ArticlePLoS pathogens2020
HER2-mediated enhancement of Ebola virus entry.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- Platelet-like particles released from Ebola virus-infected megakaryocytic cells behave like virus-like particles.PLoS pathogens · 2026Article
- Knowledge graph and machine learning-guided virtual screening prioritizes putative blockers of the PSMD11/Rpn6-EBOV glycoprotein interface.Frontiers in pharmacology · 2026Article
- Attenuated viral strains of priority pathogens for potential use in controlled human infection model studies: A scoping review.PLoS neglected tropical diseases · 2026Article
- Exploiting host kinases to combat dengue virus infection and disease.Antiviral research · 2025Review
- CD44 mediates the internalization of foot-and-mouth disease virus through macropinocytosis.Veterinary research · 2025Article
- Cellular Receptor Tyrosine Kinase Signaling Plays Important Roles in SARS-CoV-2 Infection.Pathogens (Basel, Switzerland) · 2025Article
- Generation of Biologically Contained Marburg Virus.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Multi-protomics analysis identified host cellular pathways perturbed by tick-borne encephalitis virus infection.Nature communications · 2024Article
- Molecular determinants of cross-species transmission in emerging viral infections.Microbiology and molecular biology reviews : MMBR · 2024Review
- Molecular insights into the Ebola virus life cycle.Nature microbiology · 2024Review
- A compendium of multi-omics data illuminating host responses to lethal human virus infections.Scientific data · 2024Article
- Identification and Potential Roles of Human MicroRNAs in Ebola Virus Infection and Disease Pathogenesis.Genes · 2024Article
- A genome-wide CRISPR screening uncovers that TOB1 acts as a key host factor for FMDV infection via both IFN and EGFR mediated pathways.PLoS pathogens · 2024Article
- The underlying mechanisms of arenaviral entry through matriglycan.Frontiers in molecular biosciences · 2024Review
- Identification of a receptor tyrosine kinase inhibitor CP-724714 inhibits SADS-CoV related swine diarrhea coronaviruses infection in vitro.Virologica Sinica · 2023Article
- Combinatorial Effects of miRNAs in HSV-2 Infection of Macrophages: An In Silico and In Vitro Integration Approach.Vaccines · 2023Article
- Preparing for the next viral threat with broad-spectrum antivirals.The Journal of clinical investigation · 2023Review
- Sphingosine Kinases Promote Ebola Virus Infection and Can Be Targeted to Inhibit Filoviruses, Coronaviruses, and Arenaviruses Using Late Endocytic Trafficking to Enter Cells.ACS infectious diseases · 2023Article
- Pseudotyped Viruses for Marburgvirus and Ebolavirus.Advances in experimental medicine and biology · 2023Article
- Ebola Virus Entry Inhibitors.Advances in experimental medicine and biology · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Multiple cell surface molecules including TAM receptors (TYRO3, AXL, and MERTK), a family of tyrosine kinase receptors, can serve as attachment receptors for Ebola virus (EBOV) entry into cells. The interaction of these receptors with EBOV particles is believed to trigger the initial internalization events that lead to macropinocytosis. However, the details of how these interactions lead to EBOV internalization have yet to be elucidated. Here, we screened receptor tyrosine kinase (RTK) inhibitors for anti-EBOV activity by using our previously established biologically contained Ebola virus that lacks the VP30 gene (EBOVΔVP30) and identified several RTKs, including human epidermal growth factor receptor 2 (HER2), as potential targets of anti-EBOV inhibitors and as novel host factors that have a role in EBOV infection. Of these identified RTKs, it was only HER2 whose knockdown by siRNAs impaired EBOVΔVP30-induced AKT1 phosphorylation, an event that is required for AKT1 activation and subsequent macropinocytosis. Stable expression of HER2 resulted in constitutive activation of AKT1, resulting in the enhancement of EBOVΔVP30 growth, EBOV GP-mediated entry, and macropinocytosis. Moreover, we found that HER2 interacts with the TAM receptors, and in particular forms a complex with TYRO3 and EBOVΔVP30 particles on the cell surface. Interestingly, HER2 was required for EBOVΔVP30-induced TYRO3 and AKT1 activation, but the other TAM receptors (TYRO3 and MERTK) were not essential for EBOVΔVP30-induced HER2 and AKT1 activation. Our findings demonstrate that HER2 plays an important role in EBOV entry and provide novel insights for the development of therapeutics against the virus.
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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.