ArticleThe Journal of biological chemistry2019
Heartland virus antagonizes type I and III interferon antiviral signaling by inhibiting phosphorylation and nuclear translocation of STAT2 and STAT1.
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 34 papers.
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Who cites it
34 citing papers in PubMed, 56 citations in OpenAlex.
- Functional divergence of the Bhanja virus NSs protein modulates interferon antagonism and viral fitness across divergent lineages.PLoS pathogens · 2026Article
- Marburg Virus Glycoprotein Is a Remarkable Virulent Factor Linked to Hemorrhagic Pathology: Evidence from Multimodal Experimental Systems.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Foot-and-mouth disease virus 3D polymerase antagonizes the interferon signaling pathway by blocking STAT2 nuclear translocation.Virus research · 2026Article
- Extending the temporal window of arbovirus evolutionary analysis through the recovery of a century-old bandavirus.Virus evolution · 2026Article
- Sensing of Ebinur Lake virus by distinct pattern recognition receptors dictates cell-type specific innate immunity and pathogenesis.Journal of virology · 2025Article
- VISTA expressed on tumor cells is regulated by m6A and influences immune microenvironment through STAT3/CCL22 in NSCLC.Journal of translational medicine · 2025Article
- NSs: the multifaceted bunyavirus virulence factor.Npj viruses · 2025Review
- Interferon-stimulated gene screening identifies CCND3 as a host restriction factor against emerging high-pathogenic bandaviruses.Nature communications · 2025Article
- Functional Involvement of Signal Transducers and Activators of Transcription in the Pathogenesis of Influenza A Virus.International journal of molecular sciences · 2024Review
- Review
- The long noncoding RNA loc107053557 acts as a gga-miR-3530-5p sponge to suppress the replication of vvIBDV through regulating STAT1 expression.Virulence · 2024Article
- Pathogenesis and virulence of Heartland virus.Virulence · 2024Review
- Suppression of Interferon Response and Antiviral Strategies of Bunyaviruses.Tropical medicine and infectious disease · 2024Review
- N-glycosylation of viral glycoprotein is a novel determinant for the tropism and virulence of highly pathogenic tick-borne bunyaviruses.PLoS pathogens · 2024Article
- Modeling Heartland virus disease in mice and therapeutic intervention with 4'-fluorouridine.Journal of virology · 2024Article
- Host factor MxA restricts Dabie bandavirus infection by targeting the viral NP protein to inhibit NP-RdRp interaction and ribonucleoprotein activity.Journal of virology · 2024Article
- Innate immune response against vector-borne bunyavirus infection and viral countermeasures.Frontiers in cellular and infection microbiology · 2024Review
- Viral evasion of the interferon response at a glance.Journal of cell science · 2023Review
- Antiviral activity and mechanism of the antifungal drug, anidulafungin, suggesting its potential to promote treatment of viral diseases.BMC medicine · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heartland virus (HRTV) is a pathogenic phlebovirus recently identified in the United States and related to severe fever with thrombocytopenia syndrome virus (SFTSV) emerging in Asia. We previously reported that SFTSV disrupts host antiviral responses directed by interferons (IFNs) and their downstream regulators, signal transducer and activator of transcription (STAT) proteins. However, whether HRTV infection antagonizes the IFN-STAT signaling axis remains unclear. Here, we show that, similar to SFTSV, HRTV also inhibits IFN-α- and IFN-λ-mediated antiviral responses. As expected, the nonstructural protein (NSs) of HRTV (HNSs) robustly antagonized both type I and III IFN signaling. Protein interaction analyses revealed that a common component downstream of type I and III IFN signaling, STAT2, is the target of HNSs. Of note, the DNA-binding and linker domains of STAT2 were required for an efficient HNSs-STAT2 interaction. Unlike the NSs of SFTSV (SNSs), which blocks both STAT2 and STAT1 nuclear accumulation, HNSs specifically blocked IFN-triggered nuclear translocation only of STAT2. However, upon HRTV infection, IFN-induced nuclear translocation of both STAT2 and STAT1 was suppressed, suggesting that STAT1 is an additional HRTV target for IFN antagonism. Consistently, despite HNSs inhibiting phosphorylation only of STAT2 and not STAT1, HRTV infection diminished both STAT2 and STAT1 phosphorylation. These results suggest that HRTV antagonizes IFN antiviral signaling by dampening both STAT2 and STAT1 activities. We propose that HNSs-specific targeting of STAT2 likely plays an important role but is not all of the "tactics" of HRTV in its immune evasion.
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