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
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 -