scholarly journals Molecular Mimicry, Bystander Activation, or Viral Persistence: Infections and Autoimmune Disease

2006 ◽  
Vol 19 (1) ◽  
pp. 80-94 ◽  
Author(s):  
Robert S. Fujinami ◽  
Matthias G. von Herrath ◽  
Urs Christen ◽  
J. Lindsay Whitton
Keyword(s):  
Multiple Sclerosis ◽  
Autoimmune Disease ◽  
Virus Infection ◽  
Molecular Mimicry ◽  
Viral Persistence ◽  
Target Organ ◽  
Virus Infections ◽  
Epitope Spreading ◽  
Bystander Activation ◽  
The Brain

SUMMARY Virus infections and autoimmune disease have long been linked. These infections often precede the occurrence of inflammation in the target organ. Several mechanisms often used to explain the association of autoimmunity and virus infection are molecular mimicry, bystander activation (with or without epitope spreading), and viral persistance. These mechanisms have been used separately or in various combinations to account for the immunopathology observed at the site of infection and/or sites of autoimmune disease, such as the brain, heart, and pancreas. These mechanisms are discussed in the context of multiple sclerosis, myocarditis, and diabetes, three immune-medicated diseases often linked with virus infections.

scholarly journals CD28 Costimulatory Blockade Exacerbates Disease Severity and Accelerates Epitope Spreading in a Virus-Induced Autoimmune Disease

2000 ◽  
Vol 74 (18) ◽  
pp. 8349-8357 ◽  
Author(s):  
Katherine L. Neville ◽  
Mauro C. Dal Canto ◽  
Jeffrey A. Bluestone ◽  
Stephen D. Miller
Keyword(s):  
Chronic Disease ◽  
T Cell ◽  
Autoimmune Disease ◽  
Virus Infection ◽  
Disease Severity ◽  
Demyelinating Disease ◽  
Virus Infections ◽  
Epitope Spreading ◽  
Costimulatory Blockade ◽  
Persistent Virus

ABSTRACT Theiler's murine encephalomyelitis virus (TMEV) is a natural mouse pathogen which causes a lifelong persistent infection of the central nervous system (CNS) accompanied by T-cell-mediated myelin destruction leading to chronic, progressive hind limb paralysis. TMEV-induced demyelinating disease (TMEV-IDD) is considered to be a highly relevant animal model for the human autoimmune disease multiple sclerosis (MS), which is thought to be initiated as a secondary consequence of a virus infection. Although TMEV-IDD is initiated by virus-specific CD4+ T cells targeting CNS-persistent virus, CD4+ T-cell responses against self myelin protein epitopes activated via epitope spreading contribute to chronic disease pathogenesis. We thus examined the ability of antibodies directed against B7 costimulatory molecules to regulate this chronic virus-induced immunopathologic process. Contrary to previous studies showing that blockade of B7-CD28 costimulatory interactions inhibit the initiation of experimental autoimmune encephalomyelitis, treatment of SJL mice at the time of TMEV infection with murine CTLA-4 immunoglobulin or a combination of anti-B7-1 and anti-B7-2 antibodies significantly enhanced clinical disease severity. Costimulatory blockade inhibited early TMEV-specific T-cell and antibody responses critical in clearing peripheral virus infection. The inhibition of virus-specific immune responses led to significantly increased CNS viral titers resulting in increased damage to myelin-producing oligodendrocytes. Following clearance of the costimulatory antagonists, epitope spreading to myelin epitopes was accelerated as a result of the increased availability of myelin epitopes leading to a more severe chronic disease course. Our results raise concern about the potential use of B7-CD28 costimulatory blockade to treat human autoimmune diseases potentially associated with acute or persistent virus infections.

scholarly journals Multiple Sclerosis

2020 ◽  
Author(s):  
Amirhossein Azari Jafari ◽  
Seyyedmohammadsadeq Mirmoeeni
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Optic Nerve ◽  
Autoimmune Disease ◽  
The Central Nervous System ◽  
Genetic And Environmental Factors ◽  
Chronic Autoimmune Disease ◽  
The Brain

Multiple sclerosis (MS) is a chronic autoimmune disease affecting the central nervous system (CNS), caused by genetic and environmental factors. It is characterized by intermittent and recurrent episodes of inflammation that result in the demyelination and subsequent damage of the underlying axons present in the brain, optic nerve and spinal cord [1][2][3].

