Response to Joob and Wiwanitkit re: “Genetic Polymorphisms of Tumor Necrosis Factor Alpha and Susceptibility to Dengue Virus Infection in a Mexican Population”

2017 ◽  
Vol 30 (9) ◽  
pp. 679-679
Author(s):  
Jesús Salvador Velarde-Félix ◽  
Juan Fidel Osuna-Ramos
Keyword(s):  
Tumor Necrosis Factor ◽  
Virus Infection ◽  
Dengue Virus ◽  
Genetic Polymorphisms ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Dengue Virus Infection ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Genetic Polymorphisms of Tumor Necrosis Factor Alpha and Susceptibility to Dengue Virus Infection in a Mexican Population

2017 ◽  
Vol 30 (8) ◽  
pp. 615-621 ◽  
Author(s):  
Marina Sánchez-Leyva ◽  
Jorge Guillermo Sánchez-Zazueta ◽  
Juan Fidel Osuna-Ramos ◽  
Horacio Rendón-Aguilar ◽  
Rafael Félix-Espinoza ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Virus Infection ◽  
Dengue Virus ◽  
Genetic Polymorphisms ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Dengue Virus Infection ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with schizophrenia

2017 ◽  
Vol Volume 13 ◽  
pp. 1081-1088 ◽  
Author(s):  
Saeed Kadasah ◽  
Misbahul Arfin ◽  
Sadaf Rizvi ◽  
Mohammed Al-Asmari ◽  
Abdulrahman Al-Asmari
Keyword(s):  
Risk Factor ◽  
Tumor Necrosis Factor ◽  
Genetic Polymorphisms ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor ◽  
Saudi Patients

scholarly journals Dengue Virus (DV) Replication in Monocyte-Derived Macrophages Is Not Affected by Tumor Necrosis Factor Alpha (TNF-α), and DV Infection Induces Altered Responsiveness to TNF-α Stimulation

2007 ◽  
Vol 81 (18) ◽  
pp. 10161-10171 ◽  
Author(s):  
Satiya Wati ◽  
Peng Li ◽  
Christopher J. Burrell ◽  
Jillian M. Carr
Keyword(s):  
Tumor Necrosis Factor ◽  
Dengue Virus ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Progeny Virus ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Huh7 Cells ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Tumor necrosis factor alpha (TNF-α) is believed to play a significant role in the pathogenesis of dengue virus (DV) infection, with elevated levels of TNF-α in the sera of DV-infected patients paralleling the severity of disease and TNF-α release being coincident with the peak of DV production from infected monocyte-derived macrophages (MDM) in vitro. Since macrophages are a primary cell target in vivo for DV infection, we investigated the potential antiviral role of TNF-α in regulating DV replication in MDM. While pretreatment of MDM with TNF-α had a minor inhibitory effect, addition of TNF-α to MDM with established DV infection had no effect on DV replication as measured by DV RNA levels or progeny virus production. Blocking endogenous TNF-α using short interfering RNA or inhibitory TNF-α antibodies also had no effect on infectious DV production or viral RNA synthesis. Together, these results demonstrate that DV replication in MDM is not affected by TNF-α. Additionally, normal cellular TNF-α signaling, measured by quantitation of TNF-α-induced stimulation of transcription from an NF-κB-responsive reporter plasmid or NF-κB protein nuclear translocation, was blocked in DV-infected MDM and Huh7 cells. Thus, DV replication in MDM is not affected by TNF-α, and infected cells do not respond normally to TNF-α stimulation. It is therefore unlikely that the increased production of TNF-α seen in DV infection directly effects DV clearance by reducing DV replication, and the ability of DV to alter TNF-α responsiveness highlights another example of viral subversion of cellular functions.

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