Influenza A Virus PA Antagonizes Interferon-β by Interacting with Interferon Regulatory Factor 3
نویسندگان
چکیده
منابع مشابه
Influenza A Virus PA Antagonizes Interferon-β by Interacting with Interferon Regulatory Factor 3
The influenza A virus (IAV) can be recognized by retinoic acid-inducible gene I (RIG-I) to activate the type I interferon response and induce antiviral effects. The virus has evolved several strategies to evade the innate immune response, including non-structural protein 1 (NS1) and its polymerase subunits. The mechanism by which NS1 inhibits interferon-β (IFN-β) is well understood, whereas the...
متن کاملHIST1H1C Regulates Interferon-β and Inhibits Influenza Virus Replication by Interacting with IRF3
Influenza virus NS2 is well known for its role in viral ribonucleoprotein nuclear export; however, its function has not been fully understood. A recent study showed that NS2 might interact with HIST1H1C (H1C, H1.2). Histones have been found to affect influenza virus replication, such as the H2A, H2B, H3, and H4, but H1 has not been detected. Here, we found that H1C interacts with NS2 via its C-...
متن کاملPrimary activation of interferon A and interferon B gene transcription by interferon regulatory factor 3.
The family of interferon (IFN) regulatory factors (IRFs) encodes DNA-binding transcription factors, some of which function as modulators of virus-induced signaling. The IRF-3 gene is constitutively expressed in many tissues and cell types, and neither virus infection nor IFN treatment enhances its transcription. In infected cells, however, IRF-3 protein is phosphorylated at the carboxyl terminu...
متن کاملp38-dependent activation of interferon regulatory factor 3 by lipopolysaccharide.
Interferon regulatory factor 3 (IRF3) is known to participate in the transcriptional induction of interferon (IFN) alpha and IFNbeta genes, as well as of a number of interferon-stimulated genes (ISGs), as a result of viral infection. In the present study we demonstrate the activation of IRF3 followed by ISG induction after exposure of cells to the bacterial cell wall component lipopolysaccharid...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Frontiers in Immunology
سال: 2017
ISSN: 1664-3224
DOI: 10.3389/fimmu.2017.01051