scholarly journals HL-A Frequencies in Patients with Multiple Sclerosis

1974 ◽  
Vol 1 (4) ◽  
pp. 211-213 ◽  
Author(s):  
D.W. Paty ◽  
H. Mervart ◽  
B. Campling ◽  
C.G. Rand ◽  
C.R. Stiller
Keyword(s):  
Multiple Sclerosis ◽  
Autoimmune Disease ◽  
Virus Infection ◽  
Major Histocompatibility ◽  
Histocompatibility Antigens ◽  
Experimental Animals ◽  
Major Histocompatibility Locus ◽  
Slow Virus ◽  
Histocompatibility Locus

SUMMARY:The histocompatibility antigens (HL-A) have been determined in 100 multiple sclerosis (M.S.) patients and 143 randomly selected controls. In the M.S. group there was a statistically significant increase in the frequency of HL-A 7 and W 18 with an insignificant increase in HL-A 3. The variance from normal HL-A patterns in the M.S. population may play some role in establishing the substrate for this disease. Studies in experimental animals have shown that susceptibility to autoimmune disease and to virus infection is linked to the major histocompatibility locus. This has interesting implications for both the “slow virus” and the “autoimmune” theories of the etiology of multiple sclerosis.

scholarly journals Pemphigus Vulgaris Following Influenza: A Case Report

2019 ◽  
Vol 3 (6) ◽  
pp. 418-422
Author(s):  
Kristen Bice ◽  
Channing Hood ◽  
Rawaa Almukhtar ◽  
Michelle Gerdes ◽  
Pamela Martin ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Case Report ◽  
Autoimmune Disease ◽  
Influenza Vaccine ◽  
Mucous Membrane ◽  
Influenza A ◽  
Viral Infections ◽  
Molecular Mimicry ◽  
Pemphigus Vulgaris ◽  
Epitope Spreading

Viruses have long been implicated as potential triggers of autoimmune disease. In the case of pemphigus vulgaris, members of the herpesviridae family are often associated with its development. There have also been reports of pemphigus being triggered by the influenza vaccine. We report a case of a 17-year-old male who developed mucous membrane-predominant pemphigus vulgaris after testing positive for the influenza virus and discuss proposed hypotheses for the association between viral infections and autoimmunity, such as molecular mimicry and epitope spreading.

scholarly journals Is Multiple Sclerosis an Autoimmune Disease?

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Bharath Wootla ◽  
Makoto Eriguchi ◽  
Moses Rodriguez
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Autoimmune Disease ◽  
Virus Infection ◽  
Demyelinating Disease ◽  
Immune Mediated ◽  
Clinical Presentations ◽  
The Central Nervous System ◽  
Immunological Abnormalities

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) with varied clinical presentations and heterogeneous histopathological features. The underlying immunological abnormalities in MS lead to various neurological and autoimmune manifestations. There is strong evidence that MS is, at least in part, an immune-mediated disease. There is less evidence that MS is a classical autoimmune disease, even though many authors state this in the description of the disease. We show the evidence that both supports and refutes the autoimmune hypothesis. In addition, we present an alternate hypothesis based on virus infection to explain the pathogenesis of MS.

scholarly journals Whole-brain fluorescence-MRI coregistration for precise anatomical mapping of virus infection

2021 ◽  
Author(s):  
Nunya Chotiwan ◽  
Stefanie M.A. Willekens ◽  
Erin Schexnaydre ◽  
Max Hahn ◽  
Federico Morini ◽  
...  
Keyword(s):  
Virus Infection ◽  
Type I Interferon ◽  
Ex Vivo ◽  
Interferon Response ◽  
Type I ◽  
Virus Infections ◽  
Whole Brain ◽  
Neurotropic Virus ◽  
Langat Virus ◽  
The Brain

Neurotropic virus infections cause tremendous disease burden. Methods visualizing infection in the whole brain remain unavailable which greatly impedes understanding of viral neurotropism and pathogenesis. We devised an approach to visualize the distribution of neurotropic virus infection in whole mouse brain ex vivo. Optical projection tomography (OPT) signal was coregistered with a unique magnetic resonance imaging (MRI) brain template, enabling precise anatomical mapping of viral distribution, and the effect of type I interferon on distribution of infection was analyzed. Guided by OPT-MR, we show that Langat virus specifically targets sensory brain systems and the lack of type I interferon response results in an anatomical shift in infection patterns in the brain. We confirm this regional tropism, observed with whole brain OPT-MRI, by confocal and electron microscopy to provide unprecedented insight into viral neurotropism. This approach can be applied to any fluorescently labeled target in the brain.

Sign in / Sign up

Export Citation Format

Share Document