Vesicular stomatitis virus: Immune recognition, responsiveness, and pathogenesis of infection in mice

Reiss, Carol Shoshkes; Aoki, Chiye

doi:10.1002/rmv.1980040207

Cited by 7 publications

(8 citation statements)

References 38 publications

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“…We did not observe accumulation of B cells in the brains of VSV-infected mice until after the mice had recovered from the infection. Passive transfer of mouse anti-VSV immune serum at the time of infection is protective (36), but transfer of anti-VSV Abs after infection failed to protect against CNS infection (39). This further supports our hypothesis that anti-VSV Abs are protective when they are present before or at the time of infection but not when they are present after VSV infection in the CNS has been established.…”

Section: Discussionsupporting

confidence: 83%

Vesicular stomatitis virus infection of the central nervous system activates both innate and acquired immunity

Barna

Komatsu

et al. 1995

J Virol

141

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Vesicular stomatitis virus (VSV) causes acute infection of the central nervous system (CNS) when intranasally applied. We have examined cellular inflammatory changes in the CNS following VSV infection. As early as 1 day postinfection (p.i.), astrocytes were activated in the olfactory bulb (OB). This was followed by activation of microglia, first observed in the OB at day 3 p.i. Expression of inducible nitric oxide synthase was observed in activated microglia in the OB at day 3 p.i., and increased inducible nitric oxide synthase expression coincided with decreased virus titers in tissue homogenates. Expression of major histocompatibility complex (MHC) class I molecules on astrocytes and microglial, endothelial, and ependymal cells was also rapidly induced and followed by induced expression of MHC class II molecules on astrocytes and microglial and endothelial cells. Consistent with the pattern of viral dissemination, MHC molecules were expressed temporally from the rostral-to-caudal direction. Infiltration of CD8 ؉ cells was observed as early as 1 day p.i. in the OB. CD4 ؉ cells were detected in the OB at day 4 p.i. Increasing T-cell infiltration coincided with decreased virus titers. In contrast, B-cell infiltration of the CNS was not detected until day 14 p.i., after the virus was cleared and mice were showing behavioral signs of recovery. Breakdown of the blood-brain barrier was detected beginning at day 6 p.i., was most severe at day 8 p.i., and was followed by full recovery. Collectively, these data show that both innate immunity (production of nitric oxide) and acquired immunity (expression of MHC molecules and T-cell infiltration) are activated following VSV infection in the CNS.

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Section: Discussionsupporting

confidence: 83%

Vesicular stomatitis virus infection of the central nervous system activates both innate and acquired immunity

Barna

Komatsu

et al. 1995

J Virol

141

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“…30 Dissemination of virus from the olfactory bulbs to other structures in the brain then occurs via retrograde and possibly anterograde transneuronal transport. 16,24,25,32 Similar retrograde and anterograde transneuronal transport of VSV was demonstrated within the brain following injection into the eye in NMRI strain mice. 24 A second route of viral dissemination in the brains of infected laboratory mice involves extensive spread through the ventricular system.…”

Section: Discussionmentioning

confidence: 79%

Pathogenesis of Experimental Vesicular Stomatitis Virus (New Jersey Serotype) Infection in the Deer Mouse (Peromyscus maniculatus)

