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C-terminal region of apoptin affects chicken anemia virus replication and virulence

Overview of attention for article published in Virology Journal, February 2017
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Title
C-terminal region of apoptin affects chicken anemia virus replication and virulence
Published in
Virology Journal, February 2017
DOI 10.1186/s12985-017-0713-9
Pubmed ID
Authors

Yongqiang Wang, Xiuqing Song, Honglei Gao, Xiaoyan Wang, Yonghao Hu, Yulong Gao, Xiaole Qi, Liting Qin, Huan Lin, Li Gao, Shuai Yao, Chunyan Han, Xiaomei Wang, Hualan Chen

Abstract

Chicken anemia virus (CAV) causes anemia and immune suppression, which are important diseases in the poultry industry. CAV VP3, also referred as 'apoptin', has been shown to selectively kill tumor cells, raising great hopes for its utilization as an anticancer therapy. The ability of apoptin to induce apoptosis is closely related to its nuclear localization. The C-terminal region of apoptin contains a bipartite nuclear localization signals (NLS), and a nuclear export signal (NES) is located between the arms of the NLS. Most previous studies have expressed apoptin of different lengths in vitro to understand the relationship between its localization and its induction of apoptosis. In this study, we investigated the replication of CAV and its induction of apoptosis in vitro and in vivo with VP3-truncated infectious virus. Quantitative PCR was used to detect viral replication in MDCC-MSB1 cells, and the viral localization was observed by confocal microscopy. Flow cytometry was uesed to analyze virus-induced apoptosis in MDCC-MSB1 cells. Additionally, chickens infected with the rescued viruses compared with the parental virus rM9905 to evaluate the viral replication in vivo and virulence. Based on the infectious clone, we rescued two viruses in which were deleted NES-NLS2 (rCAV-VP3N88) or NLS1-NES-NLS2 (rCAV-VP3N80) in the C-terminal region of apoptin. The viral load of rCAV-VP3N88 decreased significantly between 60 and 108 hpi, and was always 10-100-fold lower than that of the parental virus rM9905. The levels of rCAV-VP3N80 were also 10-100-fold lower than that of rM9905 and declined significantly at three time points. There was almost no difference in the viral loads of rCAV-VP3N88 and rCAV-VP3N80. Additionally, rM9905 induced 85.39 ± 2.18% apoptosis at 96 hpi, whereas rCAV-VP3N88 and rCAV-VP3N80 induced 63.08 ± 4.78% and 62.56 ± 7.35% apoptosis, respectively, which were significantly (about 20%) lower than that induced by the parental virus. The rescued viruses altered the nuclear localization in MDCC-MSB1 cells. Moreover, deletion of C-terminal region of apoptin impaired viral replication in vivo and reduced the virulence of CAV in chickens. In summary, we have demonstrated that the C-terminal deletion of apoptin in infectious CAV affected the replication of the virus. The deletion of the C-terminal region of apoptin not only significantly reduced viral replication in vitro but also reduced its induction of apoptosis, which correlated with the loss of its nuclear localization. The deletion of the C-terminal region of apoptin also impaired the replication of CAV and attenuated its virulence in chickens.

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The data shown below were collected from the profiles of 2 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 17 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 17 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 4 24%
Researcher 3 18%
Student > Doctoral Student 2 12%
Professor 2 12%
Student > Ph. D. Student 1 6%
Other 2 12%
Unknown 3 18%
Readers by discipline Count As %
Veterinary Science and Veterinary Medicine 5 29%
Pharmacology, Toxicology and Pharmaceutical Science 1 6%
Biochemistry, Genetics and Molecular Biology 1 6%
Linguistics 1 6%
Nursing and Health Professions 1 6%
Other 3 18%
Unknown 5 29%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 10 March 2017.
All research outputs
#14,798,134
of 22,958,253 outputs
Outputs from Virology Journal
#1,785
of 3,056 outputs
Outputs of similar age
#184,799
of 310,768 outputs
Outputs of similar age from Virology Journal
#31
of 70 outputs
Altmetric has tracked 22,958,253 research outputs across all sources so far. This one is in the 34th percentile – i.e., 34% of other outputs scored the same or lower than it.
So far Altmetric has tracked 3,056 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 25.7. This one is in the 40th percentile – i.e., 40% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 310,768 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 39th percentile – i.e., 39% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 70 others from the same source and published within six weeks on either side of this one. This one is in the 48th percentile – i.e., 48% of its contemporaries scored the same or lower than it.