HIV-1 RNAs whose transcription initiates from the third deoxyguanosine of GGG tract in the 5′ long terminal repeat serve as a dominant genome for efficient provirus DNA formation

Since the promoter for transcribing HIV-1 RNA is unique, all viral elements including genomic RNA and viral proteins have to be generated by the unique transcripts through ingenious mechanisms including RNA splicing and frameshifting during protein translation. Previous studies suggested a new mecha...

Full description

Saved in:
Bibliographic Details
Published inJournal of virology Vol. 98; no. 2; p. e0182523
Main Authors Yoshida, Takeshi, Kasuya, Yuho, Yamamoto, Hiroyuki, Kawai, Gota, Hanaki, Ken-ichi, Matano, Tetsuro, Masuda, Takao
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 20.02.2024
Subjects
Online AccessGet full text

Cover

Loading…
Abstract Since the promoter for transcribing HIV-1 RNA is unique, all viral elements including genomic RNA and viral proteins have to be generated by the unique transcripts through ingenious mechanisms including RNA splicing and frameshifting during protein translation. Previous studies suggested a new mechanism for diversification of HIV-1 RNA functions by heterogeneous transcriptional initiation site usage; HIV-1 RNAs whose transcription initiates from a certain nucleotide were predominant in virus particles. In this study, we established two methods to analyze heterogenous transcriptional initiation site usage by HIV-1 during viral infection and showed that RNAs beginning with one guanosine (G1-form RNAs), whose transcription initiates from the third deoxyguanosine of the GGG tract in 5′ LTR, were primarily selected as viral genome in infectious particles and thus are used as a template to generate provirus for continuous replication. This study provides insights into the mechanism for diversification of unspliced RNA functions and requisites of lentivirus infectivity.
AbstractList Since the promoter for transcribing HIV-1 RNA is unique, all viral elements including genomic RNA and viral proteins have to be generated by the unique transcripts through ingenious mechanisms including RNA splicing and frameshifting during protein translation. Previous studies suggested a new mechanism for diversification of HIV-1 RNA functions by heterogeneous transcriptional initiation site usage; HIV-1 RNAs whose transcription initiates from a certain nucleotide were predominant in virus particles. In this study, we established two methods to analyze heterogenous transcriptional initiation site usage by HIV-1 during viral infection and showed that RNAs beginning with one guanosine (G1-form RNAs), whose transcription initiates from the third deoxyguanosine of the GGG tract in 5′ LTR, were primarily selected as viral genome in infectious particles and thus are used as a template to generate provirus for continuous replication. This study provides insights into the mechanism for diversification of unspliced RNA functions and requisites of lentivirus infectivity.
Unspliced HIV-1 RNAs function as messenger RNAs for Gag or Gag-Pol polyproteins and progeny genomes packaged into virus particles. Recently, it has been reported that fate of the RNAs might be primarily determined, depending on transcriptional initiation sites among three consecutive deoxyguanosine residues (GGG tract) downstream of TATA-box in the 5' long terminal repeat (LTR). Although HIV-1 RNA transcription starts mostly from the first deoxyguanosine of the GGG tract and often from the second or third deoxyguanosine, RNAs beginning with one guanosine (G1-form RNAs), whose transcription initiates from the third deoxyguanosine, were predominant in HIV-1 particles. Despite selective packaging of G1-form RNAs into virus particles, its biological impact during viral replication remains to be determined. In this study, we revealed that G1-form RNAs are primarily selected as a template for provirus DNA rather than other RNAs. In competitions between HIV-1 and lentiviral vector transcripts in virus-producing cells, approximately 80% of infectious particles were found to generate provirus using HIV-1 transcripts, while lentiviral vector transcripts were conversely selected when we used HIV-1 mutants in which the third deoxyguanosine in the GGG tract was replaced with deoxythymidine or deoxycytidine (GGT or GGC mutants, respectively). In the other analyses of proviral sequences after infection with an HIV-1 mutant in which the GGG tract in 3' LTR was replaced with TTT, most proviral sequences of the GGG-tract region in 5' LTR were found to be TTG, which is reasonably generated using the G1-form transcripts. Our results indicate that the G1-form RNAs serve as a dominant genome to establish provirus DNA.IMPORTANCESince the promoter for transcribing HIV-1 RNA is unique, all viral elements including genomic RNA and viral proteins have to be generated by the unique transcripts through ingenious mechanisms including RNA splicing and frameshifting during protein translation. Previous studies suggested a new mechanism for diversification of HIV-1 RNA functions by heterogeneous transcriptional initiation site usage; HIV-1 RNAs whose transcription