Role of IL-6 and IL-1beta in reactivation by acetylcholine of latently infecting pseudorabies virus.
We previously reported that the latently infecting Pseudorabies virus (PrV) could be reactivated by injection of swine or mice with acetylcholine. However, the mechanism of the reactivation was not clear yet. In this study, we analyzed the kinetics of cytokines related to stress to clarify the relationship between virus reactivation by acetylcholine and the immune system. IL-6 and IL-1beta were detected in mice after stimulation with acetylcholine. This shows that acetylcholine induced physiological stress conditions. However, there seemed to be no relationship between the kinetics of the cytokine levels and PrV excretion. Moreover, neither IL-6 nor IL-1beta alone could reactivate latently infecting PrV. Thus, acetylcholine causes the reactivation of latent PrV via a mechanism not involving these immunological factors.
Tanaka
Seiichi
S
Division of Laboratory Animal Sciences, Department of Life Science, Institute of Scientific Research, Oita University, Japan.
Mannen
Kazuaki
K
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D002478:Cells, Cultured; D011558:Herpesvirus 1, Suid / Q000502:physiology*; D007375:Interleukin-1 / Q000502:physiology*; D015850:Interleukin-6 / Q000502:physiology*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D013552:Swine; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology; D014775:Virus Activation / Q000187:drug effects* / Q000276:immunology; D017735:Virus Latency / Q000187:drug effects* / Q000276:immunology
D007375:Interleukin-1; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D000109:Acetylcholine