Hydrocephalus in Mice Infected with a Theilerʼs Murine Encephalomyelitis Virus Variant

Tsunoda, Ikuo; McCright, Ingeborg J.; Kuang, Li Qing; Zurbriggen, Andreas; Fujinami, Robert S.

doi:10.1097/00005072-199712000-00005

Cited by 42 publications

(57 citation statements)

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“…The disease course and pathology seen in mice infected i.c. with VV are similar to what we have reported in communicating hydrocephalus caused by TMEV mutant H101 (Tsunoda et al, 1997). In H101 infection, mice develop acute meningitis composed of TUNEL + apoptotic meningeal infiltrates with no involvement of parenchyma.…”

Section: Discussionsupporting

confidence: 89%

Sequential polymicrobial infections lead to CNS inflammatory disease: Possible involvement of bystander activation in heterologous immunity

Tsunoda¹,

Libbey²,

Fujinami³

2007

Journal of Neuroimmunology

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VV PLP is a recombinant vaccinia virus (VV) encoding myelin proteolipid protein (PLP) that has been used to investigate molecular mimicry and autoimmunity. Since virus infections can cause bystander activation, mice were first infected with VV PLP , and later challenged with wild-type VV, lymphocytic choriomeningitis virus (LCMV), or murine cytomegalovirus (MCMV). Among the VV PLP -primed mice, only MCMV challenge induced significant Ki-67 + , CD3 + T cell infiltration into the central nervous system (CNS) with a mild PLP antibody response. While MCMV alone caused no CNS disease, control VV-infected mice followed with MCMV developed mild CNS inflammation. Thus, heterologous virus infections can induce CNS pathology.

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Section: Discussionsupporting

confidence: 89%

Sequential polymicrobial infections lead to CNS inflammatory disease: Possible involvement of bystander activation in heterologous immunity

Tsunoda¹,

Libbey²,

Fujinami³

2007

Journal of Neuroimmunology

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“…DA viral-antigen-positive cells and astrocytes were detected on paraffin sections using hyperimmune rabbit serum against TMEV and glial fibrillary acidic protein (GFAP) antibody (Dako Corp., Carpinteria, CA), respectively, as previously described (37,39). The slides were labeled using the avidin-biotin peroxidase complex technique with 3,3Ј-diaminobenzidine tetrahydrochloride (Sigma-Aldrich, St. Louis, MO) in 0.01% hydrogen peroxide (Sigma) in PBS.…”

Section: Animals and Infectionmentioning

confidence: 99%

Role for Complement in the Development of Seizures following Acute Viral Infection

Libbey

Kirkman

Wilcox

et al. 2010

J Virol

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Complement, part of the innate immune system, acts to remove pathogens and unwanted host material. Complement is known to function in all tissues, including the central nervous system (CNS). In this study, we demonstrated the importance of the complement system within the CNS in the development of behavioral seizures following Theiler's murine encephalomyelitis virus (TMEV) infection. C57BL/6 mice, deficient in complement component C3, developed significantly fewer behavioral seizures following TMEV infection, whereas mice depleted of complement component C3 in the periphery through treatment with cobra venom factor had a seizure rate comparable to that of control mice. These studies indicate that C3 participates in the induction of acute seizures during viral encephalitis.

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“…Four-micrometerthick sections were stained with luxol fast blue for myelin visualization. Histological scoring was performed as previously described (44)(45)(46)(47). Brain sections were scored for meningitis (0, no meningitis; 1, mild cellular infiltrates; 2, moderate cellular infiltrates; 3, severe cellular infiltrates) and perivascular cuffing (0, no cuffing; 1, 1 to 10 lesions; 2, 11 to 20 lesions; 3, 21 to 30 lesions; 4, 31 to 40 lesions; 5, over 50 lesions).…”

