ArticleJournal of virology2002
Endocytosis is a critical step in entry of subgroup B avian leukosis viruses.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
46 citing papers in PubMed, 75 citations in OpenAlex.
- Trial
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- Analogue discovery of safer alternatives to HCQ and CQ drugs for SAR-CoV-2 by computational design.Computers in biology and medicine · 2021Article
- Insights of Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV-2) pandemic: a current review.Biological procedures online · 2021Review
- Characterization of the Modulatory Effect of Hydroxychloroquine on ACE2 Activity: New Insights in relation to COVID-19.BioMed research international · 2021Article
- A pharmacological perspective of chloroquine in SARS-CoV-2 infection: An old drug for the fight against a new coronavirus?International journal of antimicrobial agents · 2020Review
- Research Progress of Chloroquine and Hydroxychloroquine on the COVID-19 and Their Potential Risks in Clinic Use.Frontiers in pharmacology · 2020Review
- Infection by Zika viruses requires the transmembrane protein AXL, endocytosis and low pH.Virology · 2018Article
- Chloroquine, an Endocytosis Blocking Agent, Inhibits Zika Virus Infection in Different Cell Models.Viruses · 2016Article
- MxB binds to the HIV-1 core and prevents the uncoating process of HIV-1.Retrovirology · 2014Article
- Article
- A proteolytic cascade controls lysosome rupture and necrotic cell death mediated by lysosome-destabilizing adjuvants.PloS one · 2014Article
- The ability of TNPO3-depleted cells to inhibit HIV-1 infection requires CPSF6.Retrovirology · 2013Article
- Contribution of SAM and HD domains to retroviral restriction mediated by human SAMHD1.Virology · 2013Article
- Contribution of SUMO-interacting motifs and SUMOylation to the antiretroviral properties of TRIM5α.Virology · 2013Article
- Retrovirus entry by endocytosis and cathepsin proteases.Advances in virology · 2012Article
- Trafficking of some old world primate TRIM5α proteins through the nucleus.Retrovirology · 2011Article
- PD-1 on immature and PD-1 ligands on migratory human Langerhans cells regulate antigen-presenting cell activity.The Journal of investigative dermatology · 2010Article
- A B-box 2 surface patch important for TRIM5alpha self-association, capsid binding avidity, and retrovirus restriction.Journal of virology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The avian leukosis virus (ALV) entry mechanism is controversial, with evidence for and against a low-pH requirement for viral fusion. To further address this question, we tested the entry of human immunodeficiency virus type 1 (HIV-1) pseudotyped with the envelope protein of subgroup B ALV (ALV-B) in the presence of three different lysosomotropic agents. These lysosomotropic agents were able to block the entry of wild-type and pseudotyped ALV-B in two different cell lines, strongly suggesting that ALV-B requires a low-pH step for entry. ALV-B and pH-dependent Semliki Forest virus (SFV) entered cells with slower uptake kinetics than HIV-1, which is pH independent. These slow uptake rates support the theory that ALV-B utilizes endocytic pathways to enter cells. Using immunofluorescence and electron microscopy analysis, we visualized the colocalization of virus particles with the endosomal marker transferrin and demonstrated virus particles in clathrin-coated vesicles and endosome-like structures. Surprisingly, a low-pH treatment did not overcome the inhibition of ALV-B entry by lysosomotropic agents. This indicates that, in contrast to SFV, ALV-B is unable to fuse at the cellular surface, even at a low pH. Taken together, our findings suggest that endocytosis and a subsequent low-pH step are critical for successful ALV-B infection.
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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.