ArticleViruses2022
Virus Hijacks Host Proteins and Machinery for Assembly and Budding, with HIV-1 as an Example.
Article in Viruses, 2022. 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, 12 citations in OpenAlex.
- The K247 ubiquitination site of the Newcastle disease virus M protein enhances viral budding to facilitate rapid exploitation of host cell sphingolipid metabolites.Poultry science · 2026Article
- DAMP Laden Extracellular Vesicles From the Airways of Patients With Severe SARS-CoV-2 Respiratory Infection Compromise Inflammation and Cellular Metabolism.Journal of extracellular vesicles · 2026Article
- Bioengineering of extracellular vesicles with scaffold proteins for drug delivery.Journal of nanobiotechnology · 2026Review
- Metagenomic analysis of viral communities in the polluted Varuna River reveals site-specific diversity patterns associated with environmental aspects.International microbiology : the official journal of the Spanish Society for Microbiology · 2025Article
- Insights into the function of ESCRT complex and LBPA in ASFV infection.Frontiers in cellular and infection microbiology · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viral assembly and budding are the final steps and key determinants of the virus life cycle and are regulated by virus-host interaction. Several viruses are known to use their late assembly (L) domains to hijack host machinery and cellular adaptors to be used for the requirement of virus replication. The L domains are highly conserved short sequences whose mutation or deletion may lead to the accumulation of immature virions at the plasma membrane. The L domains were firstly identified within retroviral Gag polyprotein and later detected in structural proteins of many other enveloped RNA viruses. Here, we used HIV-1 as an example to describe how the HIV-1 virus hijacks ESCRT membrane fission machinery to facilitate virion assembly and release. We also introduce galectin-3, a chimera type of the galectin family that is up-regulated by HIV-1 during infection and further used to promote HIV-1 assembly and budding via the stabilization of Alix-Gag interaction. It is worth further dissecting the details and finetuning the regulatory mechanism, as well as identifying novel candidates involved in this final step of replication cycle.
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