initiates from a certain nucleotide were predominant in virus particles. In this study, we established two methods to analyze heterogenous transcriptional initiation site usage by HIV-1 during viral infection and showed that RNAs beginning with one guanosine (G1-form RNAs), whose transcription initiates from the third deoxyguanosine of the GGG tract in 5' LTR, were primarily selected as viral genome in infectious particles and thus are used as a template to generate provirus for continuous replication. This study provides insights into the mechanism for diversification of unspliced RNA functions and requisites of lentivirus infectivity.Unspliced HIV-1 RNAs function as messenger RNAs for Gag or Gag-Pol polyproteins and progeny genomes packaged into virus particles. Recently, it has been reported that fate of the RNAs might be primarily determined, depending on transcriptional initiation sites among three consecutive deoxyguanosine residues (GGG tract) downstream of TATA-box in the 5' long terminal repeat (LTR). Although HIV-1 RNA transcription starts mostly from the first deoxyguanosine of the GGG tract and often from the second or third deoxyguanosine, RNAs beginning with one guanosine (G1-form RNAs), whose transcription initiates from the third deoxyguanosine, were predominant in HIV-1 particles. Despite selective packaging of G1-form RNAs into virus particles, its biological impact during viral replication remains to be determined. In this study, we revealed that G1-form RNAs are primarily selected as a template for provirus DNA rather than other RNAs. In competitions between HIV-1 and lentiviral vector transcripts in virus-producing cells, approximately 80% of infectious particles were found to generate provirus using HIV-1 transcripts, while lentiviral vector transcripts were conversely selected when we used HIV-1 mutants in which the third deoxyguanosine in the GGG tract was replaced with deoxythymidine or deoxycytidine (GGT or GGC mutants, respectively). In the other analyses of proviral sequences after infection with an HIV-1 mutant in which the GGG tract in 3' LTR was replaced with TTT, most proviral sequences of the GGG-tract region in 5' LTR were found to be TTG, which is reasonably generated using the G1-form transcripts. Our results indicate that the G1-form RNAs serve as a dominant genome to establish provirus DNA.IMPORTANCESince the promoter for transcribing HIV-1 RNA is unique, all viral elements including genomic RNA and viral proteins have to be generated by the unique transcripts through ingenious mechanisms including RNA splicing and frameshifting during protein translation. Previous studies suggested a new mechanism for diversification of HIV-1 RNA functions by heterogeneous transcriptional initiation site usage; HIV-1 RNAs whose transcription initiates from a certain nucleotide were predominant in virus particles. In this study, we established two methods to analyze heterogenous transcriptional initiation site usage by HIV-1 during viral infection and showed that RNAs beginning with one guanosine (G1-form RNAs), whose transcription initiates from the third deoxyguanosine of the GGG tract in 5' LTR, were primarily selected as viral genome in infectious particles and thus are used as a template to generate provirus for continuous replication. This study provides insights into the mechanism for diversification of unspliced RNA functions and requisites of lentivirus infectivity.
Unspliced HIV-1 RNAs function as messenger RNAs for Gag or Gag-Pol polyproteins and progeny genomes packaged into virus particles. Recently, it has been reported that fate of the RNAs might be primarily determined, depending on transcriptional initiation sites among three consecutive deoxyguanosine residues (GGG tract) downstream of TATA-box in the 5′ long terminal repeat (LTR). Although HIV-1 RNA transcription starts mostly from the first deoxyguanosine of the GGG tract and often from the second or third deoxyguanosine, RNAs beginning with one guanosine (G1-form RNAs), whose transcription initiates from the third deoxyguanosine, were predominant in HIV-1 particles. Despite selective packaging of G1-form RNAs into virus particles, its biological impact during viral replication remains to be determined. In this study, we revealed that G1-form RNAs are primarily selected as a template for provirus DNA rather than other RNAs. In competitions between HIV-1 and lentiviral vector transcripts in virus-producing cells, approximately 80% of infectious particles were found to generate provirus using HIV-1 transcripts, while lentiviral vector transcripts were conversely selected when we used HIV-1 mutants in which the third deoxyguanosine in the GGG tract was replaced with deoxythymidine or deoxycytidine (GGT or GGC mutants, respectively). In the other analyses of proviral sequences after infection with an HIV-1 mutant in which the GGG tract in 3′ LTR was replaced with TTT, most proviral sequences of the GGG-tract region in 5′ LTR were found to be TTG, which is reasonably generated using the G1-form transcripts. Our results indicate that the G1-form RNAs serve as a dominant genome to establish provirus DNA.
