Human Enterovirus 68 Interferes with the Host Cell Cycle to Facilitate Viral Production

Wang, Zeng Yan; Zhong, Ting; Wang, Yue; Song, Feng Mei; Yu, X.F.; Xing, Li Ping; Zhang, Wen Yan; Yu, Jing; Hua, Shu

doi:10.3389/fcimb.2017.00029

Cited by 31 publications

(48 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The 98 strain of CA6 1 was provided by the Jilin Provincial Center for Diseases Control and Prevention (Changchun, China). Viruses were propagated in RD cells, and the supernatants were collected and stored at −80 • C as our previous studies (Yu et al, 2015;Wang et al, 2017).…”

Section: Cells and Virusesmentioning

confidence: 99%

Coxsackievirus A6 Induces Necroptosis for Viral Production

Zhang

Meng

et al. 2020

Front. Microbiol.

View full text Add to dashboard Cite

Hand, foot, and mouth disease (HFMD) is a febrile exanthematous disease with typical or atypical symptoms. Typical HFMD is usually caused by enterovirus 71 (EV71) or coxsackievirus A16, while atypical HFMD is usually caused by coxsackievirus A6 (CA6). In recent years, worldwide outbreaks of CA6-associated HFMD have dramatically increased, although the pathogenic mechanism of CA6 is still unclear. EV71 has been established to induce caspase-dependent apoptosis, but in this study, we demonstrate that CA6 infection promotes a distinct pathway of cell death that involves loss of cell membrane integrity. Necrostatin-1, an inhibitor of necroptosis, blocks the cell death induced by CA6 infection, but Z-DEVD-FMK, an inhibitor of caspase-3, has no effect on CA6-induced cell death. Furthermore, CA6 infection up-regulates the expression of the necroptosis signaling molecule RIPK3. Importantly, necrostatin-1 inhibits CA6 viral production, as assessed by its ability to inhibit levels of VP1 protein and genomic RNA and infectious particles. CA6-induced necroptosis is not dependent on the generation of reactive oxygen species; however, viral 3D protein can directly bind RIPK3, which is suggestive of a direct mechanism of necroptosis induction. Therefore, these results indicate that CA6 induces a mechanism of RIPK3-dependent necroptosis for viral production that is distinct from the mechanism of apoptosis induced by typical HFMD viruses.

show abstract

Section: Cells and Virusesmentioning

confidence: 99%

Coxsackievirus A6 Induces Necroptosis for Viral Production

Zhang

Meng

et al. 2020

Front. Microbiol.

View full text Add to dashboard Cite

show abstract

“…In our previous study, we showed that the EVD68 virus induced cell cycle arrest in the G0/G1 phase to promote viral replication (Wang et al, ). Therefore, we used flow cytometry to examine the effects of rheum emodin, artemisinin, astragaloside, and pseudolaric acid B on the cell cycle upon infection with the EVD68 virus.…”

Section: Resultsmentioning

confidence: 99%

“…In a previous study, we demonstrate that the EVD68 virus manipulates cell cycle arrest in the G0/G1 phase for viral replication (Wang et al, ). This indicates the possibility of developing cell cycle‐modifying agents (especially those that induce S or G2/M phase arrest) as a novel strategy for treating EVD68‐related diseases.…”

Section: Introductionmentioning

confidence: 84%

Effect of ingredients from Chinese herbs on enterovirus D68 production

Meng

Liu

et al. 2018

Phytotherapy Research

View full text Add to dashboard Cite

Human enterovirus 68 (EVD68) is a primary causative agent for respiratory illness worldwide. Until now, there has been no available medication for treating EVD68related diseases. Rheum emodin, artemisinin, astragaloside, pseudolaric acid B, oridonin, and erianin are natural extracts from Chinese herbs that have traditionally been used for the treatment and prevention of epidemic diseases. Our results showed that pseudolaric acid B protected cells from EVD68-induced cytopathic effects and decreased viral production. However, the same effects were not observed with rheum emodin, astragaloside, or artemisinin. Pseudolaric acid B inhibited EVD68 production by manipulating the host cell cycle in G2/M phase. Further, either oridonin or erianin related G2/M arrest also inhibited viral production. Due to inducing G2/M phase arrest, pseudolaric acid B, oridonin, and erianin might be good candidates for inhibiting EVD68 production, and Chinese herbs with natural compounds inducing G2/M arrest should be considered for the treatment of EVD68-related diseases. KEYWORDS enterovirus D68 (EVD68), G2/M arrest, natural compounds, viral production

show abstract

“…Propidium iodide (PI) staining was applied for measuring the changes of cell cycle (G0/G1, S and M) through a ow cytometer (BD Biosciences, San Diego, CA, USA) as previously described [20,21].…”

Section: Cell Cycle Detectionmentioning

confidence: 99%

Circ_RPL23A acts as a miR-1233 sponge to suppress the progression of clear cell renal cell carcinoma by promoting ACAT2

Cheng

Cao

et al. 2020

Preprint

View full text Add to dashboard Cite

Background Clear cell renal cell carcinoma (CCRCC) is a prevalent urological carcinoma with high metastatic risk. Circular RNAs (circRNAs) have been identified as effective diagnostic and therapeutic biomarkers for CCRCC. This research aims to disclose the involvement of circRNA ribosomal protein L23a (circ_RPL23A) in CCRCC, and how it regulates carcinogenesis. Methods We performed quantitative real-time polymerase chain reaction (qRT-PCR) to examine circ_RPL23A, microRNA-1233 (miR-1233) and acetyl-coenzyme A acetyltransferase 2 (ACAT2). Cellular behavior detection included cell cycle, proliferation, apoptosis and metastasis, which were severally analyzed using propidium iodide (PI)-flow cytometry, 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT), Annexin V/PI-flow cytometry and transwell migration/invasion assays. ACAT2 and related proteins of cell cycle, epithelial-mesenchymal transition (EMT) were measured via western blot. Target relationship was analyzed via dual-luciferase reporter assay. A xenograft model was used to study circ_RPL23A action in mice. Results Both in CCRCC tissues and cells, circ_RPL23A had a down-regulated tendency. Explicitly, circ_RPL23A overexpression inhibited cell cycle, proliferation and metastasis but enhanced apoptosis of CCRCC cells, whereas these effects of circ_RPL23A were dependent on the suppression of its target miR-1233. Besides, miR-1233 could target ACAT2 and circ_RPL23A regulated ACAT2 by sponging miR-1233. Also importantly, miR-1233 was a pro-cancer gene in CCRCC via targeting ACAT2. CCRCC tumor growth was also decreased in vivo by circ_RPL23A through miR-1233/ACAT2 axis. Conclusion Altogether, the circ_RPL23A/miR-1233/ACAT2 axis in this report provides an in-depth cognition for CCRCC pathogenesis and circ_RPL23A may has pivotal value in diagnosing and treating CCRCC.

show abstract

Human Enterovirus 68 Interferes with the Host Cell Cycle to Facilitate Viral Production

Cited by 31 publications

References 39 publications

Coxsackievirus A6 Induces Necroptosis for Viral Production

Coxsackievirus A6 Induces Necroptosis for Viral Production

Effect of ingredients from Chinese herbs on enterovirus D68 production

Circ_RPL23A acts as a miR-1233 sponge to suppress the progression of clear cell renal cell carcinoma by promoting ACAT2

Contact Info

Product

Resources

About