A herpes simplex virus type 1 mutant containing a deletion within immediate early gene 1 is latency-competent in mice

Area of Science:

• Virology
• Immunology
• Neuroscience

Background:

• Herpes simplex virus type 1 (HSV-1) establishes lifelong latent infections.
• The immediate early protein Vmw110 plays a role in HSV-1 replication and pathogenesis.
• Understanding viral latency mechanisms is crucial for developing antiviral therapies.

Purpose of the Study:

• To investigate the role of the Vmw110 polypeptide in HSV-1 virulence, latency, and reactivation.
• To characterize the behavior of HSV-1 mutant dl1403 in a mouse model.

Main Methods:

• Infection of mice with HSV-1 mutant dl1403 via intracranial and footpad routes.
• Assessment of viral virulence and neuroinvasion.
• Detection of latent viral infection in sensory ganglia.
• Induction of viral reactivation by explantation.

Main Results:

• HSV-1 mutant dl1403 exhibited reduced virulence compared to wild-type virus.
• The mutant virus successfully reached the spinal cord and established latency in sensory ganglia.
• Spontaneous viral reactivation was observed upon explantation of infected ganglia.

Conclusions:

• The Vmw110 polypeptide is dispensable for the establishment and maintenance of HSV-1 latency.
• Vmw110 is not required for HSV-1 reactivation from a latent state in sensory ganglia.
• These findings contribute to understanding HSV-1 latency and pathogenesis.