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Review

HIV-1: To Splice or Not to Splice, That Is the Question

by 1 and 1,2,3,*
1
Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA
2
Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill, NC 27599, USA
3
Center for AIDS Research, University of North Carolina, Chapel Hill, NC 27599, USA
*
Author to whom correspondence should be addressed.
Academic Editors: Karen Beemon and Marie-Louise Hammarskjold
Viruses 2021, 13(2), 181; https://doi.org/10.3390/v13020181
Received: 5 January 2021 / Revised: 21 January 2021 / Accepted: 22 January 2021 / Published: 26 January 2021
(This article belongs to the Special Issue Retroviral RNA Processing)
The transcription of the HIV-1 provirus results in only one type of transcript—full length genomic RNA. To make the mRNA transcripts for the accessory proteins Tat and Rev, the genomic RNA must completely splice. The mRNA transcripts for Vif, Vpr, and Env must undergo splicing but not completely. Genomic RNA (which also functions as mRNA for the Gag and Gag/Pro/Pol precursor polyproteins) must not splice at all. HIV-1 can tolerate a surprising range in the relative abundance of individual transcript types, and a surprising amount of aberrant and even odd splicing; however, it must not over-splice, which results in the loss of full-length genomic RNA and has a dramatic fitness cost. Cells typically do not tolerate unspliced/incompletely spliced transcripts, so HIV-1 must circumvent this cell policing mechanism to allow some splicing while suppressing most. Splicing is controlled by RNA secondary structure, cis-acting regulatory sequences which bind splicing factors, and the viral protein Rev. There is still much work to be done to clarify the combinatorial effects of these splicing regulators. These control mechanisms represent attractive targets to induce over-splicing as an antiviral strategy. Finally, splicing has been implicated in latency, but to date there is little supporting evidence for such a mechanism. In this review we apply what is known of cellular splicing to understand splicing in HIV-1, and present data from our newer and more sensitive deep sequencing assays quantifying the different HIV-1 transcript types. View Full-Text
Keywords: HIV-1; HIV-1 splicing; HIV-1 oversplicing; HIV-1 latency HIV-1; HIV-1 splicing; HIV-1 oversplicing; HIV-1 latency
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MDPI and ACS Style

Emery, A.; Swanstrom, R. HIV-1: To Splice or Not to Splice, That Is the Question. Viruses 2021, 13, 181. https://doi.org/10.3390/v13020181

AMA Style

Emery A, Swanstrom R. HIV-1: To Splice or Not to Splice, That Is the Question. Viruses. 2021; 13(2):181. https://doi.org/10.3390/v13020181

Chicago/Turabian Style

Emery, Ann, and Ronald Swanstrom. 2021. "HIV-1: To Splice or Not to Splice, That Is the Question" Viruses 13, no. 2: 181. https://doi.org/10.3390/v13020181

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