scholarly journals Retraction: Peste des petits ruminants virus V protein inhibits cellular antiviral response by blocking the secretion of endogenous and exogenous interferons

Author(s):  
Linjie LI ◽  
Xiaoling SHI ◽  
Derong ZHANG ◽  
Xin CAO ◽  
Amjad ALI ◽  
...  
2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Zixiang Zhu ◽  
Xiaocui Zhang ◽  
Gulizhati Adili ◽  
Jiong Huang ◽  
Xiaoli Du ◽  
...  

Peste des petits ruminants virus (PPRV) is the causative agent of peste des petits ruminants (PPR). The spread of PPR often causes severe economic losses. Therefore, special attention should be paid to the surveillance of PPR emergence, spread, and geographic distribution. Here we describe a novel mutant of PPRV China/XJBZ/2015 that was isolated fromCapra ibexin Xinjiang province in China 2015. The sequence analysis and phylogenetic assessment indicate that China/XJBZ/2015 belongs to lineage IV, being closely related to China/XJYL/2013 strain. Interestingly, the V protein sequence of China/XJBZ/2015 showed lower homology with other Chinese PPRVs isolated during 2013 to 2014 (94%~95%), whereas it shared 100% identity with three Tibet strains isolated in China 2007. The 3′ UTR, V gene, and C gene were determined to be highly variable. Besides, 29 PPR genomic sequences available in GenBank were analyzed in this study. It is the first time to use PPRV genomic sequences to classify the different lineages which confirmed the lineage clustering of PPRVs using N gene 255 bp fragments and F gene 322 bp fragments. In conclusion, our findings indicate that the PPRVs continue to evolve in China, and some new mutations have emerged.


2015 ◽  
Vol 195 (11) ◽  
pp. 5358-5366 ◽  
Author(s):  
K. Zhu ◽  
X. Wang ◽  
L.-G. Ju ◽  
Y. Zhu ◽  
J. Yao ◽  
...  

2012 ◽  
Vol 9 (1) ◽  
pp. 292 ◽  
Author(s):  
Wen Pan ◽  
Xiangyang Zuo ◽  
Tingting Feng ◽  
Xiaohong Shi ◽  
Jianfeng Dai

2017 ◽  
Vol 474 (7) ◽  
pp. 1241-1257 ◽  
Author(s):  
Evelyn Chukwurah ◽  
Indhira Handy ◽  
Rekha C. Patel

Human immunodeficiency virus type 1 (HIV-1) has evolved various measures to counter the host cell's innate antiviral response during the course of infection. Interferon (IFN)-stimulated gene products are produced following HIV-1 infection to limit viral replication, but viral proteins and RNAs counteract their effect. One such mechanism is specifically directed against the IFN-induced Protein Kinase PKR, which is centrally important to the cellular antiviral response. In the presence of viral RNAs, PKR is activated and phosphorylates the translation initiation factor eIF2α. This shuts down the synthesis of both host and viral proteins, allowing the cell to mount an effective antiviral response. PACT (protein activator of PKR) is a cellular protein activator of PKR, primarily functioning to activate PKR in response to cellular stress. Recent studies have indicated that during HIV-1 infection, PACT's normal cellular function is compromised and that PACT is unable to activate PKR. Using various reporter systems and in vitro kinase assays, we establish in this report that interactions between PACT, ADAR1 and HIV-1-encoded Tat protein diminish the activation of PKR in response to HIV-1 infection. Our results highlight an important pathway by which HIV-1 transcripts subvert the host cell's antiviral activities to enhance their translation.


Virus Genes ◽  
2016 ◽  
Vol 53 (2) ◽  
pp. 233-239 ◽  
Author(s):  
Jie Tao ◽  
Jinhu Liao ◽  
Jianye Wang ◽  
Xinjun Zhang ◽  
Qian Zhang ◽  
...  

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