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The impact of p53 on the early stage replication of retrovirus

Overview of attention for article published in Virology Journal, August 2017
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Title
The impact of p53 on the early stage replication of retrovirus
Published in
Virology Journal, August 2017
DOI 10.1186/s12985-017-0820-7
Pubmed ID
Authors

Michaela Kinnetz, Faris Alghamdi, Michael Racz, Wenwei Hu, Binshan Shi

Abstract

The function of p53 in cancer biology has been studied extensively, but its role in anti-retrovirus infection has been elusive for many years. The restriction of retrovirus early stage replication by p53 was investigated in this study. VSV-G pseudotyped retrovirus with GFP reporter gene was used to infect both HCT116 p53(+/+) cells and its isogenic p53 knockout HCT116 p53(-/-) cells. The infection was detected by flow cytometry. Reverse transcription products were quantified by real time PCR. Mutation analysis was performed after 1-LTR cycle and 2-LTR cycle DNA were amplified and PCR products were sequenced. Transcription and translation of cyclin-dependent kinase inhibitor 1 (p21(Cip1)) and SAM domain and HD domain-containing protein 1 (SAMHD1) were analyzed by TaqMan PCR and Western blot experiments. siRNA experiment was applied to study the role of p53 downstream gene p21(Cip1) in the restriction of retrovirus infection. It was found that the block of retrovirus infection in non-cycling cells was significantly attenuated in HCT116 p53(-/-) cells when compared to HCT116 p53(+/+) cells. It was found that both late reverse transcription products and viral 2-LTR cycle DNA were significantly increased in infected non-cycling HCT116 p53(-/-) cells. Furthermore, the mutation frequency detected in 1-LTR DNA from HCT116 p53(+/+) cells were significantly decreased in comparison to HCT116 p53(-/-) cells. A higher number of insertion and deletion mutations were detected in the joint region of 2-LTR cycle DNA in infected p53(+/+) cells. Cell cycle analysis showed retrovirus infection promoted host cell replication. Higher levels of mRNA and protein of p21(Cip1) were found in HCT116 p53(+/+) cells in comparison to the HCT116 p53(-/-) cells. Furthermore, knockdown of p21(Cip1) in non-cycling HCT116 p53(+/+) cells significantly increased the infection. The results of this study showed that p53 is an important restriction factor that interferes with retrovirus infection in its early stage of replication. Our results suggested that p53 mediates the inhibition of retrovirus infection in non-cycling cells through it downstream gene p21(Cip1), and p53 also functions to influence formation of 1-LTR cycle and 2-LTR cycle DNA.

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Mendeley readers

The data shown below were compiled from readership statistics for 6 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 6 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 2 33%
Student > Bachelor 1 17%
Professor > Associate Professor 1 17%
Unknown 2 33%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 4 67%
Unknown 2 33%

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 15 August 2017.
All research outputs
#9,750,415
of 12,199,528 outputs
Outputs from Virology Journal
#1,628
of 2,061 outputs
Outputs of similar age
#194,413
of 266,084 outputs
Outputs of similar age from Virology Journal
#29
of 42 outputs
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So far Altmetric has tracked 2,061 research outputs from this source. They receive a mean Attention Score of 3.5. This one is in the 8th percentile – i.e., 8% of its peers scored the same or lower than it.
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