Toll-like receptor-3 mediates HIV-1 transactivation via NFκB and JNK pathways and histone acetylation, but prolonged activation suppresses Tat and HIV-1 replication
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- 作者：Biju Bhargavan bbhargavan@unmc.edu" class="auth_mail" title="E-mail the corresponding author ; Shawna M. Woollard swoollar@unmc.edu" class="auth_mail" title="E-mail the corresponding author ; Georgette D. Kanmogne ; gkanmogne@unmc.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：TLR3 ; HIV ; Viral transactivation ; LTR ; NFκB ; JNK ; STAT1 ; Histone acetylation ; Epigenetics ; Human monocyte-derived macrophages ; TZM-bl ; U38 cells
- 刊名：Cellular Signalling
- 出版年：2016
- 出版时间：February 2016
- 年：2016
- 卷：28
- 期：2
- 页码：7-22
- 全文大小：2942 K
文摘
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TLR3 activation induced transcription factors that modulate HIV promoter activity.
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TLR3 activation increased HIV transactivation via JNK and NFκB pathways.
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Epigenetic modifications modulate TLR3-induced HIV transactivation.
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Prolonged TLR3 activation suppresses HIV transactivation and viral replication.
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TLR3 ligands could help target and eliminate HIV in latently infected cells.