ArticleThe Journal of biological chemistry2019
An engineered mutant of a host phospholipid synthesis gene inhibits viral replication without compromising host fitness.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Positive-strand RNA virus genome replication organelles: structure, assembly, control.Trends in genetics : TIG · 2024Review
- Metabolic alterations upon SARS-CoV-2 infection and potential therapeutic targets against coronavirus infection.Signal transduction and targeted therapy · 2023Review
- A conserved viral amphipathic helix governs the replication site-specific membrane association.PLoS pathogens · 2022Article
- Aspartic protease inhibitor enhances resistance to potato virus Y and A in transgenic potato plants.BMC plant biology · 2022Article
- Phytosterol metabolism in plant positive-strand RNA virus replication.Plant cell reports · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viral infections universally rely on numerous hijacked host factors to be successful. It is therefore possible to control viral infections by manipulating host factors that are critical for viral replication. Given that host genes may play essential roles in certain cellular processes, any successful manipulations for virus control should cause no or mild effects on host fitness. We previously showed that a group of positive-strand RNA viruses enrich phosphatidylcholine (PC) at the sites of viral replication. Specifically, brome mosaic virus (BMV) replication protein 1a interacts with and recruits a PC synthesis enzyme, phosphatidylethanolamine methyltransferase, Cho2p, to the viral replication sites that are assembled on the perinuclear endoplasmic reticulum (ER) membrane. Deletion of the
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Registered trials
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