ArticleNature communications2018
MxB is an interferon-induced restriction factor of human herpesviruses.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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Who cites it
91 citing papers in PubMed, 130 citations in OpenAlex.
- Expulsion of nuclear DNA to the cytoplasm after viral entry: A mechanism for activation of the cGAS pathway.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Nectin4 restricts pseudorabies virus infection by blocking gD-Nectin1 interaction.Journal of virology · 2026Article
- The antiviral GTPase MxB is packaged into virions and binds via its N-terminal domain to alphaherpesvirus capsids.PLoS pathogens · 2026Article
- SUMOylation and ubiquitination reciprocally regulate SMCHD1 antiviral activity against herpes simplex virus 1.PLoS pathogens · 2026Article
- MX2 Mediates Collapse of the HIV-1 Capsid.bioRxiv : the preprint server for biology · 2026Article
- Antiviral Inflammasomes and How to Find Them.Viruses · 2026Review
- Unraveling the Biology of Interferon-Stimulated Genes: Mechanisms, Functions, and Clinical Implications.Infection and drug resistance · 2026Review
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- The interferon-inducible MxB large GTPase attenuates hepatitis B virus replication by activating the RIG-I innate immunity signaling pathway.Scientific reports · 2025Article
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- Comparative Transcriptomics Analyses Identify DDX43 as a Cellular Regulator Involved in Suppressing HSV-2 Replication.Viruses · 2025Article
- Ubiquitously expressed transcript isoform 2 (UXT-V2) restricts HSV-2 replication by targeting glycoprotein B for degradation through ubiquitin-proteasome pathway.Virologica Sinica · 2025Article
- Multi-proteomic profiling of the varicella-zoster virus-host interface reveals host susceptibilities to severe infection.Nature microbiology · 2025Article
- Clicking viruses-with chemistry toward mechanisms in infection.Journal of virology · 2025Review
- Antiviral Mx proteins have an ancient origin and widespread distribution among eukaryotes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Characterization of Human Cytomegalovirus (HCMV) Long Non-Coding RNA1.2 During Lytic Replication.Viruses · 2025Article
- FGF receptor kinase inhibitors exhibit broad antiviral activity by targeting Src family kinases.Cellular and molecular life sciences : CMLS · 2024Article
- Antiviral Mx proteins have an ancient origin and widespread distribution among eukaryotes.bioRxiv : the preprint server for biology · 2024Article
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31 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The type I interferon (IFN) system plays an important role in controlling herpesvirus infections, but it is unclear which IFN-mediated effectors interfere with herpesvirus replication. Here we report that human myxovirus resistance protein B (MxB, also designated Mx2) is a potent human herpesvirus restriction factor in the context of IFN. We demonstrate that ectopic MxB expression restricts a range of herpesviruses from the Alphaherpesvirinae and Gammaherpesvirinae, including herpes simplex virus 1 and 2 (HSV-1 and HSV-2), and Kaposi's sarcoma-associated herpesvirus (KSHV). MxB restriction of HSV-1 and HSV-2 requires GTPase function, in contrast to restriction of lentiviruses. MxB inhibits the delivery of incoming HSV-1 DNA to the nucleus and the appearance of empty capsids, but not the capsid delivery to the cytoplasm or tegument dissociation from the capsid. Our study identifies MxB as a potent pan-herpesvirus restriction factor which blocks the uncoating of viral DNA from the incoming viral capsid.
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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.