PMID- 37194028
OWN - NLM
STAT- MEDLINE
DCOM- 20230518
LR  - 20230607
IS  - 1742-4690 (Electronic)
IS  - 1742-4690 (Linking)
VI  - 20
IP  - 1
DP  - 2023 May 16
TI  - Origin and functional role of antisense transcription in endogenous and exogenous 
      retroviruses.
PG  - 6
LID - 10.1186/s12977-023-00622-x [doi]
LID - 6
AB  - Most proteins expressed by endogenous and exogenous retroviruses are encoded in 
      the sense (positive) strand of the genome and are under the control of regulatory 
      elements within the 5' long terminal repeat (LTR). A number of retroviral genomes 
      also encode genes in the antisense (negative) strand and their expression is 
      under the control of negative sense promoters within the 3' LTR. In the case of 
      the Human T-cell Lymphotropic Virus 1 (HTLV-1), the antisense protein HBZ has 
      been shown to play a critical role in the virus lifecycle and in the pathogenic 
      process, while the function of the Human Immunodeficiency Virus 1 (HIV-1) 
      antisense protein ASP remains unknown. However, the expression of 3' LTR-driven 
      antisense transcripts is not always demonstrably associated with the presence of 
      an antisense open reading frame encoding a viral protein. Moreover, even in the 
      case of retroviruses that do express an antisense protein, such as HTLV-1 and the 
      pandemic strains of HIV-1, the 3' LTR-driven antisense transcript shows both 
      protein-coding and noncoding activities. Indeed, the ability to express antisense 
      transcripts appears to be phylogenetically more widespread among endogenous and 
      exogenous retroviruses than the presence of a functional antisense open reading 
      frame within these transcripts. This suggests that retroviral antisense 
      transcripts may have originated as noncoding molecules with regulatory activity 
      that in some cases later acquired protein-coding function. Here, we will review 
      examples of endogenous and exogenous retroviral antisense transcripts, and the 
      ways through which they benefit viral persistence in the host.
CI  - (c) 2023. The Author(s).
FAU - Romerio, Fabio
AU  - Romerio F
AD  - Department of Molecular and Comparative Pathobiology, Johns Hopkins University 
      School of Medicine, Baltimore, MD, USA. fromeri2@jhmi.edu.
LA  - eng
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20230516
PL  - England
TA  - Retrovirology
JT  - Retrovirology
JID - 101216893
RN  - 0 (Viral Proteins)
SB  - IM
MH  - Humans
MH  - *Human T-lymphotropic virus 1/genetics
MH  - Deltaretrovirus/genetics
MH  - Viral Proteins/genetics
MH  - Promoter Regions, Genetic
MH  - *HIV-1/genetics
PMC - PMC10186651
COIS- The author declares that he has no competing interests
EDAT- 2023/05/17 01:07
MHDA- 2023/05/18 06:42
PMCR- 2023/05/16
CRDT- 2023/05/16 23:35
PHST- 2023/01/31 00:00 [received]
PHST- 2023/04/30 00:00 [accepted]
PHST- 2023/05/18 06:42 [medline]
PHST- 2023/05/17 01:07 [pubmed]
PHST- 2023/05/16 23:35 [entrez]
PHST- 2023/05/16 00:00 [pmc-release]
AID - 10.1186/s12977-023-00622-x [pii]
AID - 622 [pii]
AID - 10.1186/s12977-023-00622-x [doi]
PST - epublish
SO  - Retrovirology. 2023 May 16;20(1):6. doi: 10.1186/s12977-023-00622-x.