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Impaired immune responsiveness is an essential component in persistent central nervous system infection with gross
J M Korostoff1, M T Nakada, J F Markman
1Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia 19104.
Abstract:
Exposure of newborn mice to Gross murine leukemia virus (GMuLV) results in persistent viral infection of the central nervous system (CNS) white matter. Animals exposed to virus as neonates showed a marked depression in GMuLV-specific B lymphocyte function as evidenced by significant decreases in adult and neonatal anti-GMuLV antibody levels. Immunohistochemical analyses showed that the sites of GMuLV infection in the CNS were also devoid of major histocompatibility complex (MHC) class I and II protein expression, although transplantation of GMuLV-infected brain tissue to the kidney capsules of immunocompetent mice induced a potent mononuclear cell graft infiltrate. These results indicate that persistent GMuLV infection of the CNS is linked to both impairment of anti-GMuLV peripheral immune responses and deficient antigen-presenting cell function within the CNS.
Insights
Persistent Gross murine leukemia virus (GMuLV) infection in newborn mice impairs immune responses. The central nervous system (CNS) shows reduced B lymphocyte function and antigen-presenting cell activity.
Area of Science:
- Virology
- Immunology
- Neuroscience
Background:
- Gross murine leukemia virus (GMuLV) infection in newborns establishes persistent central nervous system (CNS) white matter infection.
- Neonatal viral exposure can lead to long-term immune dysregulation.
Purpose of the Study:
- To investigate the immunological consequences of persistent GMuLV infection in the CNS.
- To determine the impact on B lymphocyte function and antigen-presenting cell activity.
Main Methods:
- Exposure of newborn mice to GMuLV.
- Assessment of anti-GMuLV antibody levels.
- Immunohistochemical analysis of CNS tissue for viral infection and major histocompatibility complex (MHC) expression.
- Grafting of infected CNS tissue into immunocompetent mice.
Main Results:
- Neonatal GMuLV exposure resulted in persistent CNS white matter infection.
- GMuLV-infected mice exhibited depressed GMuLV-specific B lymphocyte function and reduced antibody levels.
- CNS sites of infection lacked MHC class I and II protein expression.
- Transplanted infected brain tissue elicited a strong mononuclear cell infiltrate, indicating immune recognition.
Conclusions:
- Persistent GMuLV CNS infection is associated with impaired peripheral anti-GMuLV immune responses.
- Deficient antigen-presenting cell function within the CNS contributes to the persistent viral infection.
- The interplay between viral persistence and host immune response in the CNS is complex.