et al. 2001

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Abstract. The pathogenesis of vesicular stomatitis virus (VSV) infection has not been investigated previously in native New World rodents that may have a role in the epidemiology of the disease. In the present study, 45 juvenile and 80 adult deer mice (Peromyscus maniculatus) were inoculated intranasally with VSV New Jersey serotype (VSV-NJ) and examined sequentially over a 7-day period. Virus was detected by means of immunohistochemistry and in situ hybridization in all tissues containing histologic lesions. Viral antigen and mRNA were observed initially in olfactory epithelium neurons, followed by olfactory bulbs and more caudal olfactory pathways in the brain. Virus also was detected throughout the ventricular system in the brain and central canal of the spinal cord. These results support both viral retrograde transneuronal transport and viral spread within the ventricular system. Other tissues containing viral antigen included airway epithelium and macrophages in the lungs, cardiac myocytes, and macrophages in cervical lymph nodes. In a second experiment, 15 adult, 20 juvenile, and 16 nestling deer mice were inoculated intradermally with VSV-NJ. Adults were refractory to infection by this route; however, nestlings and juveniles developed disseminated central nervous system infections. Viral antigen also was detected in cardiac myocytes and lymph node macrophages in these animals. Viremia was detected by virus isolation in 35/72 (49%) intranasally inoculated juvenile and adult mice and in 17/36 (47%) intradermally inoculated nestlings and juveniles from day 1 to day 3 postinoculation. The documentation of viremia in these animals suggests that they may have a role in the epidemiology of vectorborne vesicular stomatitis.

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“…In the absence of a functionally intact immune system, a variety of defects in the hosts' response to intranasal VSV infection have been observedTable 2). Mice that do not have a functional T cell compartment (severe combined immunodeficiency (SCID) mice or nude mice) readily succumb to infection, even when the virus is administered parenterally 8‐10. In BALB/c‐H‐2 dm2 mice, which do not have the class I major histocompatibility complex (MHC‐I) restricting heterodimer, H‐2L d , the infection proceeds without significant differences from mice able to use CD8 + effector T cells; this shows that CD4 + T cells are sufficient at controlling the infection and promoting recovery of mice 3,6.…”

Section: Introductionmentioning

confidence: 99%

Viral Replication in Olfactory Receptor Neurons and Entry into the Olfactory Bulb and Brain^a

Reiss

Plakhov

Komatsu

1998

Annals of the New York Academy of Sciences

102

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This communication describes our ongoing studies of the interaction of the mouse host and vesicular stomatitis virus (VSV). When VSV is applied to the nasal neuroepithelium, it initially replicates in olfactory receptor neurons, and is transmitted along the olfactory nerve to the central nervous system (CNS) within 12 hours. In the olfactory bulb, the virus replicates invasively through the layers of the olfactory bulb, reaching the olfactory ventricle by day 4-5 post infection, and the hindbrain by day 8 post infection. In mice, infection may result in a 50% mortality rate. The crucial host innate and specific immune responses responsible for restricting viral propagation and caudal spread of the virus will be discussed. The efficacy of interleukin-12 (IL-12) treatment for enhanced viral clearance and promotion of host recovery are described along with the implications for treatment of human encephalitis. The hosts' response to infection is also regulated by the sex of the host, and the age at infection. The role of specific mucosal humoral immunity and systemic cellular immunity in prevention of infection are described.

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Vesicular stomatitis virus: Immune recognition, responsiveness, and pathogenesis of infection in mice

Cited by 7 publications

References 38 publications

Vesicular stomatitis virus infection of the central nervous system activates both innate and acquired immunity

Vesicular stomatitis virus infection of the central nervous system activates both innate and acquired immunity

Pathogenesis of Experimental Vesicular Stomatitis Virus (New Jersey Serotype) Infection in the Deer Mouse (Peromyscus maniculatus)

Viral Replication in Olfactory Receptor Neurons and Entry into the Olfactory Bulb and Brain^a

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Vesicular stomatitis virus: Immune recognition, responsiveness, and pathogenesis of infection in mice

Cited by 7 publications

References 38 publications

Vesicular stomatitis virus infection of the central nervous system activates both innate and acquired immunity

Vesicular stomatitis virus infection of the central nervous system activates both innate and acquired immunity

Pathogenesis of Experimental Vesicular Stomatitis Virus (New Jersey Serotype) Infection in the Deer Mouse (Peromyscus maniculatus)

Viral Replication in Olfactory Receptor Neurons and Entry into the Olfactory Bulb and Braina

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Viral Replication in Olfactory Receptor Neurons and Entry into the Olfactory Bulb and Brain^a