Unspliced HIV-1 RNAs function as messenger RNAs for Gag or Gag-Pol polyproteins and progeny genomes packaged into virus particles. Recently, it has been reported that fate of the RNAs might be primarily determined, depending on transcriptional initiation sites among three consecutive deoxyguanosine residues (GGG tract) downstream of TATA-box in the 5′ long terminal repeat (LTR). Although HIV-1 RNA transcription starts mostly from the first deoxyguanosine of the GGG tract and often from the second or third deoxyguanosine, RNAs beginning with one guanosine (G1-form RNAs), whose transcription initiates from the third deoxyguanosine, were predominant in HIV-1 particles. Despite selective packaging of G1-form RNAs into virus particles, its biological impact during viral replication remains to be determined. In this study, we revealed that G1-form RNAs are primarily selected as a template for provirus DNA rather than other RNAs. In competitions between HIV-1 and lentiviral vector transcripts in virus-producing cells, approximately 80% of infectious particles were found to generate provirus using HIV-1 transcripts, while lentiviral vector transcripts were conversely selected when we used HIV-1 mutants in which the third deoxyguanosine in the GGG tract was replaced with deoxythymidine or deoxycytidine (GGT or GGC mutants, respectively). In the other analyses of proviral sequences after infection with an HIV-1 mutant in which the GGG tract in 3′ LTR was replaced with TTT, most proviral sequences of the GGG-tract region in 5′ LTR were found to be TTG, which is reasonably generated using the G1-form transcripts. Our results indicate that the G1-form RNAs serve as a dominant genome to establish provirus DNA.IMPORTANCESince the promoter for transcribing HIV-1 RNA is unique, all viral elements including genomic RNA and viral proteins have to be generated by the unique transcripts through ingenious mechanisms including RNA splicing and frameshifting during protein translation. Previous studies suggested a new mechanism for diversification of HIV-1 RNA functions by heterogeneous transcriptional initiation site usage; HIV-1 RNAs whose transcription initiates from a certain nucleotide were predominant in virus particles. In this study, we established two methods to analyze heterogenous transcriptional initiation site usage by HIV-1 during viral infection and showed that RNAs beginning with one guanosine (G1-form RNAs), whose transcription initiates from the third deoxyguanosine of the GGG tract in 5′ LTR, were primarily selected as viral genome in infectious particles and thus are used as a template to generate provirus for continuous replication. This study provides insights into the mechanism for diversification of unspliced RNA functions and requisites of lentivirus infectivity.
Author Kasuya, Yuho
Hanaki, Ken-ichi
Matano, Tetsuro
Yoshida, Takeshi
Masuda, Takao
Kawai, Gota
Yamamoto, Hiroyuki
Author_xml – sequence: 1
  givenname: Takeshi
  orcidid: 0000-0003-2650-7435
  surname: Yoshida
  fullname: Yoshida, Takeshi
  organization: Management Department of Biosafety, Laboratory Animal, and Pathogen Bank, National Institute of Infectious Diseases, Tokyo, Japan, AIDS Research Center, National Institute of Infectious Diseases, Tokyo, Japan
– sequence: 2
  givenname: Yuho
  surname: Kasuya
  fullname: Kasuya, Yuho
  organization: AIDS Research Center, National Institute of Infectious Diseases, Tokyo, Japan, Department of Molecular Virology, Tokyo Medical and Dental University (TMDU), Tokyo, Japan
– sequence: 3
  givenname: Hiroyuki
  surname: Yamamoto
  fullname: Yamamoto, Hiroyuki
  organization: AIDS Research Center, National Institute of Infectious Diseases, Tokyo, Japan, Department of Biomedicine, University Hospital Basel, Basel, Switzerland
– sequence: 4
  givenname: Gota
  surname: Kawai
  fullname: Kawai, Gota
  organization: Department of Life Science, Faculty of Advanced Engineering, Chiba Institute of Technology, Chiba, Japan
– sequence: 5
  givenname: Ken-ichi
  surname: Hanaki
  fullname: Hanaki, Ken-ichi
  organization: Management Department of Biosafety, Laboratory Animal, and Pathogen Bank, National Institute of Infectious Diseases, Tokyo, Japan
– sequence: 6
  givenname: Tetsuro
  surname: Matano
  fullname: Matano, Tetsuro
  organization: AIDS Research Center, National Institute of Infectious Diseases, Tokyo, Japan, Institute of Medical Science, The University of Tokyo, Tokyo, Japan, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan
