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Open AccessArticle

Amino Acid Deletions in p6Gag Domain of HIV-1 CRF07_BC Ameliorate Galectin-3 Mediated Enhancement in Viral Budding

1
Center for Tropical Medicine and Infectious Disease, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
2
Division of Infectious Disease, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
3
Department of Medical Laboratory Science and Biotechnology, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
4
Graduate Institute of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
5
Master Program in Clinical Pharmacogenomics and Pharmacoproteomics, College of Pharmacy, Taipei Medical University, Taipei 110, Taiwan
6
Institute of Biomedical Sciences, Academia Sinica 11529, Taiwan
7
Department of Medical Research, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2020, 21(8), 2910; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21082910
Received: 12 March 2020 / Revised: 13 April 2020 / Accepted: 19 April 2020 / Published: 21 April 2020
(This article belongs to the Special Issue Virus Replication)
HIV-1 CRF07_BC is a recombinant virus with amino acid (a.a.) deletions in p6Gag, which are overlapped with the Alix-binding domain. Galectin-3 (Gal3), a β-galactose binding lectin, has been reported to interact with Alix and regulate HIV-1 subtype B budding. This study aims to evaluate the role of Gal3 in HIV-1 CRF07_BC infection and the potential effect of a.a. deletions on Gal3-mediated regulation. A total of 38 HIV-1+ injecting drug users (IDUs) were enrolled in the study. Viral characterization and correlation of Gal3 were validated. CRF07_BC containing 7 a.a. deletions and wild-type in the p6Gag (CRF07_BC-7d and -wt) were isolated and infectious clones were generated. Viral growth kinetic and budding assays using Jurkat-CCR5/Jurkat-CCR5-Gal3 cells infected with CRF07_BC were performed. Results indicate that 69.4% (25/38) of the recruited patients were identified as CRF07_BC, and CRF07_BC-7d was predominant. Slow disease progression and significantly higher plasma Gal3 were noted in CRF07_BC patients (p < 0.01). Results revealed that CRF07_BC infection resulted in Gal3 expression, which was induced by Tat. Growth dynamic and budding assays indicated that Gal3 expression in Jurkat-CCR5 cells significantly enhanced CRF07_BC-wt replication and budding (p < 0.05), while the promoting effect was ameliorated in CRF07_BC-7d. Co-immunoprecipitation found that deletions in the p6Gag reduced Gal-3-mediated enhancement of the Alix–Gag interaction. View Full-Text
Keywords: Galectin-3; HIV-1; CRF07_BC; p6Gag; Alix Galectin-3; HIV-1; CRF07_BC; p6Gag; Alix
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MDPI and ACS Style

Wang, W.-H.; Yeh, C.-S.; Lin, C.-Y.; Yuan, R.-Y.; Urbina, A.N.; Lu, P.-L.; Chen, Y.-H.; Chen, Y.-M.A.; Liu, F.-T.; Wang, S.-F. Amino Acid Deletions in p6Gag Domain of HIV-1 CRF07_BC Ameliorate Galectin-3 Mediated Enhancement in Viral Budding. Int. J. Mol. Sci. 2020, 21, 2910. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21082910

AMA Style

Wang W-H, Yeh C-S, Lin C-Y, Yuan R-Y, Urbina AN, Lu P-L, Chen Y-H, Chen Y-MA, Liu F-T, Wang S-F. Amino Acid Deletions in p6Gag Domain of HIV-1 CRF07_BC Ameliorate Galectin-3 Mediated Enhancement in Viral Budding. International Journal of Molecular Sciences. 2020; 21(8):2910. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21082910

Chicago/Turabian Style

Wang, Wen-Hung; Yeh, Chun-Sheng; Lin, Chih-Yen; Yuan, Ruei-Yu; Urbina, Aspiro N.; Lu, Po-Liang; Chen, Yen-Hsu; Chen, Yi-Ming A.; Liu, Fu-Tong; Wang, Sheng-Fan. 2020. "Amino Acid Deletions in p6Gag Domain of HIV-1 CRF07_BC Ameliorate Galectin-3 Mediated Enhancement in Viral Budding" Int. J. Mol. Sci. 21, no. 8: 2910. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21082910

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