TY - JOUR
T1 - Complementation of vaccinia virus deleted of the E3L gene by mutants of E3L
AU - Shors, Teri
AU - Kibler, Karen
AU - Perkins, Kim B.
AU - Seidler-Wulff, Renee
AU - Banaszak, Matthew P.
AU - Jacobs, Bertram
N1 - Funding Information:
We thank Jim Tartaglia for providing the virus stocks of VVDE3L and wtVV and the transfer vector pMPE3LDGPT#748. We also thank Cruz Lotz for assistance in preparing the manuscript. This work was supported by Public Health Service Grant CA-48654 from the National Cancer Institute, Contract CNTR 9610 from the Arizona Disease Control Research Commission and Grant VM-151 from the American Cancer Society. T. Shors and K. Kibler were also supported by the ARCS foundation (T.S. sponsored by Millie Windrow).
PY - 1997/12/22
Y1 - 1997/12/22
N2 - Vaccinia virus devoid of its E3L gene is sensitive to treatment of RK- 13 cells with interferon-α and fails to replicate or form plaques in HeLa cells. In order to determine function of the E3L gene, vaccinia virus recombinants were constructed by inserting mutant E3L genes or a gene coding for an alternative dsRNA-binding protein into virus deleted of its wild type E3L gene. Those viruses that expressed proteins that retained dsRNA binding activity were resistant to the effects of interferon in RK-13 cells and could replicate in HeLa cells. Recombinant viruses that expressed E3L mutant proteins which were unable to bind to dsRNA were interferon sensitive in RK- 13 cells and could not replicate in HeLa cells. In addition, a virus that expressed a mutant E3L protein previously characterized as having a low binding affinity for dsRNA exhibited an intermediate phenotype: it was interferon resistant in RK-13 cells but could not replicate in HeLa cells. This work suggests that the E3L gene of vaccinia virus functions primarily as a dsRNA-binding protein in allowing resistance to interferon and in promoting replication in HeLa cells.
AB - Vaccinia virus devoid of its E3L gene is sensitive to treatment of RK- 13 cells with interferon-α and fails to replicate or form plaques in HeLa cells. In order to determine function of the E3L gene, vaccinia virus recombinants were constructed by inserting mutant E3L genes or a gene coding for an alternative dsRNA-binding protein into virus deleted of its wild type E3L gene. Those viruses that expressed proteins that retained dsRNA binding activity were resistant to the effects of interferon in RK-13 cells and could replicate in HeLa cells. Recombinant viruses that expressed E3L mutant proteins which were unable to bind to dsRNA were interferon sensitive in RK- 13 cells and could not replicate in HeLa cells. In addition, a virus that expressed a mutant E3L protein previously characterized as having a low binding affinity for dsRNA exhibited an intermediate phenotype: it was interferon resistant in RK-13 cells but could not replicate in HeLa cells. This work suggests that the E3L gene of vaccinia virus functions primarily as a dsRNA-binding protein in allowing resistance to interferon and in promoting replication in HeLa cells.
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U2 - 10.1006/viro.1997.8881
DO - 10.1006/viro.1997.8881
M3 - Article
C2 - 9434718
AN - SCOPUS:0031583869
SN - 0042-6822
VL - 239
SP - 269
EP - 276
JO - Virology
JF - Virology
IS - 2
ER -