– sequence: 7
  givenname: Takao
  surname: Masuda
  fullname: Masuda, Takao
  organization: Department of Life Science, Faculty of Advanced Engineering, Chiba Institute of Technology, Chiba, Japan, Graduate school of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan
BackLink https://www.ncbi.nlm.nih.gov/pubmed/38289105$$D View this record in MEDLINE/PubMed
BookMark eNp1kc1u1DAURiNURKeFHWvkJUhN8U-cOCs0KmVaqSoSAsTOcpLrGY8Se2o7A93xTIgn4klwZloECFaWfM89-nS_o-zAOgtZ9pTgU0KoeLnemlNMBOU5ZQ-yGcG1yDknxUE2w5jSnDPx6TA7CmGNMSmKsniUHTJBRU0wn2XfLy4_5gS9u54H9HnlAqDolQ2tN5tonEXGmmhUhIC0dwOKqwSsjO9QB-7L7XJU1gVjATmNFovFtNzGtLQD-Y-v31Dv7BJF8IOxqkceNqAiCuC3gFRACnVumtiIlmDdAEg7j0Br0xpInxvvtsaPAb2-nk-jQU2pHmcPteoDPLl7j7MPb87fn13kV28Xl2fzq1wVgsecVS3mTaWhFFjVmje66HhZUcbKhhVMNyXveKEbzDDjtBRKVzWvCwodgaZrS3acvdp7N2MzQNemRF71cuPNoPytdMrIPyfWrOTSbSXBohK4ZMnw_M7g3c0IIcrBhBb6XllwY5C0pqm7sqhIQl_sURUGKtdu9OlgIankVLNMNctdzZJO2me_B_uV6L7XBNA90HoXggctWxN3t0s5Tf8_68lfS_fef-I_AWphyPs
CitedBy_id crossref_primary_10_1016_j_sbi_2024_102896
crossref_primary_10_1128_jvi_02139_24
crossref_primary_10_1073_pnas_2407400121
crossref_primary_10_1128_mbio_03576_24
Cites_doi 10.1073/pnas.2112475118
10.1111/j.1600-0854.2007.00700.x
10.1073/pnas.86.21.8343
10.1126/science.1210460
10.1016/j.jmb.2011.04.029
10.1038/s41598-021-90427-9
10.1186/1742-4690-1-23
10.1038/srep17680
10.1073/pnas.0906822106
10.1128/spectrum.01053-22
10.1016/j.tim.2019.04.003
10.1073/pnas.1616627113
10.3390/v14051113
10.1016/S0021-9258(19)50101-6
10.1128/JVI.01527-21
10.1073/pnas.2114494118
10.1038/nrmicro903
10.1038/nrmicro3490
10.1016/j.virol.2014.01.019
10.1016/j.semcdb.2018.03.015
10.1126/science.aaz7959
10.1093/nar/22.2.137
10.1093/nar/gkac062
10.1128/JVI.01669-19
10.1002/bies.950070611
10.1146/annurev-virology-092917-043448
10.1038/nrmicro1210
ContentType Journal Article
Copyright Copyright © 2024 American Society for Microbiology.
Copyright © 2024 American Society for Microbiology. 2024 American Society for Microbiology.
Copyright_xml – notice: Copyright © 2024 American Society for Microbiology.
– notice: Copyright © 2024 American Society for Microbiology. 2024 American Society for Microbiology.
DBID AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
7X8
5PM
DOI 10.1128/jvi.01825-23
DatabaseName CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
MEDLINE - Academic
PubMed Central (Full Participant titles)
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
MEDLINE - Academic
DatabaseTitleList CrossRef
MEDLINE - Academic


MEDLINE
Database_xml – sequence: 1
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 2
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
DeliveryMethod fulltext_linktorsrc
Discipline Biology
EISSN 1098-5514
Editor Simon, Viviana
Editor_xml – sequence: 1
  givenname: Viviana
  surname: Simon
  fullname: Simon, Viviana
ExternalDocumentID PMC10878063
01825-23
38289105
10_1128_jvi_01825_23
Genre Research Support, Non-U.S. Gov't
Journal Article
GrantInformation_xml – fundername: Takeda Science Foundation (TSF)
  grantid: 1224
– fundername: Japan Agency for Medical Research and Development (AMED)
  grantid: 23fk0410041h9903
– fundername: ;
  grantid: 23fk0410041h9903
– fundername: ;
  grantid: 1224
GroupedDBID ---
-~X
0R~
18M
29L
2WC
39C
4.4
53G
5GY
5RE
5VS
85S
AAFWJ
AAGFI
AAYXX
ABPPZ
ACGFO
ACNCT
ADBBV
AENEX
AGVNZ
ALMA_UNASSIGNED_HOLDINGS
AOIJS
BAWUL
BTFSW
CITATION
CS3
DIK
E3Z
EBS
F5P
FRP
GX1
H13
HYE
HZ~
IH2
KQ8
N9A
O9-
OK1
P2P
RHI
RNS
RPM
RSF
TR2
UPT
W2D
W8F
WH7
WOQ
YQT
~02
~KM
CGR
CUY
CVF
ECM
EIF
NPM
RHF
UCJ
ZA5
7X8
5PM
ID FETCH-LOGICAL-a485t-37c05b7fe680a9f5bf4d5672336b343fb65d54fb03035268af795942ed1ebdc63
ISSN 0022-538X
1098-5514
IngestDate Thu Aug 21 18:33:59 EDT 2025
Fri Jul 11 01:17:52 EDT 2025
Tue May 21 18:31:39 EDT 2024
Thu Jun 12 01:52:47 EDT 2025
Thu Apr 24 22:56:15 EDT 2025
Tue Jul 01 01:32:44 EDT 2025
IsDoiOpenAccess false
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 2
Keywords HIV-1
genome
RNA
transcriptional initiation site
LTR
diversification
infectivity
Language English
License All Rights Reserved. https://doi.org/10.1128/ASMCopyrightv2
All Rights Reserved.
LinkModel OpenURL
MergedId FETCHMERGED-LOGICAL-a485t-37c05b7fe680a9f5bf4d5672336b343fb65d54fb03035268af795942ed1ebdc63
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
The authors declare no conflict of interest.
