HERPES-SIMPLEX VIRUS TYPE-1 (HSV-1) U(L)56 GENE IS INVOLVED IN VIRAL INTRAPERITONEAL PATHOGENICITY TO IMMUNOCOMPETENT MICE

A comparison of the pathogenicity in mice of the recombinant herpes si mplex virus type 1 (HSV-1) strain HSV-1-M- LacZ, in which the U(L)56 g ene has been deleted, was made with its parental strain F, following i nfection in different mouse strains. The polymerase chain reaction (PC R) technique was used to study the migration of virus DNA in the mouse model. Tissues from adult mice infected intraperitoneally (IP) with o ne of three HSV-1 strains (F, HFEM or HSV-1-LacZ) were examined for th e presence of viral DNA. DNA of the pathogenic strain F was detected i n the adrenal glands, spinal cord, brain, liver and pancreas. DNA of H SV-1-M-LacZ was detected in the same tissues. However, DNA of the apat hogenic strain HFEM was detected transiently (on days 2 and 3 p.i., bu t not days 1, 5 or 7), only in the adrenal glands and no viral DNA was detected in any of the other tissues. HSV-1 pathogenic strains inject ed intraperitoneally into newborn mice (7 days old) killed most of the mice. In the surviving mice viral DNA of the three virus strains was found in peritoneal exudate cells (PEC), adrenal glands, spinal cord, liver and spleen. It was found that HSV-1-M-LacZ, which lacks the U(L) 56 gene, resembled in pathogenicity to the newborn mice the pathogenic HSV-1 strains F and KOS. The PCR technique was used to trace viral DN A in tissues of the mice which survived HSV-1 infection at 7 weeks of age. Only HSV-1 (KOS) DNA was detected in the pancreas. The brains of these mice did not contain viral DNA. It is suggested that HSV-1 DNA m ay reside in surviving HSV-1- infected newborn mice in a ''latent'' st ate in nonneural tissues.