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BMC Infectious Diseases

Open Access

DC SIGNR silencing reduces HIV-1 infection in Dendritic cells

  • Omkar Chaudhary1,
  • Sanjeev Kumar1,
  • Heena Aggarwal1,
  • Muzamil A Makhdoomi1,
  • Jasbir Singh2, 3,
  • Anjali Hazarika3 and
  • Kalpana Luthra1Email author
BMC Infectious Diseases201414(Suppl 3):O8

https://doi.org/10.1186/1471-2334-14-S3-O8

Published: 27 May 2014

Background

Dendritic cells (DCs) capture HIV-1 from periphery via DC SIGN/R receptors and transfer to T cells. It has been reported that siRNA directed against DC SIGN significantly inhibits HIV infection of DCs. In this study, the expression of DC SIGN/R and its role in HIV-1 infectivity of DCs were assessed.

Methods

DCs were cultured from monocytes from healthy donors and infected with HIV-1 Indian clade C virus. DC SIGN/R expression on DCs was determined by RealTime PCR. The effect of down regulation of this receptor in DCs using DC SIGN/R siRNA on the infection with HIV-1 was assessed. Statistical significance was calculated by Student’s t test.

Results

High expression of DC SIGN/R was observed on DCs infected with HIV-1 (p= 0.01). DC sIGNR expression in DCs was maximally downregulated by siRNA at 24 hrs (p=0.002) and was associated with significant reduction in expression of CD40 (p= 0.003), CD80 (p=0.008), CD86 (p=0.007) and P38 MAPK (p=0.005). Transfection of DC SIGNR on DCs at 24 hours followed by infection with clade C HIV-1 demonstrated lower levels of p24 compared to that in untransfected DCs (p=0.0008).

Conclusion

Data demonstrates that down regulation of DC SIGNR expression on DCs decreases activation that in turn may inhibit DC T cell interactions needed for progression of HIV-1 infection. Reduced p24 antigen production may be mediated by P38 MAPK inhibition. Our finding suggests that blocking DC SIGNR expression on DCs may prevent initial binding of HIV-1 and serve as a first step in prevention of HIV-1 infection.

Authors’ Affiliations

(1)
Dept. of Biochemistry, All India Institute of Medical Sciences, New Delhi, India
(2)
Dept. of Biochemistry, Kurukshetra University, Kurukshetra, India
(3)
Blood Transfusion Services, Cardiothoracic and Neurosciences Center, All India Institute of Medical Sciences, New Delhi, India

Copyright

© Chaudhary et al; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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