ORCID 0000-0003-2650-7435
OpenAccessLink https://www.ncbi.nlm.nih.gov/pmc/articles/10878063
PMID 38289105
PQID 2920186471
PQPubID 23479
PageCount 17
ParticipantIDs pubmedcentral_primary_oai_pubmedcentral_nih_gov_10878063
proquest_miscellaneous_2920186471
asm2_journals_10_1128_jvi_01825_23
pubmed_primary_38289105
crossref_citationtrail_10_1128_jvi_01825_23
crossref_primary_10_1128_jvi_01825_23
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate 2024-02-20
PublicationDateYYYYMMDD 2024-02-20
PublicationDate_xml – month: 02
  year: 2024
  text: 2024-02-20
  day: 20
PublicationDecade 2020
PublicationPlace United States
PublicationPlace_xml – name: United States
– name: 1752 N St., N.W., Washington, DC
PublicationTitle Journal of virology
PublicationTitleAbbrev J Virol
PublicationTitleAlternate J Virol
PublicationYear 2024
Publisher American Society for Microbiology
Publisher_xml – name: American Society for Microbiology
References e_1_3_2_26_2
e_1_3_2_27_2
e_1_3_2_28_2
e_1_3_2_20_2
e_1_3_2_21_2
e_1_3_2_22_2
e_1_3_2_23_2
e_1_3_2_24_2
e_1_3_2_25_2
e_1_3_2_9_2
e_1_3_2_15_2
e_1_3_2_8_2
e_1_3_2_16_2
e_1_3_2_7_2
e_1_3_2_17_2
e_1_3_2_6_2
e_1_3_2_18_2
e_1_3_2_19_2
e_1_3_2_10_2
e_1_3_2_5_2
e_1_3_2_11_2
e_1_3_2_4_2
e_1_3_2_12_2
e_1_3_2_3_2
e_1_3_2_13_2
e_1_3_2_2_2
e_1_3_2_14_2
Chen, J, Nikolaitchik, O, Singh, J, Wright, A, Bencsics, CE, Coffin, JM, Ni, N, Lockett, S, Pathak, VK, Hu, WS (B7) 2009; 106
Olson, ED, Musier-Forsyth, K (B3) 2019; 86
Lu, K, Heng, X, Summers, MF (B8) 2011; 410
Yoshida, T, Kawano, Y, Sato, K, Ando, Y, Aoki, J, Miura, Y, Komano, J, Tanaka, Y, Koyanagi, Y (B26) 2008; 9
Perrino, FW, Preston, BD, Sandell, LL, Loeb, LA (B24) 1989; 86
Kuzembayeva, M, Dilley, K, Sardo, L, Hu, W-S (B6) 2014; 454–455
Rawson, JMO, Nikolaitchik, OA, Shakya, S, Keele, BF, Pathak, VK, Hu, WS (B25) 2022; 10
D’Souza, V, Summers, MF (B9) 2005; 3
Lu, K, Heng, X, Garyu, L, Monti, S, Garcia, EL, Kharytonchyk, S, Dorjsuren, B, Kulandaivel, G, Jones, S, Hiremath, A, Divakaruni, SS, LaCotti, C, Barton, S, Tummillo, D, Hosic, A, Edme, K, Albrecht, S, Telesnitsky, A, Summers, MF (B10) 2011; 334
Brown, JD, Kharytonchyk, S, Chaudry, I, Iyer, AS, Carter, H, Becker, G, Desai, Y, Glang, L, Choi, SH, Singh, K, Lopresti, MW, Orellana, M, Rodriguez, T, Oboh, U, Hijji, J, Ghinger, FG, Stewart, K, Francis, D, Edwards, B, Chen, P, Case, DA, Telesnitsky, A, Summers, MF (B16) 2020; 368
Ding, P, Kharytonchyk, S, Kuo, N, Cannistraci, E, Flores, H, Chaudhary, R, Sarkar, M, Dong, X, Telesnitsky, A, Summers, MF (B17) 2021; 118
Yao, W, Yoshida, T, Hashimoto, S, Takeuchi, H, Strebel, K, Yamaoka, S (B19) 2020; 94
Yao, W, Strebel, K, Yamaoka, S, Yoshida, T (B21) 2022; 96
Bieniasz, P, Telesnitsky, A (B2) 2018; 5
Klaver, B, Berkhout, B (B22) 1994; 22
Obayashi, CM, Shinohara, Y, Masuda, T, Kawai, G (B18) 2021; 11
Freed, EO (B1) 2015; 13
Nikolaitchik, OA, Liu, S, Kitzrow, JP, Liu, Y, Rawson, JMO, Shakya, S, Cheng, Z, Pathak, VK, Hu, WS, Musier-Forsyth, K (B27) 2021; 118
