We report the construction of a deletion mutant (del22Z) that is unabl
e to synthesize any detectable messenger RNA or protein products from
the herpes simplex virus type 1 (HSV-1) immediate early ICP22 gene upo
n infection. The del22Z deletion mutant lacks all but 18 nucleotides o
f the ICP22 coding sequence and carries the bacterial lacZ gene at the
site of the deletion. No other known open reading frames or flanking
sequences were disrupted. Del22Z was able to infect Vero cells product
ively but was severely restricted in human and rodent cells that were
permissive for the parental HSV-1(F). The yield of del22Z was not enha
nced significantly, either by increasing the multiplicity of infection
or by increasing the duration of the infection. There was a prolonged
expression of some early gene products and a delayed appearance of so
me late gene products in both permissive and restrictive cells. This p
henotype of cell-line restricted growth and alteration of the normal g
ene expression cascade maps specifically to the ICP22 coding region.