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Liu, Limei; Xiang, Kun–san; Zheng, Tao; Zhang, Rong; Li, Ming; Wang, Yanqing; Lu, Huijuan; Li, Jie

doi:10.1023/a:1022870128494

Cited by 4 publications

(1 citation statement)

References 19 publications

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“…HS is a negatively chargedd linear carbohydrate polymer composed of repeating disaccharide of glucosamine and hexuronic acids that are sulfated at various positions [15]. Apart from the essential functions in animal development and homeostasis, demonstrated by targeted disruption of the enzymes involved in biosynthesis of HS [16], [17], HS is drawing attention as a potential target for prevention of viral infection. Previous investigations on the SINV-HS interaction indicate that HS-dependent phenotype has a selective advantage through the adaptive mutation for positively charged animo acid (aa) during tissue culture.…”

Section: Introductionmentioning

confidence: 99%

Interaction of E2 Glycoprotein with Heparan Sulfate Is Crucial for Cellular Infection of Sindbis Virus

et al. 2010

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Cell culture-adapted strains of Sindbis virus (SINV) initially attach to cells by the ability to interact with heparan sulfate (HS) through selective mutation for positively charged amino acid (aa) scattered in E2 glycoprotein (W. B. Klimstra, K. D. Ryman, and R. E. Johnston, J. Virol. 72: 7357–7366, 1998). Here we have further confirmed that interaction of E2 protein with HS is crucial for cellular infection of SINV based on the reverse genetic system of XJ-160 virus, a Sindbis-like virus (SINLV). Both SINV YN87448 and SINLV XJ-160 displayed similar infectivity on BHK-21, Vero, or C6/36 cells, but XJ-160 failed to infect mouse embryonic fibroblast (MEF) cells. The molecular mechanisms underlying the selective infectivity of XJ-160 were approached by substituting the E1, E2, or both genes of XJ-160 with that of YN87448, and the chimeric virus was denominated as XJ-160/E1, XJ-160/E2, or XJ-160/E1E2, respectively. In contrast to the parental XJ-160, all chimeric viruses became infectious to wild-type MEF cells (MEF-wt). While MEF-Ext −/− cells, producing shortened HS chains, were resistant not only to XJ-160, but also to YN87448 as well as the chimeric viruses, indicating that the inability of XJ-160 to infect MEF-wt cells likely due to its incompetent discrimination of cellular HS. Treatment with heparin or HS-degrading enzyme resulted in a substantial decrease in plaque formation by YN87448, XJ-160/E2, and XJ-160/E1E2, but had marginal effect on XJ-160 and XJ-160/E1, suggesting that E2 glycoprotein from YN87448 plays a more important role than does E1 in mediating cellular HS-related cell infection. In addition, the peptide containing 145–150 aa from E2 gene of YN87448 specifically bound to heparin, while the corresponding peptide from the E2 gene of XJ-160 essentially showed no binding to heparin. As a new dataset, these results clearly confirm an essential role of E2 glycoprotein, especially the domain of 145–150 aa, in SINV cellular infection through the interaction with HS.

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Section: Introductionmentioning

confidence: 99%

Interaction of E2 Glycoprotein with Heparan Sulfate Is Crucial for Cellular Infection of Sindbis Virus

et al. 2010

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Heparan sulfate gene polymorphism in calcium oxalate nephrolithiasis

et al. 2008

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Calcium oxalate (CaOx) nephrolithiasis has a complex pathogenic mechanism. Besides environmental factors, genetic factors also have influence on stone formation. This study represents the effects of heparan sulfate (HSPG2) gene polymorphism for determining the risk of urolithiasis. We investigated 143 CaOx stone formers with 158 healthy individuals for the BamHI restriction site polymorphism located in intron 6 of the HSPG gene using the polymerase chain reaction, restriction fragments length polymorphism method. After digestion with BamHI, the polymorphism was assumed to cause three genotypes according to the banding types as GG (242 bp), GT (242, 144, and 98 bp) and TT (144 and 98 bp). According to the genotype frequencies between the groups, TT genotype showed significantly increased risk for urolithiasis than TG and GG genotypes. We concluded that HSPG2 gene polymorphism might be one of the genetic factors affecting the CaOx stone formation.

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Preliminary Results in a Study Regarding the Relationship Between Perlecan Gene Polymorphism and Spinal Muscular Atrophy Type I Disease

Stavarachi

Toma²,

Butoianu³

et al. 2009

Genetic Testing and Molecular Biomarkers

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Spinal muscular atrophy (SMA) is a neuromuscular disease characterized by weakness and atrophy of proximal muscles. Despite the fact that the disease transmission suggests an autosomal recessive trait, the wide spectrum of clinical manifestations indicates that other genes may contribute to the SMA phenotype. To identify possible modifier genes, the aim of our study was to investigate the relationship between BamH1 perlecan gene polymorphism and SMA type I, the classical severe form of the disease. We genotyped 40 patients with SMA type I disease and 50 subjects without personal or heredo-colateral neuromuscular problems, using the polymerase chain reaction-restriction fragment length polymorphism method. After statistical analysis of the observed genotypes, a significant difference (p = 0.03) could be observed regarding the incidence of TT genotype and T allele in boys with SMA type I compared with affected girls. However, this result cannot be assessed because of the small and unequal number of subjects. We concluded that there might be no association between perlecan gene polymorphism and SMA type I disease.

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Cited by 4 publications

References 19 publications

Interaction of E2 Glycoprotein with Heparan Sulfate Is Crucial for Cellular Infection of Sindbis Virus

Interaction of E2 Glycoprotein with Heparan Sulfate Is Crucial for Cellular Infection of Sindbis Virus

Heparan sulfate gene polymorphism in calcium oxalate nephrolithiasis

Preliminary Results in a Study Regarding the Relationship Between Perlecan Gene Polymorphism and Spinal Muscular Atrophy Type I Disease

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