Academic Journal

Host Innate Antiviral Response to Influenza A Virus Infection: From Viral Sensing to Antagonism and Escape

التفاصيل البيبلوغرافية
العنوان: Host Innate Antiviral Response to Influenza A Virus Infection: From Viral Sensing to Antagonism and Escape
المؤلفون: Wenlong An, Simran Lakhina, Jessica Leong, Kartik Rawat, Matloob Husain
المصدر: Pathogens, Vol 13, Iss 7, p 561 (2024)
بيانات النشر: MDPI AG, 2024.
سنة النشر: 2024
المجموعة: LCC:Medicine
مصطلحات موضوعية: influenza virus, Toll-like receptors, RIG-I, NOD-like receptors, NLRP3 inflammasome, ZBP1, Medicine
الوصف: Influenza virus possesses an RNA genome of single-stranded, negative-sensed, and segmented configuration. Influenza virus causes an acute respiratory disease, commonly known as the “flu” in humans. In some individuals, flu can lead to pneumonia and acute respiratory distress syndrome. Influenza A virus (IAV) is the most significant because it causes recurring seasonal epidemics, occasional pandemics, and zoonotic outbreaks in human populations, globally. The host innate immune response to IAV infection plays a critical role in sensing, preventing, and clearing the infection as well as in flu disease pathology. Host cells sense IAV infection through multiple receptors and mechanisms, which culminate in the induction of a concerted innate antiviral response and the creation of an antiviral state, which inhibits and clears the infection from host cells. However, IAV antagonizes and escapes many steps of the innate antiviral response by different mechanisms. Herein, we review those host and viral mechanisms. This review covers most aspects of the host innate immune response, i.e., (1) the sensing of incoming virus particles, (2) the activation of downstream innate antiviral signaling pathways, (3) the expression of interferon-stimulated genes, (4) and viral antagonism and escape.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2076-0817
Relation: https://www.mdpi.com/2076-0817/13/7/561; https://doaj.org/toc/2076-0817
DOI: 10.3390/pathogens13070561
URL الوصول: https://doaj.org/article/77ff552fed964a83ae89c691df71f7fe
رقم الانضمام: edsdoj.77ff552fed964a83ae89c691df71f7fe
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:20760817
DOI:10.3390/pathogens13070561