LIU Gong, DONG Xiao-Beng, LIU Yan-Na and CHU Yong-Lie. Construction of HPV 16 genomes containing mutated and deleted long control regions from cevical cancers[J]. Virologica Sinica, 1996, 11(3).
Citation: LIU Gong, DONG Xiao-Beng, LIU Yan-Na, CHU Yong-Lie. Construction of HPV 16 genomes containing mutated and deleted long control regions from cevical cancers .VIROLOGICA SINICA, 1996, 11(3) : 237.

构建来自宫颈癌并带有突变及缺失LCR的HPVl6重组体

  • 白纹伊蚊和埃及伊蚊通过吸食病毒液或叮吸有病毒血症的小鸡血后,能感染登革1~4型病毒,并能在蚊体内增萌。对感染雌蚊子1和子2代幼虫、雌性或雄性成虫4559只,分101批进行了病毒检测。白纹伊蚊子1代的批阳性率:登革1型为10%(1/10),2型为22.22%(2/9),3型为33.33%(4/12),4型为28.95%(11/38);登革1~4型的最低子代感染率依次为0.20%、0.71%、0.70%和0.63%。子2代对登革4型的批阳性率和最低子代的感染率分别为35.29%(6/17)和0.93%。登革4型感染埃及伊蚊子1和子2代的最低子代感染率分别为0.63%和0.60%。实验表明,白纹伊蚊和埃及伊蚊能经卵传递登革病毒。在本病地方性疫区中,这两种蚊虫在维持登革病毒的自然循环中起重要作用。

Construction of HPV 16 genomes containing mutated and deleted long control regions from cevical cancers

  • Y1 is an imporiant cellular transcriptional regulator which is ubiquitously expressed in vari-ous kinds of cells.The specific binding sites of YY1 protein are found in the flanking sequences ofnlany cellular aiid viral promoters.In the "high risk"huinan papilloniaviruses(HPVs)YY1 works as a traxiscriptional repressor for the viral early gene promoter.In the episomal HPV 16 genomesextracted from cervieal cancers,removal of YY1 binding sites in LCR is a repeated event, resultingin increasing the activity of viral oncogene promoter P97.In order to study the effect of revomal ofYY1 binding sites in LCR on the viral tumorigenicity,HPV16 wild-tny plasmid p1203 was usedas basic sequences,through mltiple-step-clone to construct the new HPV16 plasnuds containingdeleted and mutated LCRs. houence analysis coofirmed that pDV390 had a G to A exchiinge inthe second YY1 site,whereas PDV 1326 and pDV401 contained 115 bp aiid 143 bp deletions in therespective LCRs that revomed 2 and 4 YY1 binding sites.

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    Construction of HPV 16 genomes containing mutated and deleted long control regions from cevical cancers

    • 1. Xi~an Medical University,Xi'an 710061

    Abstract: Y1 is an imporiant cellular transcriptional regulator which is ubiquitously expressed in vari-ous kinds of cells.The specific binding sites of YY1 protein are found in the flanking sequences ofnlany cellular aiid viral promoters.In the "high risk"huinan papilloniaviruses(HPVs)YY1 works as a traxiscriptional repressor for the viral early gene promoter.In the episomal HPV 16 genomesextracted from cervieal cancers,removal of YY1 binding sites in LCR is a repeated event, resultingin increasing the activity of viral oncogene promoter P97.In order to study the effect of revomal ofYY1 binding sites in LCR on the viral tumorigenicity,HPV16 wild-tny plasmid p1203 was usedas basic sequences,through mltiple-step-clone to construct the new HPV16 plasnuds containingdeleted and mutated LCRs. houence analysis coofirmed that pDV390 had a G to A exchiinge inthe second YY1 site,whereas PDV 1326 and pDV401 contained 115 bp aiid 143 bp deletions in therespective LCRs that revomed 2 and 4 YY1 binding sites.

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