Influenza A virus uses the aggresome processing machinery for host cell entry (Science, 2014, 346 (6208): 473-477)

報告日期: 2015/03/31
報告時間: 15:10/16:00
報告學生: 鄭又瑋
講評老師: 張堯
附件下載: 下載[1459-1425857226-1.pdf] 

Influenza A virus uses the aggresome processing machinery       for host cell entry

Indranil Banerjee, Yasuyuki Miyake, Samuel Philip Nobs, Christoph Schneider,  Peter Horvath, Manfred Kopf, Patrick Matthias, Ari Helenius, Yohei Yamauchi

Science. 2014 October 346(6208):473-477.

Student:Yu-Wei Cheng

Time:2015/03/31  15:10

Commentator:Dr. Yao Chang

Place:Room 602



      Influenza A virus (IAV) is a virus with eight single-stranded, and negative-sense genomic RNA segments. IAV infection is a global medical issue which may cause epidemic and pandemic through antigenic drift/shift by gene mutation/reassortment. It is important to explore the interaction between virus and host to develop common antiviral targets. The authors previously found that some histone deacetylases (HDACs) play important roles through viral entry process by the function of deacetylation of cytoskeletal motor component, tubulin1. In this study, they found that viral infection was reduced in HDAC6 deficiency model, and the affected stage was post-fusion during uncoating and vRNP import. Zinc-finger ubiquitin binding domain (ZnF-UBP) was found to be a key binding region which mediated this process. Since HDAC6 is mainly participated in ubiquitin (Ub)-dependent aggresome formation and disassembly for the degradation of misfolded proteins by binding to dynein motor complexes2, 3, HDAC6-dynein-binding domain was also found to contribute to IAV uncoating process. Furthermore, the authors showed that myosin II, microtubules (MTs) and actin were also involved in uncoating by using different inhibitors. In summary, this study identified that IAV processes uncoating for dispersing viral proteins and vRNPs by HDAC6-dependent aggresome machinery, and need the assistance of some cytoskeletal motors. This revealing offers a new aspect for potential antiviral targets which may be beneficial for treating frequent change antigenicity of influenza viruses. 


  1. Y. Yamauchi et al., PLOS Pathog. 7, e1002316 (2011).
  2. R. Hao et al., Mol. Cell 51, 819–828 (2013).
  3. Y. Kawaguchi et al., Cell 115, 727–738 (2003).