kidney removed during tumor nephrectomy. RESULTS: The FGF-2 expression pattern in the kidneys as detected by immunohistochemistry was variable and depended on the antibody used. The most consistent expression of FGF-2 protein was demonstrated in glomerular parietal epithelial cells, tubular cells (mainly of the distal nephron), as well as arterial endothelial cells. These locations also corresponded to areas of FGF-2 mRNA expression. Additionally, by immunohistochemistry, FGF-2 protein was detected in arterial smooth muscle cells and occasional podocytes. The expression of FGFR1 protein and mRNA was most consistently present in tubular cells of the distal nephron and in vascular smooth muscle cells. In situ hybridization, but not immunohistochemistry, also suggested FGFR1 expression in cells that could not be precisely identified within the glomerular tuft as well as some interstitial cells. CONCLUSION: These data suggest potential autocrine and paracrine pathways within the FGF-2 system, particularly within the vascular walls and in the distal nephron, and thereby provide information for further mechanistic understanding of the role of the FGF-2 system in human renal disease.

Adult↗
PubMed1999

Ovarian morphology and follicular systems in yaks of different ages.

Forty-five female yaks of different ages with known reproductive histories were used to determine the morphology and follicular systems of their ovaries. The histological structure of the ovaries in each age group was found to be similar and resembled that of cattle and buffalo. The atresia of primordial follicles took one form (oocyte atresia); that of growing follicles could be divided into two stages (early and late); and that of Graafian follicular were classified as early, definite and late stage. The details of the several types of atresia are described herein. The average total numbers of primordial follicles per ovary pair in 1-month-old calves, 1-year-old heifers, 2-year-old heifers and 7-10-year-old cows were 53,500 +/- 6300, 32,870 +/- 4500, 22,850 +/- 2800 and 9500 +/- 1200, respectively; those of growing follicles were 210 +/- 76, 815 +/- 95, 895 +/- 142 and 445 +/- 88, respectively; and those of Graafian follicles were 36.5 +/- 14.2, 41.7 +/- 12.3, 37.8 +/- 9.8 and 42.5 +/- 14.5, respectively. The percentage of atretic primordial follicles per ovary pair in 1-month-old calves, 1-year-old heifers, 2-year-old heifers and 7 to 10 year-old cows were 51.6, 55.5, 56.7 and 47.4%, respectively. The average total numbers of atretic growing follicles per ovary pair were 119.5 +/- 21.5, 605.5 +/- 74.3, 721.6 +/- 78.5 and 275.8 +/- 66.3, respectively; those of atretic Graafian follicles were 22.1 +/- 5.6, 21.2 +/- 7.6, 21.5 +/- 4.7 and 25.3 +/- 6.7, respectively.

Aging↗
PubMed1999

An anatomical study of the internal genital organs of the yak at different ages.

Forty-five female yaks of different ages with known reproductive histories were used to determine the anatomical characteristics of their internal genital organs. The results showed that there were several follicles of different sizes present on the surface of each examined ovary, up to a maximum of 13. In each age group, a greater number of follicles < 5 mm was observed in the right than in the left ovary (P < 0.05), while the number of follicles > 5 mm in the right ovary was almost the same as that in the left one. The average sizes and/or weights of the ovary, oviduct and uterus became larger or heavier with increasing age, and significant differences occurred between age groups (P < 0.05). The shapes, locations and other anatomical characteristics of the different internal genital organs are also described.

Aging↗
PubMed1999

Structural and transcriptional comparative analysis of the S locus regions in two self-incompatible Brassica napus lines.

