J Gen Virol Tips for Better Browsing
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Narita, M.
Right arrow Articles by Arao, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Narita, M.
Right arrow Articles by Arao, Y.
Agricola
Right arrow Articles by Narita, M.
Right arrow Articles by Arao, Y.

Journal of General Virology, Vol 79, 565-572, Copyright © 1998 by Society for General Microbiology

ARTICLES

The BglII-N fragment of herpes simplex virus type 2 contains a region responsible for resistance to antiviral effects of interferon

M Narita, Y Ando, S Soushi, T Kurata and Y Arao
Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.

Double infection with two interferon (IFN)-sensitive strains of herpes simplex virus (HSV), HSV-1(17syn) and HSV-2(UW268), showed reduced inhibition of virus growth by IFN. Intertypic recombinants with IFN resistance were obtained from the doubly infected cultures. These results indicate that HSV IFN resistance is controlled by at least two genetic regions. Restriction endonuclease analysis demonstrated that the recombinants were similar to HSV-2 in their genomic structure but the BamHI-A, BglII-I and BglII-N fragments of HSV-2 were commonly lost in the recombinants, suggesting that any of these fragments could be associated with HSV-2 IFN resistance. We cloned these fragments and BamHI-E, which overlaps BglII-N, from an IFN-resistant HSV-2 strain, HSV-2(G), and examined each fragment for its ability to rescue IFN resistance of HSV-2(UW268) by co-transfecting with the HSV-2(UW268) genome. Of the HSV-2(G) fragments, only BglII-N increased plating efficiency of progeny viruses in IFN-treated cells. An IFN-resistant HSV-2 clone was obtained from the BglII-N of HSV-2(G) and HSV-2(UW268) genome co-transfected culture, and a part of BglII-N of HSV-2(UW268) was replaced with that of HSV-2(G) in the HSV-2 clone. Thus, it was concluded that one of the HSV regions encoding IFN resistance is located on the BglII-N fragment of HSV-2.


This article has been cited by other articles:


Home page
 J. Virol.Home page
J. A. Murphy, R. J. Duerst, T. J. Smith, and L. A. Morrison
Herpes Simplex Virus Type 2 Virion Host Shutoff Protein Regulates Alpha/Beta Interferon but Not Adaptive Immune Responses during Primary Infection In Vivo
J. Virol., September 1, 2003; 77(17): 9337 - 9345.
[Abstract] [Full Text] [PDF]

Home page
 JEMHome page
D. A. Leib, T. E. Harrison, K. M. Laslo, M. A. Machalek, N. J. Moorman, and H. W. Virgin
Interferons Regulate the Phenotype of Wild-type and Mutant Herpes Simplex Viruses In Vivo
J. Exp. Med., February 15, 1999; 189(4): 663 - 672.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL MICROBIOLOGY J GEN VIROL
J MED MICROBIOL ALL SGM JOURNALS
Copyright © 1998 by the Society for General Microbiology.