Journal
VIROLOGICA SINICA
Volume 36, Issue 4, Pages 796-809Publisher
KEAI PUBLISHING LTD
DOI: 10.1007/s12250-021-00363-1
Keywords
Human immunodeficiency virus (HIV); RNA polymerase II (RNA Pol II); Viral transcription; Infection; Virology; CREB regulated transcription coactivator 2 (CRTC2); Long terminal repeat (LTR); Latency
Categories
Funding
- National Mega-Project for Infectious Disease [2018ZX10301408]
- National Key Research and Development program of China [2018YFE0107600]
- National Natural Science Foundation of China [81903679, 81772205]
- Peking Union Medical College Youth Fund [332017075]
- CAMS innovation fund for Medical Sciences [2018-I2M-3-004]
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CRTCs can inhibit HIV-1 transcription and decrease viral RNA expression, having a negative impact on HIV-1 infection, and may drive HIV-1 into latency.
The CREB-regulated transcriptional co-activators (CRTCs), including CRTC1, CRTC2 and CRTC3, enhance transcription of CREB-targeted genes. In addition to regulating host gene expression in response to cAMP, CRTCs also increase the infection of several viruses. While human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) promoter harbors a cAMP response element and activation of the cAMP pathway promotes HIV-1 transcription, it remains unknown whether CRTCs have any effect on HIV-1 transcription and HIV-1 infection. Here, we reported that CRTC2 expression was induced by HIV-1 infection, but CRTC2 suppressed HIV-1 infection and diminished viral RNA expression. Mechanistic studies revealed that CRTC2 inhibited transcription from HIV-1 LTR and diminished RNA Pol II occupancy at the LTR independent of its association with CREB. Importantly, CRTC2 inhibits the activation of latent HIV-1. Together, these data suggest that in response to HIV-1 infection, cells increase the expression of CRTC2 which inhibits HIV-1 gene expression and may play a role in driving HIV-1 into latency.
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