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MS strain of type 2 herpes simplex virus produces necrotizing retinitis in mice

S Love1, T J Hill, N J Maitland

  • 1Department of Pathology & Microbiology, University of Bristol, UK.

Insights

Herpes simplex virus type 2 (HSV-2) infection in mice causes encephalitis and significant ocular disease, including impaired pupillary light reflex and necrotizing retinitis. This study details the progression of HSV-2 ocular pathology in mice.

Area of Science:

  • Neurovirology
  • Ophthalmology
  • Immunology

Background:

  • Herpes simplex virus type 2 (HSV-2) intracerebral inoculation in mice leads to encephalitis and central nervous system demyelination.
  • Ocular manifestations, such as pupillary light reflex impairment, are common sequelae in HSV-2 infected mice.

Purpose of the Study:

  • To investigate the development and characteristics of ocular disease following intracerebral inoculation of HSV-2 (MS strain) in NIH mice.
  • To determine the temporal progression of viral presence and pathological changes in ocular tissues.

Main Methods:

  • Intracerebral inoculation of inbred NIH mice with a low dose (10 pfu) of HSV-2 (MS strain).
  • Monitoring of encephalitis, pupillary light reflex, and mortality rates.
  • Isolation of infectious virus, immunohistochemical detection of viral antigen, and electron microscopy in ocular tissues and nervous system.
  • Histopathological examination of eyes, optic nerves, trigeminal ganglia, and brain.

Main Results:

  • Acute encephalitis was fatal in 30-50% of mice; 80% of survivors showed impaired pupillary response by 1 month.
  • Infectious HSV-2 was isolated from eyes by day 4 and viral antigen detected in optic nerves (day 5) and retinae (day 6).
  • Necrotizing retinitis developed in up to half of mice during the second week, with high viral titers and antigen presence in the retina.
  • Viral particles were confirmed in retinal glia and degenerating neurons via electron microscopy.
  • Infectious virus persisted longer in eyes than in trigeminal ganglia or optic nerves, with titers declining to undetectable levels by 1 month.

Conclusions:

  • Intracerebral HSV-2 infection in mice induces significant ocular pathology, including retinitis and visual reflex impairment.
  • The eyes serve as a significant site for HSV-2 replication and persistence following central nervous system inoculation.
  • Understanding the pathogenesis of HSV-2 ocular disease is crucial for developing effective therapeutic strategies.

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