TY - JOUR
T1 - Virulence of and establishment of latency by genetically engineered deletion mutants of herpes simplex virus I
AU - Meignier, Bernard
AU - Longnecker, Richard
AU - Mavromara-Nazos, Penelope
AU - Sears, Amy E.
AU - Roizman, Bernard
N1 - Funding Information:
We thank Marie-Clothilde Bernard and Demetra Lagen for expert technical assistance. The studies at the University of Chicago were aided by Public Health Service Grants CA08494, CA19264, Al24009 and by the American Cancer Society Grant MV-2R. Additional support was provided by lnstitut Merieux. R.L. was a predoctoral trainee supported by PHS Training Grant T32 Al07 182 from the National Institute of Allergy and Infectious Diseases. P.M.N. was a Damon Runyon postdoctoral fellow (DRG767).
PY - 1988/1
Y1 - 1988/1
N2 - We report the results of studies on the biologic properties of seven deletion mutants of herpes simplex virus 1 (HSV-1). The genes deleted from six of these mutants map in the S component of HSV-1 DNA and include those specifying the α protein 47, the glycoproteins G and E, the viral protein kinase, and two proteins whose functions are not yet known (open reading frames US2 and US11). The seventh virus [HSV-1(F)Δ305] contained a 700-bp deletion in the thymidine kinase gene. The results of intracerebral inoculation of Balb/c mice indicated that all but one of the deletion mutants in the S component were significantly attenuated. The PFU/LD50 ratios for these mutants ranged from 104- to 105-fold higher than that of the wild-type, HSV-1(F). The PFU/LD50 for mutant R7032, from which the glycoprotein E gene had been deleted, was less than 100-fold higher than that of the parent virus. All of the mutants, with one exception, were able to establish latency in mice; the exception, HSV-1(F)Δ305, was able to establish latency in rabbits.
AB - We report the results of studies on the biologic properties of seven deletion mutants of herpes simplex virus 1 (HSV-1). The genes deleted from six of these mutants map in the S component of HSV-1 DNA and include those specifying the α protein 47, the glycoproteins G and E, the viral protein kinase, and two proteins whose functions are not yet known (open reading frames US2 and US11). The seventh virus [HSV-1(F)Δ305] contained a 700-bp deletion in the thymidine kinase gene. The results of intracerebral inoculation of Balb/c mice indicated that all but one of the deletion mutants in the S component were significantly attenuated. The PFU/LD50 ratios for these mutants ranged from 104- to 105-fold higher than that of the wild-type, HSV-1(F). The PFU/LD50 for mutant R7032, from which the glycoprotein E gene had been deleted, was less than 100-fold higher than that of the parent virus. All of the mutants, with one exception, were able to establish latency in mice; the exception, HSV-1(F)Δ305, was able to establish latency in rabbits.
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U2 - 10.1016/0042-6822(88)90417-5
DO - 10.1016/0042-6822(88)90417-5
M3 - Article
C2 - 2827384
AN - SCOPUS:0023845903
VL - 162
SP - 251
EP - 254
JO - Virology
JF - Virology
SN - 0042-6822
IS - 1
ER -