Section: Methodsmentioning

confidence: 99%

“…The total number of positive quadrants for each pathologic class was determined, then divided by the total number of quadrants present on the slide, and multiplied by 100 to give the percent involvement for each pathologic class. TMEV antigen-positive cells were detected by the avidinbiotin peroxidase complex technique, using hyperimmune rabbit serum to DA virus (44)(45)(46)(47). Enumeration of TMEV antigen-positive cells was carried out with a light microscope at a magnification of ϫ200, using 5 coronal brain sections and 10 horizontal sections per mouse as described previously (47).…”

Section: Methodsmentioning

confidence: 99%

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Prolonged Gray Matter Disease without Demyelination Caused by Theiler's Murine Encephalomyelitis Virus with a Mutation in VP2 Puff B

Tsunoda

Wada

Libbey

et al. 2001

J Virol

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Theiler's murine encephalomyelitis virus (TMEV) is divided into two subgroups based on neurovirulence. During the acute phase, DA virus infects cells in the gray matter of the central nervous system (CNS).Throughout the chronic phase, DA virus infects glial cells in the white matter, causing demyelinating disease. Although GDVII virus also infects neurons in the gray matter, infected mice developed a severe polioencephalomyelitis, and no virus is detected in the white matter or other areas in the CNS in rare survivors. Several sequence differences between the two viruses are located in VP2 puff B and VP1 loop II, which are located near each other, close to the proposed receptor binding site. We constructed a DA virus mutant, DApBL2M, which has the VP1 loop II of GDVII virus and a mutation at position 171 in VP2 puff B. While DApBL2M virus replicated less efficiently than DA virus during the acute phase, DApBL2M-induced acute polioencephalitis was comparable to that in DA virus infection. Interestingly, during the chronic phase, DApBL2M caused prolonged gray matter disease in the brain without white matter involvement in the spinal cord. This is opposite what is observed during wild-type DA virus infection. Our study is the first to demonstrate that conformational differences via interaction of VP2 puff B and VP1 loop II between GDVII and DA viruses can play an important role in making the transition of infection from the gray matter in the brain to the spinal cord white matter during TMEV infection.Theiler's murine encephalomyelitis virus (TMEV) belongs to the family Picornaviridae and is divided into two subgroups based on neurovirulence in mice, i.e., GDVII and TO (14,41,42). Strains in the first subgroup, GDVII, include the highly neurovirulent GDVII and FA strains, infect neurons in the gray matter of the central nervous system (CNS), and cause an acute polioencephalomyelitis with extensive apoptosis of neurons. Most mice infected with GDVII virus die within 10 days (43), and the virus has never been isolated from the rare survivor (22). The second subgroup, TO, including DA and BeAn strains, causes a biphasic disease. Similar to GDVII virus, DA virus infects neurons in the gray matter, mainly in the brain, and causes polioencephalomyelitis with mild neuronal apoptosis 1 week after infection (the acute phase). However, the mice survive the acute phase and progress to develop a chronic demyelinating disease in the white matter of the spinal cord 1 month postinfection (the chronic phase). During the chronic phase, virus or viral products are detected in glial cells and macrophages in the white matter of the spinal cord but not in the neurons of the brain. This chronic phase is a well-characterized experimental animal model for multiple sclerosis (2,4,31,41,42).We do not know why GDVII virus predominantly infects neurons in the gray matter is not known, and the mechanism by which DA virus infects neurons in the gray matter during the acute phase and persistently infects glial cells and macrophages in the white ...

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Hydrocephalus in Mice Infected with a Theilerʼs Murine Encephalomyelitis Virus Variant

Cited by 42 publications

References 0 publications

Sequential polymicrobial infections lead to CNS inflammatory disease: Possible involvement of bystander activation in heterologous immunity

Sequential polymicrobial infections lead to CNS inflammatory disease: Possible involvement of bystander activation in heterologous immunity

Role for Complement in the Development of Seizures following Acute Viral Infection

Prolonged Gray Matter Disease without Demyelination Caused by Theiler's Murine Encephalomyelitis Virus with a Mutation in VP2 Puff B

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