ArticleJournal of virology2012
Accumulation of autophagosomes in Semliki Forest virus-infected cells is dependent on expression of the viral glycoproteins.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Dynamic regulation of autophagy during Semliki Forest virus infection of neuroblastoma cells.The Journal of general virology · 2025Article
- Next generation self-replicating RNA vectors for vaccines and immunotherapies.Cancer gene therapy · 2023Review
- Review
- The impact of autophagy on arbovirus infection of mosquito cells.PLoS neglected tropical diseases · 2020Article
- Review
- Chikungunya Virus: An Emergent Arbovirus to the South American Continent and a Continuous Threat to the World.Frontiers in microbiology · 2020Review
- The Autophagy Protein ATG16L1 Is Required for Sindbis Virus-Induced eIF2α Phosphorylation and Stress Granule Formation.Viruses · 2019Article
- Autophagy-dependent secretion: mechanism, factors secreted, and disease implications.Autophagy · 2019Review
- Role of autophagy during the replication and pathogenesis of common mosquito-borne flavi- and alphaviruses.Open biology · 2019Review
- Origin of the Autophagosome Membrane in Mammals.BioMed research international · 2018Review
- Alphavirus-induced hyperactivation of PI3K/AKT directs pro-viral metabolic changes.PLoS pathogens · 2018Article
- Implications of autophagy on arbovirus infection of mosquitoes.Current opinion in insect science · 2017Review
- An siRNA screen for ATG protein depletion reveals the extent of the unconventional functions of the autophagy proteome in virus replication.The Journal of cell biology · 2016Article
- Effects of an In-Frame Deletion of the 6k Gene Locus from the Genome of Ross River Virus.Journal of virology · 2016Article
- A potent betulinic acid analogue ascertains an antagonistic mechanism between autophagy and proteasomal degradation pathway in HT-29 cells.BMC cancer · 2016Article
- Upregulation of ULK1 expression in PC-3 cells following tumor protein P53 transfection by sonoporation.Oncology letters · 2016Article
- HCV induces the expression of Rubicon and UVRAG to temporally regulate the maturation of autophagosomes and viral replication.PLoS pathogens · 2015Article
- Protective and Pathogenic Responses to Chikungunya Virus Infection.Current tropical medicine reports · 2015Article
- Viral and cellular proteins containing FGDF motifs bind G3BP to block stress granule formation.PLoS pathogens · 2015Article
- Species-specific impact of the autophagy machinery on Chikungunya virus infection.EMBO reports · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is a cellular process that sequesters cargo in double-membraned vesicles termed autophagosomes and delivers this cargo to lysosomes to be degraded. It is enhanced during nutrient starvation to increase the rate of amino acid turnover. Diverse roles for autophagy have been reported for viral infections, including the assembly of viral replication complexes on autophagic membranes and protection of host cells from cell death. Here, we show that autophagosomes accumulate in Semliki Forest virus (SFV)-infected cells. Despite this, disruption of autophagy had no effect on the viral replication rate or formation of viral replication complexes. Also, viral proteins rarely colocalized with autophagosome markers, suggesting that SFV did not utilize autophagic membranes for its replication. Further, we found that SFV infection, unlike nutrient starvation, did not inactivate the constitutive negative regulator of autophagosome formation, mammalian target of rapamycin, suggesting that SFV-dependent accumulation of autophagosomes was not a result of enhanced autophagosome formation. In starved cells, addition of NH(4)Cl, an inhibitor of lysosomal acidification, caused a dramatic accumulation of starvation-induced autophagosomes, while in SFV-infected cells, NH(4)Cl did not further increase levels of autophagosomes. These results suggest that accumulation of autophagosomes in SFV-infected cells is due to an inhibition of autophagosome degradation rather than enhanced rates of autophagosome formation. Finally, we show that the accumulation of autophagosomes in SFV-infected cells is dependent on the expression of the viral glycoprotein spike complex.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.