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Induction of Atypical Autophagy by Porcine Hemagglutinating Encephalomyelitis Virus Contributes to Viral Replication

Overview of attention for article published in Frontiers in Cellular and Infection Microbiology, February 2017
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Title
Induction of Atypical Autophagy by Porcine Hemagglutinating Encephalomyelitis Virus Contributes to Viral Replication
Published in
Frontiers in Cellular and Infection Microbiology, February 2017
DOI 10.3389/fcimb.2017.00056
Pubmed ID
Authors

Ning Ding, Kui Zhao, Yungang Lan, Zi Li, Xiaoling Lv, Jingjing Su, Huijun Lu, Feng Gao, Wenqi He

Abstract

Autophagy is a basic biological metabolic process involving in intracellular membrane transport pathways that recycle cellular components and eliminate intracellular microorganisms within the lysosome. Autophagy also plays an important part in virus infection and propagation. However, some pathogens, including viruses, have evolved unique trick to escape or exploit autophagy. This study explores the mechanism of autophagy induction by porcine hemagglutinating encephalomyelitis virus (PHEV) in Neuro-2a cells, and examines the role of autophagy in PHEV replication. PHEV triggered autophagy in Neuro-2a cells is dependent on the presence of bulk double- or single-membrane vacuoles, the accumulation of GFP-LC3 fluorescent dots, and the LC3 lipidation. In addition, PHEV induced an incomplete autophagic effect because the degradation level of p62 did not change in PHEV-infected cells. Further validation was captured using LysoTracker and lysosome-associated membrane protein by indirect immunofluorescence labeling in PHEV-infected cells. We also investigated the change in viral replication by pharmacological experiments with the autophagy inducer rapamycin or the autophagy inhibitor 3-MA, and the lysosomal inhibitor chloroquine (CQ). Suppression of autophagy by 3-MA increased viral replication, compared with the mock treatment, while promoting of autophagy by rapamycin reduced PHEV replication. CQ treatment enhanced the LC3 lipidation in PHEV-infected Neuro-2a cells but lowered PHEV replication. These results show that PHEV infection induces atypical autophagy and causes the appearance of autophagosomes but blocks the fusion with lysosomes, which is necessary for the replication of PHEV in nerve cells.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 42 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 42 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 11 26%
Student > Master 8 19%
Student > Bachelor 6 14%
Professor 4 10%
Professor > Associate Professor 3 7%
Other 7 17%
Unknown 3 7%
Readers by discipline Count As %
Medicine and Dentistry 7 17%
Veterinary Science and Veterinary Medicine 5 12%
Agricultural and Biological Sciences 5 12%
Biochemistry, Genetics and Molecular Biology 4 10%
Pharmacology, Toxicology and Pharmaceutical Science 3 7%
Other 11 26%
Unknown 7 17%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. 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 31 July 2018.
All research outputs
#17,880,829
of 22,957,478 outputs
Outputs from Frontiers in Cellular and Infection Microbiology
#4,132
of 6,462 outputs
Outputs of similar age
#223,970
of 310,863 outputs
Outputs of similar age from Frontiers in Cellular and Infection Microbiology
#79
of 123 outputs
Altmetric has tracked 22,957,478 research outputs across all sources so far. This one is in the 19th percentile – i.e., 19% of other outputs scored the same or lower than it.
So far Altmetric has tracked 6,462 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.3. This one is in the 24th percentile – i.e., 24% 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 310,863 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 23rd percentile – i.e., 23% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 123 others from the same source and published within six weeks on either side of this one. This one is in the 26th percentile – i.e., 26% of its contemporaries scored the same or lower than it.