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Herpes simplex virus type 1 (HSV-1) UL56 gene is involved in viral intraperitoneal pathogenicity to immunocompetent
C Berkowitz1, M Moyal, A Rösen-Wolff
1Department of Molecular Virology, Faculty of Medicine, Hebrew University of Jerusalem, Israel.
Abstract:
A comparison of the pathogenicity in mice of the recombinant herpes simplex virus type 1 (HSV-1) strain HSV-1-M-LacZ, in which the UL56 gene has been deleted, was made with its parental strain F, following infection in different mouse strains. The polymerase chain reaction (PCR) technique was used to study the migration of virus DNA in the mouse model. Tissues from adult mice infected intraperitoneally (IP) with one of three HSV-1 strains (F, HFEM or HSV-1-LacZ) were examined for the presence of viral DNA. DNA of the pathogenic strain F was detected in the adrenal glands, spinal cord, brain, liver and pancreas. DNA of HSV-1-M-LacZ was detected in the same tissues. However, DNA of the apathogenic strain HFEM was detected transiently (on days 2 and 3 p.i., but 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 injected 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 UL56 gene, resembled in pathogenicity to the newborn mice the pathogenic HSV-1 strains F and KOS. The PCR technique was used to trace viral DNA 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 may reside in surviving HSV-1- infected newborn mice in a "latent" state in nonneural tissues.
Insights
Herpes simplex virus type 1 (HSV-1) pathogenicity was compared in mice. Deleting the UL56 gene in HSV-1-M-LacZ did not affect pathogenicity, suggesting viral DNA may persist in nonneural tissues.
Area of Science:
- Virology
- Immunology
- Genetics
Background:
- Herpes simplex virus type 1 (HSV-1) is a significant human pathogen.
- Understanding HSV-1 pathogenicity and latency is crucial for developing effective treatments.
Purpose of the Study:
- To compare the pathogenicity of a recombinant HSV-1 strain (HSV-1-M-LacZ) lacking the UL56 gene with its parental strain.
- To investigate the tissue distribution and potential for latency of different HSV-1 strains in mice.
Main Methods:
- Recombinant and parental HSV-1 strains were used to infect different mouse strains.
- Polymerase chain reaction (PCR) was employed to detect viral DNA in various tissues.
- Pathogenicity was assessed by survival rates and viral DNA presence in surviving mice.
Main Results:
- The recombinant HSV-1-M-LacZ strain showed similar pathogenicity to pathogenic strains (F and KOS) in newborn mice.
- Viral DNA from pathogenic strains was detected in multiple organs, including the brain and spinal cord.
- The apathogenic strain HFEM showed transient DNA presence only in adrenal glands.
Conclusions:
- The UL56 gene deletion did not attenuate HSV-1 pathogenicity in this mouse model.
- HSV-1 DNA was detected in various tissues, suggesting potential for systemic spread.
- Evidence suggests that HSV-1 DNA may establish a latent state in nonneural tissues of surviving mice.