Pereira-Montecinos, C, Toro-Ascuy, D, Ananías-Sáez, C, Gaete-Argel, A, Rojas-Fuentes, C, Riquelme-Barrios, S, Rojas-Araya, B, García-de-Gracia, F, Aguilera-Cortés, P, Chnaiderman, J, Acevedo, ML, Valiente-Echeverría, F, Soto-Rifo, R (B12) 2022; 50
Russell, RS, Liang, C, Wainberg, MA (B11) 2004; 1
Shatkin, AJ (B20) 1987; 7
Paillart, JC, Shehu-Xhilaga, M, Marquet, R, Mak, J (B13) 2004; 2
Rein, A (B5) 2019; 27
Yu, H, Goodman, MF (B23) 1992; 267
Masuda, T, Sato, Y, Huang, Y-L, Koi, S, Takahata, T, Hasegawa, A, Kawai, G, Kannagi, M (B14) 2015; 5
Beemon, KL (B4) 2022; 14
Kharytonchyk, S, Monti, S, Smaldino, PJ, Van, V, Bolden, NC, Brown, JD, Russo, E, Swanson, C, Shuey, A, Telesnitsky, A, Summers, MF (B15) 2016; 113
References_xml – ident: e_1_3_2_18_2
  doi: 10.1073/pnas.2112475118
– ident: e_1_3_2_27_2
  doi: 10.1111/j.1600-0854.2007.00700.x
– ident: e_1_3_2_25_2
  doi: 10.1073/pnas.86.21.8343
– ident: e_1_3_2_11_2
  doi: 10.1126/science.1210460
– ident: e_1_3_2_9_2
  doi: 10.1016/j.jmb.2011.04.029
– ident: e_1_3_2_19_2
  doi: 10.1038/s41598-021-90427-9
– ident: e_1_3_2_12_2
  doi: 10.1186/1742-4690-1-23
– ident: e_1_3_2_15_2
  doi: 10.1038/srep17680
– ident: e_1_3_2_8_2
  doi: 10.1073/pnas.0906822106
– ident: e_1_3_2_26_2
  doi: 10.1128/spectrum.01053-22
– ident: e_1_3_2_6_2
  doi: 10.1016/j.tim.2019.04.003
– ident: e_1_3_2_16_2
  doi: 10.1073/pnas.1616627113
– ident: e_1_3_2_5_2
  doi: 10.3390/v14051113
– ident: e_1_3_2_24_2
  doi: 10.1016/S0021-9258(19)50101-6
– ident: e_1_3_2_22_2
  doi: 10.1128/JVI.01527-21
– ident: e_1_3_2_28_2
  doi: 10.1073/pnas.2114494118
– ident: e_1_3_2_14_2
  doi: 10.1038/nrmicro903
– ident: e_1_3_2_2_2
  doi: 10.1038/nrmicro3490
– ident: e_1_3_2_7_2
  doi: 10.1016/j.virol.2014.01.019
– ident: e_1_3_2_4_2
  doi: 10.1016/j.semcdb.2018.03.015
– ident: e_1_3_2_17_2
  doi: 10.1126/science.aaz7959
– ident: e_1_3_2_23_2
  doi: 10.1093/nar/22.2.137
– ident: e_1_3_2_13_2
  doi: 10.1093/nar/gkac062
– ident: e_1_3_2_20_2
  doi: 10.1128/JVI.01669-19
– ident: e_1_3_2_21_2
  doi: 10.1002/bies.950070611
– ident: e_1_3_2_3_2
  doi: 10.1146/annurev-virology-092917-043448
– ident: e_1_3_2_10_2
  doi: 10.1038/nrmicro1210
– volume: 5
  year: 2015
  ident: B14
  article-title: Fate of HIV-1 cDNA intermediates during reverse transcription is dictated by transcription initiation site of virus genomic RNA
  publication-title: Sci Rep
  doi: 10.1038/srep17680
– volume: 7
  start-page: 275
  year: 1987
  end-page: 277
  ident: B20
  article-title: mRNA caps – old and newer hats
  publication-title: Bioessays
  doi: 10.1002/bies.950070611
– volume: 96
  year: 2022
  ident: B21
  article-title: Simian immunodeficiency virus SIVgsn-99CM71 Vpu employs different amino acids to antagonize human and greater spot-nosed monkey BST-2
  publication-title: J Virol
  doi: 10.1128/JVI.01527-21
– volume: 2
  start-page: 461
  year: 2004
  end-page: 472
  ident: B13
  article-title: Dimerization of retroviral RNA genomes: an inseparable pair
  publication-title: Nat Rev Microbiol
  doi: 10.1038/nrmicro903
– volume: 1
  year: 2004
  ident: B11
  article-title: Is HIV-1 RNA dimerization a prerequisite for packaging? yes, no, probably?
