Wild-type rabies virus phosphoprotein is associated with viral sensitivity to type I interferon treatment

Wild-type rabies virus phosphoprotein is associated with viral sensitivity to type I interferon... Rabies virus (RABV) is a single-stranded, negative-sense RNA virus that causes a fatal neurological disease in humans and animals. Our previous studies have shown that lab-adapted, but not wild-type (wt), RABV enhances innate immune responses including type I interferon (IFN) and chemokines. To determine if treatment with type I IFN can inhibit RABV infection, mouse neuroblastoma and baby hamster kidney cells were treated with IFN-α before being infected with lab-adapted or wt RABV. It was found that lab-adapted, but not the wt, RABV was able to replicate in IFN-α-pretreated cells. To determine the genes in wt RABV that confer sensitivity to IFN-α treatment, the P and the glycoprotein (G) genes from the wt RABV were used to replace the respective genes in the lab-adapted RABV. The results revealed that it is the P, not the G, gene that is associated with IFN sensitivity. Further studies have identified the regions containing the self-association domain (residues 59-139) and the C-terminal (residue 175-297) region on the P that might be associated with IFN sensitivity. The expression of ISGs, such as ISG15, ISG56, PKR, OAS-1G, was also investigated and found to be greatly increased in wt, but not in lab-adapted RABV-infected cells. It is possible that the P protein from the lab-adapted RABV can interfere with the downstream events in the interferon-signaling cascade. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

Wild-type rabies virus phosphoprotein is associated with viral sensitivity to type I interferon treatment

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Publisher
Springer Journals
Copyright
Copyright © 2013 by Springer-Verlag Wien
Subject
Biomedicine; Virology; Medical Microbiology; Infectious Diseases
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s00705-013-1743-2
Publisher site
See Article on Publisher Site

Abstract

Rabies virus (RABV) is a single-stranded, negative-sense RNA virus that causes a fatal neurological disease in humans and animals. Our previous studies have shown that lab-adapted, but not wild-type (wt), RABV enhances innate immune responses including type I interferon (IFN) and chemokines. To determine if treatment with type I IFN can inhibit RABV infection, mouse neuroblastoma and baby hamster kidney cells were treated with IFN-α before being infected with lab-adapted or wt RABV. It was found that lab-adapted, but not the wt, RABV was able to replicate in IFN-α-pretreated cells. To determine the genes in wt RABV that confer sensitivity to IFN-α treatment, the P and the glycoprotein (G) genes from the wt RABV were used to replace the respective genes in the lab-adapted RABV. The results revealed that it is the P, not the G, gene that is associated with IFN sensitivity. Further studies have identified the regions containing the self-association domain (residues 59-139) and the C-terminal (residue 175-297) region on the P that might be associated with IFN sensitivity. The expression of ISGs, such as ISG15, ISG56, PKR, OAS-1G, was also investigated and found to be greatly increased in wt, but not in lab-adapted RABV-infected cells. It is possible that the P protein from the lab-adapted RABV can interfere with the downstream events in the interferon-signaling cascade.

Journal

Archives of VirologySpringer Journals

Published: Nov 1, 2013

References

  • An improved method for recovering rabies virus from cloned cDNA
    Inoue, K; Shoji, Y; Kurane, I; Iijima, T; Sakai, T; Morimoto, K
  • Role of chemokines in the enhancement of BBB permeability and inflammatory infiltration after rabies virus infection
    Kuang, Y; Lackay, SN; Zhao, L; Fu, ZF
  • Interferon-inducible protein, P56, inhibits HPV DNA replication by binding to the viral protein E1
    Terenzi, F; Saikia, P; Sen, GC
  • Rabies virus glycoprotein is an important determinant for the induction of innate immune responses and the pathogenic mechanisms
    Zhang, G; Wang, H; Mahmood, F; Fu, ZF

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