Journal article
The Cellular Autophagy Pathway Modulates Human T-Cell Leukemia Virus Type 1 Replication
Journal of virology, v 87(3), pp 1699-1707
01 Feb 2013
PMID: 23175371
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
Autophagy, a general homeostatic process for degradation of cytosolic proteins or organelles, has been reported to modulate the replication of many viruses. The role of autophagy in human T-cell leukemia virus type 1 (HTLV-1) replication has, however, been uncharacterized. Here, we report that HTLV-1 infection increases the accumulation of autophagosomes and that this accumulation increases HTLV-1 production. We found that the HTLV-1 Tax protein increases cellular autophagosome accumulation by acting to block the fusion of autophagosomes to lysosomes, preventing the degradation of the former by the latter. Interestingly, the inhibition of cellular autophagosome-lysosome fusion using bafilomycin A increased the stability of the Tax protein, suggesting that cellular degradation of Tax occurs in part through autophagy. Our current findings indicate that by interrupting the cell's autophagic process, Tax exerts a positive feedback on its own stability.
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Details
- Title
- The Cellular Autophagy Pathway Modulates Human T-Cell Leukemia Virus Type 1 Replication
- Creators
- Sai-Wen Tang - National Institute of Allergy and Infectious DiseasesChia-Yen Chen - NIAID, Mol Virol Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USAZachary Klase - National Institute of Allergy and Infectious DiseasesLinda Zane - National Institute of Allergy and Infectious DiseasesKuan-Teh Jeang - NIAID, Mol Virol Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA
- Publication Details
- Journal of virology, v 87(3), pp 1699-1707
- Publisher
- Amer Soc Microbiology
- Number of pages
- 9
- Grant note
- NIAID; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Allergy & Infectious Diseases (NIAID) ZIAAI001023 / NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Allergy & Infectious Diseases (NIAID)
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Pharmacology and Physiology
- Web of Science ID
- WOS:000313558100036
- Scopus ID
- 2-s2.0-84873038774
- Other Identifier
- 991021902597704721
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- Web of Science research areas
- Virology