Myricetin antagonizes semen-derived enhancer of viral infection (SEVI) formation and influences its infection-enhancing activity
| العنوان: | Myricetin antagonizes semen-derived enhancer of viral infection (SEVI) formation and influences its infection-enhancing activity |
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| المؤلفون: | Jiayong Wen, Baolong Lai, Xuanxuan Zhang, Lingzhen Ma, Yin Shuwen, Fangyuan Lai, Ruxia Ren, Shuwen Liu, Lin Li |
| المصدر: | Retrovirology, Vol 15, Iss 1, Pp 1-24 (2018) Retrovirology |
| بيانات النشر: | Springer Science and Business Media LLC, 2018. |
| سنة النشر: | 2018 |
| مصطلحات موضوعية: | Male, Models, Molecular, lcsh:Immunologic diseases. Allergy, 0301 basic medicine, Amyloid, Sexual transmission, Anti-HIV Agents, Molecular Conformation, Virus Attachment, HIV Infections, Peptide, Cell Line, Protein Aggregates, 03 medical and health sciences, chemistry.chemical_compound, Semen, Virology, Microbicide, Humans, Enhancer, Amyloid fibrils, Flavonoids, chemistry.chemical_classification, Dose-Response Relationship, Drug, 030102 biochemistry & molecular biology, biology, Research, Myricetin, Virion, HIV, Drug Synergism, Synergistic antiviral effects, In vitro, 030104 developmental biology, Infectious Diseases, chemistry, Host-Pathogen Interactions, SEVI, HIV-1, biology.protein, Protein Multimerization, Antibody, lcsh:RC581-607, Protein Binding |
| الوصف: | Background Semen is a critical vector for human immunodeficiency virus (HIV) sexual transmission and harbors seminal amyloid fibrils that can markedly enhance HIV infection. Semen-derived enhancer of viral infection (SEVI) is one of the best-characterized seminal amyloid fibrils. Due to their highly cationic properties, SEVI fibrils can capture HIV virions, increase viral attachment to target cells, and augment viral fusion. Some studies have reported that myricetin antagonizes amyloid β-protein (Aβ) formation; myricetin also displays strong anti-HIV activity in vitro. Results Here, we report that myricetin inhibits the formation of SEVI fibrils by binding to the amyloidogenic region of the SEVI precursor peptide (PAP248–286) and disrupting PAP248–286 oligomerization. In addition, myricetin was found to remodel preformed SEVI fibrils and to influence the activity of SEVI in promoting HIV-1 infection. Moreover, myricetin showed synergistic effects against HIV-1 infection in combination with other antiretroviral drugs in semen. Conclusions Incorporation of myricetin into a combination bifunctional microbicide with both anti-SEVI and anti-HIV activities is a highly promising approach to preventing sexual transmission of HIV. Electronic supplementary material The online version of this article (10.1186/s12977-018-0432-3) contains supplementary material, which is available to authorized users. |
| تدمد: | 1742-4690 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fded1c4b11fd30268ce6511d196cfb16Test https://doi.org/10.1186/s12977-018-0432-3Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....fded1c4b11fd30268ce6511d196cfb16 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 17424690 |
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