Self-incompatibility (SI) in Brassica is controlled by a single locus, termed the S locus. There is evidence that two of the S locus genes, SLG, which encodes a secreted glycoprotein, and SRK, which encodes a putative receptor kinase, are required for SI on the stigma side. The current model postulates that a pollen ligand recognizing the SLG/SRK receptors is encoded in the genomic region defined by the SLG and SRK genes. A fosmid contig of approximately 65 kb spanning the SLG-910 and SRK-910 genes was isolated from the Brassica napus W1 line. A new gene, SLL3, was identified using a novel approach combining cDNA subtraction and direct selection. This gene encodes a putative secreted small peptide and exists as multiple copies in the Brassica genome. Sequencing analysis of the 65-kb contig revealed seven additional genes and a transposon. None of these seven genes exhibited features expected of S genes on the pollen side. An approximately 88-kb contig of the A14 S region also was isolated from the B. napus T2 line and sequenced. Comparison of the two S regions revealed that (1) the gene organization downstream of SLG in both S haplotypes is highly colinear; (2) the distance between SLG-A14 and SRK-A14 genes is much larger than that between SLG-910 and SRK-910, with the intervening region filled with retroelements and haplotype-specific genes; and (3) the gene organization downstream of SRK in the two haplotypes is divergent. These observations lead us to propose that the SLG downstream region might be one border of the S locus and that the accumulation of heteromorphic sequences, such as retroelements as well as haplotype-unique genes, may act as a mechanism to suppress recombination between SLG and SRK.

Amino Acid Sequence↗
PubMed1999

rsmC of the soft-rotting bacterium Erwinia carotovora subsp. carotovora negatively controls extracellular enzyme and harpin(Ecc) production and virulence by modulating levels of regulatory RNA (rsmB) and RNA-binding protein (RsmA).

Previous studies have shown that the production of extracellular enzymes (pectate lyase [Pel], polygalacturonase [Peh], cellulase [Cel], and protease [Prt]) and harpin(Ecc) (the elicitor of hypersensitive reaction) in Erwinia carotovora subsp. carotovora is regulated by RsmA, an RNA-binding protein, and rsmB, a regulatory RNA (Rsm stands for regulator of secondary metabolites) (Y. Liu et al., Mol. Microbiol. 29:219-234, 1998). We have cloned and characterized a novel regulatory gene, rsmC, that activates RsmA production and represses extracellular enzyme and harpin(Ecc) production, rsmB transcription, and virulence in E. carotovora subsp. carotovora. In an rsmC knockout mutant of E. carotovora subsp. carotovora Ecc71 carrying the chromosomal copy of the wild-type rsmA(+) allele, the basal levels of Pel, Peh, Cel, Prt, and harpin(Ecc) as well as the amounts of rsmB, pel-1, peh-1, celV, and hrpN(Ecc) transcripts are high, whereas the levels of rsmA transcripts and RsmA protein are low. Furthermore, the expression of an rsmA-lacZ gene fusion is lower in the RsmC(-) mutant than in the RsmC(+) parent. Conversely, the expression of an rsmB-lacZ operon fusion is higher in the RsmC(-) mutant than in the RsmC(+) parent. These observations establish that RsmC negatively regulates rsmB transcription but positively affects RsmA production. Indeed, comparative studies with an RsmC(-) mutant, an RsmA(-) mutant, and an RsmA(-) RsmC(-) double mutant have revealed that the negative effects on exoprotein production and virulence are due to the cumulative regulatory effects of RsmC on rsmA and rsmB. Exoprotein production by the RsmC(-) mutant is partially dependent on the quorum sensing signal, N-(3-oxohexanoyl)-L-homoserine lactone. Southern blot data and analysis of PCR products disclosed the presence of rsmC sequences in E. carotovora subsp. atroseptica, E. carotovora subsp. betavasculorum, and E. carotovora subsp. carotovora. These findings collectively support the idea that rsmA and rsmB expression in these plant pathogenic Erwinia species is controlled by RsmC or a functional homolog of RsmC.

Amino Acid Sequence↗
PubMed1999

kdgREcc negatively regulates genes for pectinases, cellulase, protease, HarpinEcc, and a global RNA regulator in Erwinia carotovora subsp. carotovora.