  publication-title: Retrovirology
  doi: 10.1186/1742-4690-1-23
– volume: 113
  start-page: 13378
  year: 2016
  end-page: 13383
  ident: B15
  article-title: Transcriptional start site heterogeneity modulates the structure and function of the HIV-1 genome
  publication-title: Proc Natl Acad Sci U S A
  doi: 10.1073/pnas.1616627113
– volume: 11
  year: 2021
  ident: B18
  article-title: Influence of the 5′-terminal sequences on the 5′-UTR structure of HIV-1 genomic RNA
  publication-title: Sci Rep
  doi: 10.1038/s41598-021-90427-9
– volume: 86
  start-page: 129
  year: 2019
  end-page: 139
  ident: B3
  article-title: Retroviral Gag protein-RNA interactions: implications for specific genomic RNA packaging and virion assembly
  publication-title: Semin Cell Dev Biol
  doi: 10.1016/j.semcdb.2018.03.015
– volume: 334
  start-page: 242
  year: 2011
  end-page: 245
  ident: B10
  article-title: NMR detection of structures in the HIV-1 5′-leader RNA that regulate genome packaging
  publication-title: Science
  doi: 10.1126/science.1210460
– volume: 22
  start-page: 137
  year: 1994
  end-page: 144
  ident: B22
  article-title: Premature strand transfer by the HIV-1 reverse transcriptase during strong-stop DNA synthesis
  publication-title: Nucleic Acids Res
  doi: 10.1093/nar/22.2.137
– volume: 10
  year: 2022
  ident: B25
  article-title: Transcription start site heterogeneity and preferential packaging of specific full-length RNA species are conserved features of primate lentiviruses
  publication-title: Microbiol Spectr
  doi: 10.1128/spectrum.01053-22
– volume: 454–455
  start-page: 362
  year: 2014
  end-page: 370
  ident: B6
  article-title: Life of psi: how full-length HIV-1 RNAs become packaged genomes in the viral particles
  publication-title: Virology
  doi: 10.1016/j.virol.2014.01.019
– volume: 3
  start-page: 643
  year: 2005
  end-page: 655
  ident: B9
  article-title: How retroviruses select their genomes
  publication-title: Nat Rev Microbiol
  doi: 10.1038/nrmicro1210
– volume: 106
  start-page: 13535
  year: 2009
  end-page: 13540
  ident: B7
  article-title: High efficiency of HIV-1 genomic RNA packaging and heterozygote formation revealed by single virion analysis
  publication-title: Proc Natl Acad Sci U S A
  doi: 10.1073/pnas.0906822106
– volume: 410
  start-page: 609
  year: 2011
  end-page: 633
  ident: B8
  article-title: Structural determinants and mechanism of HIV-1 genome packaging
  publication-title: J Mol Biol
  doi: 10.1016/j.jmb.2011.04.029
– volume: 118
  year: 2021
  ident: B17
  article-title: 5′-cap sequestration is an essential determinant of HIV-1 genome packaging
  publication-title: Proc Natl Acad Sci U S A
  doi: 10.1073/pnas.2112475118
– volume: 86
  start-page: 8343
  year: 1989
  end-page: 8347
  ident: B24
  article-title: Extension of mismatched 3′ termini of DNA is a major determinant of the infidelity of human immunodeficiency virus type 1 reverse transcriptase
  publication-title: Proc Natl Acad Sci U S A
  doi: 10.1073/pnas.86.21.8343
– volume: 118
  year: 2021
  ident: B27
  article-title: Selective packaging of HIV-1 RNA genome is guided by the stability of 5′ untranslated region polyA stem
  publication-title: Proc Natl Acad Sci U S A
  doi: 10.1073/pnas.2114494118
– volume: 14
  year: 2022
  ident: B4
  article-title: Retroviral RNA processing
  publication-title: Viruses
  doi: 10.3390/v14051113
– volume: 13
  start-page: 484
  year: 2015
  end-page: 496
  ident: B1
  article-title: HIV-1 assembly, release and maturation
  publication-title: Nat Rev Microbiol
  doi: 10.1038/nrmicro3490
– volume: 368
  start-page: 413
  year: 2020
  end-page: 417
  ident: B16
  article-title: Structural basis for transcriptional start site control of HIV-1 RNA fate
  publication-title: Science
  doi: 10.1126/science.aaz7959
– volume: 9
  start-page: 540
  year: 2008
  end-page: 558
  ident: B26
  article-title: A CD63 mutant inhibits T-cell tropic human immunodeficiency virus type 1 entry by disrupting CXCR4 trafficking to the plasma membrane
  publication-title: Traffic
  doi: 10.1111/j.1600-0854.2007.00700.x
– volume: 50
  start-page: 2302
  year: 2022
  end-page: 2318
  ident: B12
  article-title: Epitranscriptomic regulation of HIV-1 full-length RNA packaging
  publication-title: Nucleic Acids Res
  doi: 10.1093/nar/gkac062
– volume: 27
  start-page: 715
  year: 2019
  end-page: 723
  ident: B5
  article-title: RNA packaging in HIV
  publication-title: Trends Microbiol
  doi: 10.1016/j.tim.2019.04.003
– volume: 94
  year: 2020
  ident: B19
  article-title: Vpu of a simian immunodeficiency virus isolated from greater spot-nosed monkey antagonizes human BST-2 via two AxxxxxxxW motifs
  publication-title: J Virol
  doi: 10.1128/JVI.01669-19
– volume: 267
  start-page: 10888
  year: 1992
  end-page: 10896
  ident: B23
  article-title: Comparison of HIV-1 and avian myeloblastosis virus reverse transcriptase fidelity on RNA and DNA templates
  publication-title: J Biol Chem
  doi: 10.1016/S0021-9258(19)50101-6
– volume: 5
  start-page: 165
  year: 2018
  end-page: 183
  ident: B2
  article-title: Multiple, switchable protein:RNA interactions regulate human immunodeficiency virus type 1 assembly
  publication-title: Annu Rev Virol
  doi: 10.1146/annurev-virology-092917-043448
SSID ssj0014464
Score 2.4646254
Snippet Since the promoter for transcribing HIV-1 RNA is unique, all viral elements including genomic RNA and viral proteins have to be generated by the unique...
