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Neurovirulent strains of herpes simplex virus type 1 are not necessarily competent for reactivatable latency
Abstract:
Ability of two neurovirulent strains (F and +GC (LPV) Miyama) of herpes simplex virus type 1 (HSV-1) to establish and maintain reactivatable latency in trigeminal ganglia (TG) was compared after intranasal inoculation of mice. The +GC (LPV) Miyama strain showed a very low rate of virus reactivation in explant cultures of TG, while the F strain showed a high rate of reactivation. These data indicate that neurovirulent strains of HSV-1 are not always competent for reactivatable latency, although most virulent strains of HSV-1 thus far reported were competent for reactivatable latency.
Insights
Neurovirulent herpes simplex virus type 1 (HSV-1) strains differ in their ability to establish latent infections. The F strain reactivated readily from trigeminal ganglia, unlike the +GC (LPV) Miyama strain.
Area of Science:
- Virology
- Neuroscience
- Immunology
Background:
- Herpes simplex virus type 1 (HSV-1) establishes lifelong latency, primarily in sensory neurons.
- Reactivation of latent HSV-1 from trigeminal ganglia (TG) causes recurrent disease.
- The relationship between HSV-1 neurovirulence and the ability to establish reactivatable latency is not fully understood.
Purpose of the Study:
- To compare the ability of two neurovirulent HSV-1 strains (F and +GC (LPV) Miyama) to establish and maintain reactivatable latency in mouse TG.
- To investigate if neurovirulence correlates with the capacity for viral reactivation from latency.
Main Methods:
- Intranasal inoculation of mice with neurovirulent HSV-1 strains F and +GC (LPV) Miyama.
- Explant cultures of trigeminal ganglia (TG) to assess HSV-1 reactivation.
- Quantification of viral reactivation rates.
Main Results:
- The F strain demonstrated a high rate of HSV-1 reactivation from TG.
- +GC (LPV) Miyama strain exhibited a very low rate of virus reactivation.
- Significant differences in reactivatable latency were observed between the two neurovirulent strains.
Conclusions:
- Neurovirulent HSV-1 strains are not uniformly competent for establishing reactivatable latency.
- The capacity for reactivation from latency may be strain-dependent, irrespective of neurovirulence.
- These findings challenge the assumption that highly virulent HSV-1 strains are always capable of maintaining reactivatable latency.