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Persistent infection of human fibroblasts by hepatitis A virus
Abstract:
Infection of human embryo fibroblasts with hepatitis A virus (HAV), a picornavirus, leads to an inapparent, persistent infection; cultures can be passed serially with consistent recovery of the virus in the supernatant. All of the cells of a HAV carrier culture are infected and proliferate. Subcultivation under HAV-immune serum cannot achieve a cure or even a reduction in the number of infected cells in HAV carrier cultures. No interferon activity can be detected during HAV infection and persistence. Addition of exogenous interferon eliminates HAV infection in vitro. Persistence of HAV in vitro appears to contradict the clinical course of HAV infection in vivo. The system presented offers the possibility of evaluating the role of immunological injury of HAV-infected cells, an injury which may lead to damage of these cells and to elimination of HAV during an HAV infection in vivo.
Insights
Hepatitis A virus (HAV) establishes persistent infections in human cells, unaffected by immune serum but cleared by exogenous interferon. This in vitro model may explain in vivo HAV clearance through immune-mediated cell damage.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Hepatitis A virus (HAV) causes persistent, inapparent infections in human embryo fibroblasts.
- HAV-infected cells proliferate, maintaining a carrier state resistant to immune serum.
- No endogenous interferon activity is detected during persistent HAV infection.
Purpose of the Study:
- To investigate the mechanisms of persistent Hepatitis A virus infection in vitro.
- To explore the potential of interferon in clearing HAV infection.
- To establish a model for studying immune-mediated HAV clearance in vivo.
Main Methods:
- Serial passage of HAV-infected human embryo fibroblast cultures.
- Treatment of cultures with HAV-immune serum.
- Assay for interferon activity.
- In vitro treatment with exogenous interferon.
- Comparison of in vitro persistence with in vivo clinical course.
Main Results:
- HAV established persistent infections in fibroblast cultures, with virus consistently recovered.
- Immune serum failed to cure or reduce infected cell numbers.
- No detectable interferon activity was observed during persistent infection.
- Exogenous interferon effectively eliminated HAV infection in vitro.
- In vitro persistence contrasted with in vivo clinical outcomes.
Conclusions:
- Persistent HAV infection in vitro is resistant to immune serum but sensitive to exogenous interferon.
- The in vitro model suggests immune-mediated cell injury may be crucial for HAV elimination in vivo.
- This system provides a platform for evaluating the role of immunological damage in resolving HAV infections.