کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5906435 | 1159970 | 2013 | 6 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Inhibition of CXCR4 expression by recombinant adenoviruses containing anti-sense RNA resists HIV-1 infection on MT4 cell lines Inhibition of CXCR4 expression by recombinant adenoviruses containing anti-sense RNA resists HIV-1 infection on MT4 cell lines](/preview/png/5906435.png)
- We established recombinant adenoviruses containing anti-sense CXCR4 cDNA.
- Recombinant adenoviruses containing anti-sense can inhibit CXCR4 expression.
- Recombinant adenoviruses containing anti-sense can resist HIV-1 infection on MT4 cell lines.
CXCR4-tropic (X4) variants are associated with faster disease progression than CCR5-tropic variants in HIV infection. We previously reported inhibition of CCR5 expression on U937 cells could protect the cells from HIV-1 infection. Here, we established recombinant adenoviruses containing anti-sense CXCR4 cDNA, to investigate its role in the protection of HIV entering into target cells. A fragment of 636Â bp cDNA from CXCR4 mRNA was recombined into adenoviral vector and the recombinant adenovirus was obtained from AD-293 cells. The rates of CXCR4 expression on the MT4 cells infected with recombinant adenovirus were measured by FACS. The MT4 cells infected by recombinant adenovirus were challenged by T-tropic HIV-1 strains and then P24 antigen was assayed. The rate of expression of CXCR4 on MT4 cell infected with recombinant adenovirus was decreased from 42% to 1.12% at 24Â h, and to 1.03%, 1.39%, and 1.23% at 48Â h, 72Â h and 10Â days respectively. Compared with Ad-control cells, recombinant adenovirus infected MT4 cells produced much less P24 antigen after being challenged with HIV-1. Furthermore, the recombinant adenovirus had no effects on chemotactic activity and proliferation of the MT4 cells. In conclusion, recombinant adenoviruses containing anti-sense can inhibit CXCR4 expression and resist HIV-1 infection on MT4 cell lines.
Journal: Gene - Volume 526, Issue 2, 10 September 2013, Pages 443-448