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Neuropathology of experimental autoimmune encephalomyelitis modified by retroviral infection
Hidefumi Fukumitsu1, Sayaka Takase-Yoden, Rihito Watanabe
1Institute of Life Science, Soka University, Hachioji, Tokyo, Japan.
Abstract:
The A8 virus is a molecular clone of the neuropathogenic FrC6 virus derived from the Friend murine leukemia virus (F-MuLV). To elucidate the effects of A8 virus-infection on immune-mediated diseases in the central nervous system, we investigated the development of acute and monophasic experimental autoimmune encephalomyelitis (EAE) in A8 virus-infected Lewis rats. In EAE rats after A8 virus infection (A8-EAE), many inflammatory cells were found in the gray matter including the frontal lobe, where almost no inflammatory cells were found in rats with EAE alone. The modified distribution of inflammatory cells was not dependent on the ages of A8 virus-infected rats, although the frequency of the modified distribution was reduced in older rats. The chimeric virus Rec2, which contains the pol and env genes of 57 virus on the background of A8 and does not induce spongiform degeneration in the CNS, caused the same distributional modification of inflammatory cells in the rats with EAE as in A8-EAE rats. Furthermore, the incidence and intensity of spongiform degeneration, thymoma and splenomegaly caused by A8 virus were reduced by the induction of EAE.
Insights
A8 virus infection alters inflammatory cell distribution in the central nervous system during experimental autoimmune encephalomyelitis (EAE). This modification impacts gray matter inflammation, even in chimeric virus infections.
Area of Science:
- Neurovirology
- Immunology
- Central Nervous System (CNS) Diseases
Background:
- The A8 virus, a clone of the neuropathogenic FrC6 virus (derived from Friend murine leukemia virus), is studied for its effects on immune-mediated CNS diseases.
- Experimental autoimmune encephalomyelitis (EAE) serves as a model for studying immune-mediated CNS inflammation.
Purpose of the Study:
- To investigate the impact of A8 virus infection on the development and characteristics of EAE in Lewis rats.
- To determine how A8 virus influences the distribution of inflammatory cells within the CNS during EAE.
- To assess the role of specific viral genes and the interplay between viral infection and EAE pathology.
Main Methods:
- Induction of acute, monophasic EAE in Lewis rats.
- Infection of EAE rats with the A8 virus (A8-EAE).
- Analysis of inflammatory cell infiltration in the gray matter, including the frontal lobe.
- Comparison with EAE rats without viral infection.
- Investigation using a chimeric virus (Rec2) with modified genetic components.
- Evaluation of spongiform degeneration, thymoma, and splenomegaly.
Main Results:
- A8 virus infection significantly altered inflammatory cell distribution in EAE rats, with increased infiltration in gray matter areas like the frontal lobe.
- This modified distribution was observed even with a chimeric virus (Rec2), suggesting a conserved mechanism.
- The frequency of this altered distribution decreased in older rats.
- EAE induction concurrently reduced the incidence and severity of A8 virus-induced spongiform degeneration, thymoma, and splenomegaly.
Conclusions:
- A8 virus infection profoundly modifies inflammatory cell localization in the CNS during EAE, extending beyond typical EAE patterns.
- Viral genetic components, as exemplified by the Rec2 chimeric virus, play a role in this altered inflammatory response.
- A complex interplay exists where EAE induction can mitigate certain neuropathological and systemic effects of A8 virus infection.