Unspliced HIV-1 RNAs function as messenger RNAs for Gag or Gag-Pol polyproteins and progeny genomes packaged into virus particles. Recently, it has been...
SourceID pubmedcentral
proquest
asm2
pubmed
crossref
SourceType Open Access Repository
Aggregation Database
Index Database
Enrichment Source
StartPage e0182523
SubjectTerms Deoxyguanosine - genetics
Genome and Regulation of Viral Gene Expression
Genome Replication and Regulation of Viral Gene Expression
Guanosine - genetics
HIV Long Terminal Repeat - genetics
HIV-1 - physiology
Proviruses - genetics
RNA, Viral - genetics
Terminal Repeat Sequences
Virology
Title HIV-1 RNAs whose transcription initiates from the third deoxyguanosine of GGG tract in the 5′ long terminal repeat serve as a dominant genome for efficient provirus DNA formation
URI https://www.ncbi.nlm.nih.gov/pubmed/38289105
https://journals.asm.org/doi/10.1128/jvi.01825-23
https://www.proquest.com/docview/2920186471
https://pubmed.ncbi.nlm.nih.gov/PMC10878063
Volume 98
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnZ1Lb9NAEIBXpQiJC-JNeGlAcLJcHNtrr4_llYDUHFCK2pO1ttfEtImr2qaEE78J8Sv4GfwSZtaPOKWVCpcosderJPN5d2Y8D8aeCT-N0dqJUHPjvkk7hhnEkpu-lfiO7SdRmlCC887EG--67_f43sbGr17UUlVGW_G3M_NK_keqeAzlSlmy_yDZblI8gO9RvviKEsbXC8l4_O6jOTQ-TLYL42RGgecl7TzdOpBRYBDpkqskknKWHSdGovKvy0-VXOQU9U764mg0oovjso175E0UxEvbOKR2RE3QDHUBOCKnAjlzFTWpkUaS1-E01I05nzdFxHVlCooz0D6L46owXk-2V6mS5-jElHTXd_Pv58UsS7R-O5UHCj90G4QsqqU-sV_N8m68nEtkT7t_xzjXsjroXXFSt94e5aXsOztsVyePWys826dY_ZDWnWxVsqq_1JOV7ei-xbjR1as7FU8lFbG__Aeih7l99q5iU6bE5y_ZloXmGDfrDOlTdbrbU5fYZRtNFqf1HDVPtNDsdtvK9fS12iQMW7zoT4yagSzm9rqW9JfpczqCt6cSTa-za43cYLsG8wbbUIub7Erd3XR5i_3UeALhCRpPWMMTOjyB8ASkDjSesI4n5CkgnqDxxIv0QP77-w8gMKEFE2owQYMJsgAJLZhQgwkoRujAhBZMQDChA_M22337ZvpqbDZNQkzpCl7iBhlbPPJT5QlLBimnwFPu4f_veJHjOmnk8YS7aYSbGbWCEDL1Ax64tkqGKkpiz7nDNhf5Qt1jEDt1-T-lZOBKmUqlhJMOg1T5cSCsZMCekmzCZgUoQm1A2yJEAYZagKHtDJjRSi6MmzL71O3l8JzRz7vRR3V5mXPGPWkhCHH9p4d6cqHyqgip29xQeKhjDtjdGopuJofcKWhADZhYw6UbQLXl188sspmuMT-0hC_QfLl_kd_8gF1d3awP2WZ5XKlHqKuX0WN9E_wBSarzEg
linkProvider National Library of Medicine
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=HIV-1+RNAs+whose+transcription+initiates+from+the+third+deoxyguanosine+of+GGG+tract+in+the+5%E2%80%B2+long+terminal+repeat+serve+as+a+dominant+genome+for+efficient+provirus+DNA+formation&rft.jtitle=Journal+of+virology&rft.au=Yoshida%2C+Takeshi&rft.au=Kasuya%2C+Yuho&rft.au=Yamamoto%2C+Hiroyuki&rft.au=Kawai%2C+Gota&rft.date=2024-02-20&rft.pub=American+Society+for+Microbiology&rft.issn=0022-538X&rft.eissn=1098-5514&rft.volume=98&rft.issue=2&rft_id=info:doi/10.1128%2Fjvi.01825-23&rft.externalDocID=01825-23
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0022-538X&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0022-538X&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0022-538X&client=summon