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Role of interferon in persistent infection of macrophages with herpes simplex virus

Virology
|August 1, 1987
PubMed

Insights

Macrophages from resistant mice can harbor persistent herpes simplex virus (HSV) infections, with interferon (IFN) playing a role in maintaining the infection. This highlights genetically controlled macrophage properties in HSV persistence.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Herpes simplex virus (HSV) infection outcomes vary significantly between mouse strains.
  • Macrophages play a crucial role in the immune response to viral infections.

Purpose of the Study:

  • To investigate the susceptibility of splenic macrophages from different mouse strains to HSV infection.
  • To elucidate the mechanisms underlying persistent HSV infection in macrophages.

Main Methods:

  • In vitro culture of splenic macrophages from C57BL/6 (resistant) and DBA/2 (susceptible) mice.
  • Infection of macrophage cultures with HSV.
  • Assessment of viral DNA replication, viral antigen expression, and infectious virus production.
  • Interferon (IFN) involvement was studied using anti-IFN serum and (2'-5')oligoadenylate synthetase activity.

Main Results:

  • Macrophages from resistant C57BL/6 mice survived HSV infection in vitro, establishing persistent infections with infectious virus production.
  • Macrophages from susceptible DBA/2 mice were lysed by HSV.
  • Interferon (IFN) was found to be involved in maintaining the persistent HSV infection in C57BL/6 macrophages.
  • While viral DNA replication was initially similar, later stages showed decreased viral DNA and antigen expression in C57BL/6 macrophages, with some cells retaining viral protein expression and particle production.

Conclusions:

  • Macrophages possess genetically determined properties that allow for persistent herpes simplex virus (HSV) infection.
  • Interferon (IFN) is implicated in the maintenance of HSV persistence within macrophages.
  • Macrophage susceptibility and response to HSV are influenced by host genetic factors.

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