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Investigating SREBP2 as a Potential Zika Virus Host Cofactor

Title: Investigating SREBP2 as a Potential Zika Virus Host Cofactor.

Inaccessible until Apr 27, 2020 due to copyright restrictions.

Name(s): Bell, Alexander Bell, author
Lee, Emily, author
Tang, Hengli, author
Type of Resource: text
Genre: Text
Bachelor Thesis
Date Issued: 2018-04-27
Physical Form: computer
online resource
Extent: 1 online resource
Language(s): English
Abstract/Description: Zika virus (ZIKV) is an Aedes mosquito transmitted flavivirus that has drawn global concern during the 2015-2016 epidemic in the Americas. The identification of host proteins and pathways may elucidate potential drug targets for antiviral therapy. Cholesterol synthesis has been shown to play an important role in the pathogenesis of several members of the flaviviridae family.16,18 Cholesterol biosynthesis occurs via the mevalonate pathway, and all participating enzymes are transcriptionally regulated by sterol regulatory-element binding proteins (SREBPs). 12,13 RNAi mediated expression knockdown of SREBP2 followed by NS1 FRET analysis reveals a 43% decrease in ZIKV infectivity in SNB-19 cells. Interestingly, RNAi mediated expression knockdown of individual genes that are transcriptionally activated by SREBP2 results in an increase of ZIKV infectivity. This suggests that the antiviral effect of SREBP2 knockdown is not solely mediated by depletion of mevalonate pathway products such as cholesterol. We hypothesize that the SREBP2 post-translational processing pathway contains pro-viral elements, and that ZIKV infectivity can be modulated by the activity of the pathway. Knockdown of SREBP2 does not induce spontaneous interferon beta (IFN-β) expression, but may increase IFN-β expression in the response to an infection. Overexpression of SREBP2 and SREBP1a result in increased transcription of mevalonate pathway enzymes, and increased ZIKV infection. SREBP1a’s enhancement of ZIKV infectivity indicates that SREBP2’s pro-viral role is likely mediated through the activity of it’s transcriptional targets. The specific mechanism of SREBP2’s interaction with ZIKV is not known, and is the subject of potential future plans for investigation.
Identifier: FSU_libsubv1_scholarship_submission_1524861754_b7c9463e (IID)
Keywords: Zika, Virus, Cholesterol, SREBP, Virology
Grant Number: NIH U19AI31130
Persistent Link to This Record:
Owner Institution: FSU

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Bell, A. B., Lee, E., & Tang, H. (2018). Investigating SREBP2 as a Potential Zika Virus Host Cofactor. Retrieved from