Erwinia carotovora subsp. carotovora produces extracellular pectate lyase (Pel), polygalacturonase (Peh), cellulase (Cel), and protease (Prt). The concerted actions of these enzymes largely determine the virulence of this plant-pathogenic bacterium. E. carotovora subsp. carotovora also produces HarpinEcc, the elicitor of the hypersensitive reaction. We document here that KdgREcc (Kdg, 2-keto-3-deoxygluconate; KdgR, general repressor of genes involved in pectin and galacturonate catabolism), a homolog of the E. chrysanthemi repressor, KdgREch and the Escherichia coli repressor, KdgREco, negatively controls not only the pectinases, Pel and Peh, but also Cel, Prt, and HarpinEcc production in E. carotovora subsp. carotovora. The levels of pel-1, peh-1, celV, and hrpNEcc transcripts are markedly affected by KdgREcc. The KdgREcc- mutant is more virulent than the KdgREcc+ parent. Thus, our data for the first time establish a global regulatory role for KdgREcc in E. carotovora subsp. carotovora. Another novel observation is the negative effect of KdgREcc on the transcription of rsmB (previously aepH), which specifies an RNA regulator controlling exoenzyme and HarpinEcc production. The levels of rsmB RNA are higher in the KdgREcc- mutant than in the KdgREcc+ parent. Moreover, by DNase I protection assays we determined that purified KdgREcc protected three 25-bp regions within the transcriptional unit of rsmB. Alignment of the protected sequences revealed the 21-mer consensus sequence of the KdgREcc-binding site as 5'-G/AA/TA/TGAAA[N6]TTTCAG/TG/TA-3'. Two such KdgREcc-binding sites occur in rsmB DNA in a close proximity to each other within nucleotides +79 and +139 and the third KdgREcc-binding site within nucleotides +207 and +231. Analysis of lacZ transcriptional fusions shows that the KdgR-binding sites negatively affect the expression of rsmB. KdgREcc also binds the operator DNAs of pel-1 and peh-1 genes and represses expression of a pel1-lacZ and a peh1-lacZ transcriptional fusions. We conclude that KdgREcc affects extracellular enzyme production by two ways: (i) directly, by inhibiting the transcription of exoenzyme genes; and (ii) indirectly, by preventing the production of a global RNA regulator. Our findings support the idea that KdgREcc affects transcription by promoter occlusion, i.e., preventing the initiation of transcription, and by a roadblock mechanism, i.e., by affecting the elongation of transcription.

Amino Acid Sequence↗
PubMed1999

Contributions of viral splice sites and cis-regulatory elements to lentivirus vector function.

The mobile transgene constructs of most human immunodeficiency virus (HIV)-based lentivirus vectors currently in use contain viral long terminal repeats, a 5' untranslated region, gag sequences, and env sequences that include the Rev-responsive element (RRE). In this study, we examined the possibility of deleting HIV splice sites and gag and env sequences from an HIV type 1 recombinant vector established in our laboratory as part of our ongoing efforts to improve this vector system. Mutations in the major splice donor site (SD) markedly reduced viral RNA expression but had little effect on vector titer. Deletion of gag or env sequences, excluding RRE, led to a moderate reduction in vector titer. Interestingly, deletion of RRE slightly reduced viral RNA expression but markedly impaired vector function. Combined deletions of RRE, gag (except for the first 40 nucleotides), env, and the SD mutation resulted in a twofold increase in cytoplasmic viral RNA expression and a recovery of vector efficiency to approximately 50% of the wild-type level. This increase in cytoplasmic RNA levels is likely to be due, at least in part, to effects of the TE671 host cells, a human rhabdomyosarcoma cell line used for vector production in our system, on the cytoplasmic distribution of spliced and unspliced viral RNA. These results show that optimal lentivirus vector function can be maintained in the absence of multiple essential viral elements.

5' Untranslated Regions↗