Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 565-572 |
| Number of pages | 8 |
| Journal | Journal of General Virology |
| Volume | 79 |
| Issue number | 3 |
| Publication status | Published - Mar 1998 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Virology
- Immunology
Cite this
The BglII-N fragment of herpes simplex virus type 2 contains a region responsible for resistance to antiviral effects of interferon. / Narita, Masaya; Ando, Yasutaka; Soushi, Sumi; Kurata, Takeshi; Arao, Yujiro.
In: Journal of General Virology, Vol. 79, No. 3, 03.1998, p. 565-572.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The BglII-N fragment of herpes simplex virus type 2 contains a region responsible for resistance to antiviral effects of interferon
AU - Narita, Masaya
AU - Ando, Yasutaka
AU - Soushi, Sumi
AU - Kurata, Takeshi
AU - Arao, Yujiro
PY - 1998/3
Y1 - 1998/3
N2 - 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.
AB - 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.
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UR - http://www.scopus.com/inward/citedby.url?scp=0031929191&partnerID=8YFLogxK
M3 - Article
C2 - 9519835
AN - SCOPUS:0031929191
VL - 79
SP - 565
EP - 572
JO - Journal of General Virology
JF - Journal of General Virology
SN - 0022-1317
IS - 3
ER -