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[Induction of messenger RNA of cytokines by Herpes simplex virus infection in mice].

Abstract
The induction of the cytokine mRNA after infection with Herpes simplex virus (HSV) was studied using RT-PCR method capable of detecting low levels of mRNA. Total RNA was prepared from spleen lymphocytes 3 h after infection with HSV-1 (+GC virulent variant and -GCr attenuated variant of Miyama strain) by acid guanidinium thiocyanate-phenol-chloroform (AGPC) method. cDNA was synthesized by M-MLV reverse transcriptase, and amplified using the specific oligonucleotide primers for IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, TNF-alpha, IFN-alpha, IFN-beta and IFN-gamma by PCR method. After HSV-1 infection, IFN-alpha, IFN-beta, IFN-gamma, IL-1 beta, IL-4, IL-6 and TNF-alpha mRNA were significantly induced, but IL-2, IL-3 and IL-5 mRNA were not induced. Although IFN-alpha, IFN-gamma and IL-6 mRNA were more strongly induced by infection with +GC virulent variant than -GCr attenuated variant, there was no significant difference in the expression of other cytokine mRNA between two variants. These results demonstrate that cytokine mRNA in addition to IFN was induced by HSV infection, and suggest that cytokines as well as IFNs may play a role in the defense mechanism against HSV infection.
AuthorsM Kita, L J Tong, J Imanishi
JournalComptes rendus des seances de la Societe de biologie et de ses filiales (C R Seances Soc Biol Fil) Vol. 187 Issue 4 Pg. 561-8 ( 1993) ISSN: 0037-9026 [Print] France
Vernacular TitleInduction de l'ARN messager des cytokines par l'infection de l'Herpès simplex virus chez la souris.
PMID7517338 (Publication Type: English Abstract, Journal Article)
Chemical References
  • Cytokines
  • Interleukins
  • RNA, Messenger
  • Interferons
Topics
  • Animals
  • Cytokines (metabolism)
  • Disease Models, Animal
  • Female
  • Herpes Simplex (metabolism)
  • Interferons (metabolism)
  • Interleukins (metabolism)
  • Lymphocytes (metabolism)
  • Mice
  • Mice, Inbred BALB C
  • Polymerase Chain Reaction
  • RNA, Messenger (metabolism)
  • Spleen (immunology)

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