Vitamin D receptor protects glioblastoma A172 cells against Coxsackievirus A16 infection induced cell death in the pathogenesis of hand, foot, and mouth disease

2017 ◽  
Vol 493 (2) ◽  
pp. 952-956 ◽  
Author(s):  
Meiling Qu ◽  
Shunxiang Di ◽  
Shuyun Zhang ◽  
Zhiqun Xia ◽  
Guohong Quan
Keyword(s):  
Vitamin D ◽  
Cell Death ◽  
Vitamin D Receptor ◽  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Coxsackievirus A16 ◽  
Foot And Mouth

Vitamin D receptor gene methylation in patients with hand, foot, and mouth disease caused by enterovirus 71

2020 ◽  
Vol 165 (9) ◽  
pp. 1979-1985
Author(s):  
Ya-Ping Li ◽  
Hui-Ling Deng ◽  
Wen-Jun Wang ◽  
Mu-Qi Wang ◽  
Mei Li ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Receptor Gene ◽  
Enterovirus 71 ◽  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Vitamin D Receptor Gene ◽  
Gene Methylation ◽  
Foot And Mouth

scholarly journals RSAD2 and AIM2 Modulate Coxsackievirus A16 and Enterovirus A71 Replication in Neuronal Cells in Different Ways That May Be Associated with Their 5′ Nontranslated Regions

2017 ◽  
Vol 92 (6) ◽  
Author(s):  
Thinesshwary Yogarajah ◽  
Kien Chai Ong ◽  
David Perera ◽  
Kum Thong Wong
Keyword(s):  
Viral Replication ◽  
Neuronal Cells ◽  
Neuroblastoma Cells ◽  
Foot And Mouth Disease ◽  
Neurological Complications ◽  
Mouth Disease ◽  
Host Responses ◽  
Coxsackievirus A16 ◽  
Enterovirus A71 ◽  
Foot And Mouth

ABSTRACT Coxsackievirus A16 (CV-A16) and enterovirus A71 (EV-A71) are closely related enteroviruses that cause the same hand, foot, and mouth disease (HFMD), but neurological complications occur only very rarely in CV-A16 compared to EV-A71 infections. To elucidate host responses that may be able to explain these differences, we performed transcriptomic analysis and real-time quantitative PCR (RT-qPCR) in CV-A16-infected neuroblastoma cells (SK-N-SH), and the results showed that the radical S -adenosylmethionine domain containing 2 (RSAD2) was the highest upregulated gene in the antimicrobial pathway. Increased RSAD2 expression was correlated with reduced viral replication, while RSAD2 knockdown cells were correlated with increased replication. EV-A71 replication showed no apparent correlation to RSAD2 expressions. Absent in melanoma 2 (AIM2), which is associated with pyroptotic cell death, was upregulated in EV-A71-infected neurons but not in CV-A16 infection, suggesting that the AIM2 inflammasome played a significant role in suppressing EV-A71 replication. Chimeric viruses derived from CV-A16 and EV-A71 but containing swapped 5′ nontranslated regions (5′ NTRs) showed that RSAD2 expression/viral replication and AIM2 expression/viral replication patterns may be linked to the 5′ NTRs of parental viruses. Differences in secondary structure of internal ribosomal entry sites within the 5′ NTR may be responsible for these findings. Overall, our results suggest that CV-A16 and EV-A71 elicit different host responses to infection, which may help explain the apparent lower incidence of CV-A16-associated neurovirulence in HFMD outbreaks compared to EV-A71 infection. IMPORTANCE Although coxsackievirus A16 (CV-A16) and enterovirus A17 (EV-A71) both cause hand, foot, and mouth disease, EV-A71 has emerged as a leading cause of nonpolio, enteroviral fatal encephalomyelitis among young children. The significance of our research is in the identification of the possible differing and novel mechanisms of CV-A16 and EV-A71 inhibition in neuronal cells that may impact viral neuropathogenesis. We further showed that viral 5′ NTRs may play significant roles in eliciting different host response mechanisms.

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