ArticleNature communications2024
Evolution of STAT2 resistance to flavivirus NS5 occurred multiple times despite genetic constraints.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Article
- Integrated Evolutionary and Multi-Omic Analysis of STAT Family Activation Across Solid Tumors.Genes · 2026Article
- Development and validation of a DNA-launched, intron-stabilized Langat virus infectious clone and reporter viruses.Virology · 2026Article
- Comparative susceptibility of Old World and New World bat cell lines to Zika virus: Insights into viral replication and inflammatory responses.PLoS neglected tropical diseases · 2026Article
- Reduced dengue virus pre-membrane protein-HMGB1 interaction activates host cell transcription to attenuate infection.NPJ vaccines · 2026Article
- Innate Immune and Inflammatory Responses to Dengue Virus Infection.Current topics in microbiology and immunology · 2026Review
- Coevolutionary constraints of Zika virus nonstructural protein 5 replication and interferon antagonism activities.bioRxiv : the preprint server for biology · 2025Article
- Viral interferon antagonism shapes host tropism.PLoS pathogens · 2025Review
- Viral-host molecular interactions and metabolic modulation: Strategies to inhibit flaviviruses pathogenesis.World journal of virology · 2024Review
- E2 Ubiquitin-Conjugating Enzymes Regulates Dengue Virus-2 Replication inMicroorganisms · 2024Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Zika and dengue virus nonstructural protein 5 antagonism of STAT2, a critical interferon signaling transcription factor, to suppress the host interferon response is required for viremia and pathogenesis in a vertebrate host. This affects viral species tropism, as mouse STAT2 resistance renders only immunocompromised or humanized STAT2 mice infectable. Here, we explore how STAT2 evolution impacts antagonism. By measuring the susceptibility of 38 diverse STAT2 proteins, we demonstrate that resistance arose numerous times in mammalian evolution. In four species, resistance requires distinct sets of multiple amino acid changes that often individually disrupt STAT2 signaling. This reflects an evolutionary ridge where progressive resistance is balanced by the need to maintain STAT2 function. Furthermore, resistance may come with a fitness cost, as resistance that arose early in lemur evolution was subsequently lost in some lemur lineages. These findings underscore that while it is possible to evolve resistance to antagonism, complex evolutionary trajectories are required to avoid detrimental host fitness consequences.
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