Amino Acid Deletions in p6Gag Domain of HIV-1 CRF07_BC Ameliorate Galectin-3 Mediated Enhancement in Viral Budding
| Autor: | Aspiro Nayim Urbina, Wen Hung Wang, Ruei Yu Yuan, Yen-Hsu Chen, Chun Sheng Yeh, Fu-Tong Liu, Chih Yen Lin, Po-Liang Lu, Sheng-Fan Wang, Yi Ming Arthur Chen |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Viral budding 030106 microbiology Human immunodeficiency virus (HIV) Biology medicine.disease_cause Recombinant virus Catalysis lcsh:Chemistry Inorganic Chemistry 03 medical and health sciences medicine Galectin-3 Physical and Theoretical Chemistry Slow disease progression lcsh:QH301-705.5 Molecular Biology Spectroscopy p6Gag chemistry.chemical_classification Budding Organic Chemistry Lectin General Medicine Molecular biology Computer Science Applications Amino acid Alix 030104 developmental biology lcsh:Biology (General) lcsh:QD1-999 chemistry HIV-1 biology.protein CRF07_BC |
| Zdroj: | International Journal of Molecular Sciences, Vol 21, Iss 2910, p 2910 (2020) International Journal of Molecular Sciences Volume 21 Issue 8 |
| ISSN: | 1422-0067 |
| DOI: | 10.3390/ijms21082910 |
| Popis: | 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 &beta 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&ndash Gag interaction. |
| Databáze: | OpenAIRE |
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