ArticleFrontiers in microbiology2021
Rabies Virus-Induced Autophagy Is Dependent on Viral Load in BV2 Cells.
Article in Frontiers in microbiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Autophagy in emerging and highly concerned severe zoonotic infectious diseases.Frontiers in immunology · 2026Review
- Temporal trends and determinants of delayed care-seeking after rabies exposure: a 27,930-patient analysis in Tianjin.Frontiers in public health · 2026Article
- Andrographolide Inhibits Rabies Virus Replication.Transboundary and emerging diseases · 2026Article
- Article
- Review
- Bif-1c Attenuates Viral Proliferation by Regulating Autophagic Flux Blockade Induced by the Rabies Virus CVS-11 Strain in N2a Cells.Microbiology spectrum · 2023Article
- Regulation of innate immune responses by rabies virus.Animal models and experimental medicine · 2022Review
- The Multi-Faceted Role of Autophagy During Animal Virus Infection.Frontiers in cellular and infection microbiology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An increasing number of studies are showing that autophagy plays a vital role in viral replication and escape. Rabies virus (RABV), a typical neurotropic virus, has been proven to induce autophagy in neurons. However, there are no reports indicating that RABV can cause autophagy in other cells of the central nervous system. Thus, we aimed to explore the relationship between autophagy and RABV infection in BV2 cells in this study. Results of viral growth curves showed that the titers of microglial BV2 cells infected with RABV peaked at 12 hours post-infection (hpi) and then decreased continuously over time. However, it was found that the viral genome RNA and structural proteins can express normally in BV2 cells. In addition, Western blotting indicated that RABV infection increased LC3-II and p62 expression in BV2 cells. LC3 punctate increased with RABV infection in BV2 cells after the transfection of fluorescent protein-tagged LC3 plasmids. Moreover, autophagy cargo protein further accumulated with RABV infection in Bafilomycin A1-treated cells. Subsequently, RABV infection inhibited the fusion of autophagosomes with lysosomes by using a tandem fluorescent marker. Furthermore, a higher multiplicity of infection induced stronger autophagy. Thus, RABV can induce autophagy in BV2 cells, and the autophagy is positively associated with the viral load.
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Registered trials
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