{"id":389,"title":"Oropouche virus disrupts neurodevelopment and exhibits congenital infection potential","title_zh":"Oropouche 病毒破坏神经发育并具有先天性感染潜能","url":"https://pubmed.ncbi.nlm.nih.gov/42907468","doi":"10.1038/s41467-026-77859-5","pmid":"42907468","journal":"Nat Commun","kind":"paper","lang":"en","published_at":"2026-09-22T00:00:00+00:00","fetched_at":"2026-11-08T03:44:12+00:00","authors":["Bannerman C","Philip DT","Kennedy EA","Liu S","Hewins P","Barajas Y","Miller-Ensminger T","Walsh K","Negatu SG","Ming GL","Jurado KA"],"primary_topic":"early-pregnancy","topics":[{"slug":"endometrium","score":2.0,"hits":["placenta","placental"]},{"slug":"early-pregnancy","score":1.0,"hits":["pregnancy outcomes"]}],"topic_score":2.0,"preference_score":0.0,"preference_labels":[],"llm_score":78.0,"final_score":86.0,"score_dims":{"novelty":85,"rigor":80,"impact":72,"relevance":58,"translation":65},"recommend_reason":"该研究将 OROV 作为潜在先天性病原体，用类器官、新生小鼠和胎盘感染模型系统比较其与 ZIKV 的神经致病性，对孕期感染与胎儿发育研究有提示价值；但研究对象并非 ART 或胚胎种植核心环节，生殖医学相关性中等。","keywords":["Oropouche 病毒","先天性感染","神经发育","前脑类器官","胎儿生长受限","I 型干扰素"],"selected":1,"story_id":435,"llm_provider":"deepseek","llm_model":"deepseek-flash","llm_effort":"low","source_key":"pubmed-top-journals","source_name":"PubMed · CNS/大子刊/四大医学刊（生殖相关）","source_tier":1,"mention_count":1,"has_interpretation":false,"journal_key":"nat-commun","journal_tier":"cns-sub","journal_if":14.7,"is_mock":false,"summary_zh":"研究以历史株和当前流行株，在人前脑类器官及新生小鼠中比较 Oropouche 病毒（OROV）与寨卡病毒。结果显示，OROV 可感染不同分化状态的神经元，神经嗜性与病理损伤更强，部分源于更广的神经元嗜性及对 I 型干扰素应答不敏感；新生小鼠神经感染可致快速严重病理和脑出血。I 型干扰素阻断模型进一步显示 OROV 可感染鼠胎盘并导致胎儿生长受限。作者提出胎盘和胎儿屏障可限制胎儿脑感染，但 OROV 一旦进入发育中的神经组织即具显著致病潜能，需警惕其与不良妊娠结局和先天性疾病的关系。","summary":"Oropouche virus (OROV) historically caused a self-limiting disease, yet recent strains have been clinically linked to congenital infection and neurodevelopmental disease. These observations highlight the need to study OROV as a congenital pathogen. Here, using both a historical and currently circulating strain, we show OROV infects neurons across differentiation states in human forebrain organoids. Compared with the neurotropic congenital pathogen Zika virus (ZIKV), OROV exhibits a heightened capacity for neuroinfection and pathology in both forebrain organoids and neonatal mice. The increased permissiveness of OROV is driven, in part, by a broader neuronal tropism and a relative insensitivity to neuronal type I interferon-mediated antiviral responses. Consistent with clinical observations, neonatal neuroinfection results in rapid and severe neuropathology marked by cerebral hemorrhage. Finally, using a transient type I interferon-blockade model, we demonstrate that OROV can productively infect the murine placenta and cause fetal growth restriction. Together, our complementary models support a unified framework in which placental and fetal barriers limit productive fetal brain infection, yet OROV exhibits marked neurotropism and neuropathogenic potential upon gaining access to developing neural tissues. These findings reinforce the need for vigilant monitoring of OROV as an emerging pathogen associated with adverse pregnancy outcomes and congenital disease.","interpretation_basis":null,"fulltext_status":"ok","interpretation":null,"fulltext":{"available":true,"status":"ok","reason":"已取得 Europe PMC OA 全文","pmcid":"PMC13687063","license":"CC BY-NC-ND 4.0","chars":29996,"source":"Europe PMC","fetched_at":"2026-11-08T04:19:35+00:00"}}