Antiviral role of IFITM3 in prototype foamy virus infection
Abstract Background Foamy viruses (FVs) are retroviruses with unique replication strategies that cause lifelong latent infections in their hosts. FVs can also produce foam-like cytopathic effects in vitro. However, the effect of host cytokines on FV replication requires further investigation. Althou...
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BMC
2022-11-01
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Online Access: | https://doi.org/10.1186/s12985-022-01931-x |
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author | Zhaohuan Wang Xiaopeng Tuo Junshi Zhang Keli Chai Juan Tan Wentao Qiao |
author_facet | Zhaohuan Wang Xiaopeng Tuo Junshi Zhang Keli Chai Juan Tan Wentao Qiao |
author_sort | Zhaohuan Wang |
collection | DOAJ |
description | Abstract Background Foamy viruses (FVs) are retroviruses with unique replication strategies that cause lifelong latent infections in their hosts. FVs can also produce foam-like cytopathic effects in vitro. However, the effect of host cytokines on FV replication requires further investigation. Although interferon induced transmembrane (IFITMs) proteins have become the focus of antiviral immune response research due to their broad-spectrum antiviral ability, it remains unclear whether IFITMs can affect FV replication. Method In this study, the PFV virus titer was characterized by measuring luciferase activity after co-incubation of PFVL cell lines with the cell culture supernatants (cell-free PFV) or the cells transfected with pcPFV plasmid/infected with PFV (cell-associated PFV). The foam-like cytopathic effects of PFV infected cells was observed to reflect the virus replication. The total RNA of PFV infected cells was extracted, and the viral genome was quantified by Quantitative reverse transcription PCR to detect the PFV entry into target cells. Results In the present study, we demonstrated that IFITM1-3 overexpression inhibited prototype foamy virus (PFV) replication. In addition, an IFITM3 knockdown by small interfering RNA increased PFV replication. We further demonstrated that IFITM3 inhibited PFV entry into host cells. Moreover, IFITM3 also reduced the number of PFV envelope proteins, which was related to IFITM3 promoted envelope degradation through the lysosomal pathway. Conclusions Taken together, these results demonstrate that IFITM3 inhibits PFV replication by inhibiting PFV entry into target cells and reducing the number of PFV envelope. |
first_indexed | 2024-04-11T07:36:11Z |
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id | doaj.art-37c4761ec7a4480a89c20492b4da4036 |
institution | Directory Open Access Journal |
issn | 1743-422X |
language | English |
last_indexed | 2024-04-11T07:36:11Z |
publishDate | 2022-11-01 |
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series | Virology Journal |
spelling | doaj.art-37c4761ec7a4480a89c20492b4da40362022-12-22T04:36:43ZengBMCVirology Journal1743-422X2022-11-0119111010.1186/s12985-022-01931-xAntiviral role of IFITM3 in prototype foamy virus infectionZhaohuan Wang0Xiaopeng Tuo1Junshi Zhang2Keli Chai3Juan Tan4Wentao Qiao5Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, College of Life Sciences, Nankai UniversityKey Laboratory of Molecular Microbiology and Technology, Ministry of Education, College of Life Sciences, Nankai UniversityKey Laboratory of Molecular Microbiology and Technology, Ministry of Education, College of Life Sciences, Nankai UniversityKey Laboratory of Molecular Microbiology and Technology, Ministry of Education, College of Life Sciences, Nankai UniversityKey Laboratory of Molecular Microbiology and Technology, Ministry of Education, College of Life Sciences, Nankai UniversityKey Laboratory of Molecular Microbiology and Technology, Ministry of Education, College of Life Sciences, Nankai UniversityAbstract Background Foamy viruses (FVs) are retroviruses with unique replication strategies that cause lifelong latent infections in their hosts. FVs can also produce foam-like cytopathic effects in vitro. However, the effect of host cytokines on FV replication requires further investigation. Although interferon induced transmembrane (IFITMs) proteins have become the focus of antiviral immune response research due to their broad-spectrum antiviral ability, it remains unclear whether IFITMs can affect FV replication. Method In this study, the PFV virus titer was characterized by measuring luciferase activity after co-incubation of PFVL cell lines with the cell culture supernatants (cell-free PFV) or the cells transfected with pcPFV plasmid/infected with PFV (cell-associated PFV). The foam-like cytopathic effects of PFV infected cells was observed to reflect the virus replication. The total RNA of PFV infected cells was extracted, and the viral genome was quantified by Quantitative reverse transcription PCR to detect the PFV entry into target cells. Results In the present study, we demonstrated that IFITM1-3 overexpression inhibited prototype foamy virus (PFV) replication. In addition, an IFITM3 knockdown by small interfering RNA increased PFV replication. We further demonstrated that IFITM3 inhibited PFV entry into host cells. Moreover, IFITM3 also reduced the number of PFV envelope proteins, which was related to IFITM3 promoted envelope degradation through the lysosomal pathway. Conclusions Taken together, these results demonstrate that IFITM3 inhibits PFV replication by inhibiting PFV entry into target cells and reducing the number of PFV envelope.https://doi.org/10.1186/s12985-022-01931-xIFITM3Prototype foamy virusEntryEnvelope |
spellingShingle | Zhaohuan Wang Xiaopeng Tuo Junshi Zhang Keli Chai Juan Tan Wentao Qiao Antiviral role of IFITM3 in prototype foamy virus infection Virology Journal IFITM3 Prototype foamy virus Entry Envelope |
title | Antiviral role of IFITM3 in prototype foamy virus infection |
title_full | Antiviral role of IFITM3 in prototype foamy virus infection |
title_fullStr | Antiviral role of IFITM3 in prototype foamy virus infection |
title_full_unstemmed | Antiviral role of IFITM3 in prototype foamy virus infection |
title_short | Antiviral role of IFITM3 in prototype foamy virus infection |
title_sort | antiviral role of ifitm3 in prototype foamy virus infection |
topic | IFITM3 Prototype foamy virus Entry Envelope |
url | https://doi.org/10.1186/s12985-022-01931-x |
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