Yellow Fever Virus Encephalitis: Properties of the Brain-Associated T-Cell Response during Virus Clearance in Normal and Gamma Interferon-Deficient Mice and Requirement for CD4+ Lymphocytes

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Published inJournal of Virology Vol. 75; no. 5; pp. 2107 - 2118
Main Authors Liu, T, Chambers, T J
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.03.2001
Subjects
Animals
Brain - immunology
Brain - virology
CD4-Positive T-Lymphocytes
Cytokines - biosynthesis
Encephalitis, Viral - immunology
Encephalitis, Viral - virology
Female
Immunization
Interferon-gamma - genetics
Lymphocyte Activation
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Pathogenesis and Immunity
T-Lymphocytes - immunology
T-Lymphocytes - metabolism
Virus Replication
Yellow Fever - immunology
Yellow Fever - virology
Yellow fever virus - immunology
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Abstract Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue JVI About JVI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy JVI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0022-538X Online ISSN: 1098-5514 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to JVI .asm.org, visit: JVI       
AbstractList Viral encephalitis caused by neuroadapted yellow fever 17D virus (PYF) was studied in parental and gamma interferon (IFN-γ)-deficient (IFN-γ knockout [GKO]) C57BL/6 mice. The T-cell responses which enter the brain during acute fatal encephalitis of nonimmunized mice, as well as nonfatal encephalitis of immunized mice, were characterized for relative proportions of CD4 + and CD8 + cells, their proliferative responses, and antigen-specific expression of cytokines during stimulation in vitro. Unimmunized mice accumulated only low levels of T cells within the brain during fatal disease, whereas the brains of immunized mice contained higher levels of both T-cell subsets in response to challenge, with CD8 + cells increased relative to the CD4 + subset. The presence of T cells correlated with the time at which virus was cleared from the central nervous system in both parental and GKO mice. Lymphocytes isolated from the brains of challenged immunized mice failed to proliferate in vitro in response to T-cell mitogens or viral antigens; however, IFN-γ, interleukin 4 (IL-4), and, to a lesser extent, IL-2 were detectable after stimulation. The levels of IFN-γ, but not IL-2 or IL-4, were augmented in response to viral antigen, and this specificity was detectable in the CD4 + compartment. When tested for the ability to survive both immunization and challenge with PYF virus, GKO and CD8 knockout mice did not differ from parental mice (80 to 85% survival), although GKO mice exhibited a defect in virus clearance. In contrast, CD4 knockout and Igh-6 mice were unable to resist challenge. The data implicate antibody in conjunction with CD4 + lymphocytes bearing a Th1 phenotype as the critical factors involved in virus clearance in this model.
ABSTRACT Viral encephalitis caused by neuroadapted yellow fever 17D virus (PYF) was studied in parental and gamma interferon (IFN-γ)-deficient (IFN-γ knockout [GKO]) C57BL/6 mice. The T-cell responses which enter the brain during acute fatal encephalitis of nonimmunized mice, as well as nonfatal encephalitis of immunized mice, were characterized for relative proportions of CD4 + and CD8 + cells, their proliferative responses, and antigen-specific expression of cytokines during stimulation in vitro. Unimmunized mice accumulated only low levels of T cells within the brain during fatal disease, whereas the brains of immunized mice contained higher levels of both T-cell subsets in response to challenge, with CD8 + cells increased relative to the CD4 + subset. The presence of T cells correlated with the time at which virus was cleared from the central nervous system in both parental and GKO mice. Lymphocytes isolated from the brains of challenged immunized mice failed to proliferate in vitro in response to T-cell mitogens or viral antigens; however, IFN-γ, interleukin 4 (IL-4), and, to a lesser extent, IL-2 were detectable after stimulation. The levels of IFN-γ, but not IL-2 or IL-4, were augmented in response to viral antigen, and this specificity was detectable in the CD4 + compartment. When tested for the ability to survive both immunization and challenge with PYF virus, GKO and CD8 knockout mice did not differ from parental mice (80 to 85% survival), although GKO mice exhibited a defect in virus clearance. In contrast, CD4 knockout and Igh-6 mice were unable to resist challenge. The data implicate antibody in conjunction with CD4 + lymphocytes bearing a Th1 phenotype as the critical factors involved in virus clearance in this model.
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Viral encephalitis caused by neuroadapted yellow fever 17D virus (PYF) was studied in parental and gamma interferon (IFN-gamma)-deficient (IFN-gamma knockout [GKO]) C57BL/6 mice. The T-cell responses which enter the brain during acute fatal encephalitis of nonimmunized mice, as well as nonfatal encephalitis of immunized mice, were characterized for relative proportions of CD4+ and CD8+ cells, their proliferative responses, and antigen-specific expression of cytokines during stimulation in vitro. Unimmunized mice accumulated only low levels of T cells within the brain during fatal disease, whereas the brains of immunized mice contained higher levels of both T-cell subsets in response to challenge, with CD8+ cells increased relative to the CD4+ subset. The presence of T cells correlated with the time at which virus was cleared from the central nervous system in both parental and GKO mice. Lymphocytes isolated from the brains of challenged immunized mice failed to proliferate in vitro in response to T-cell mitogens or viral antigens; however, IFN-gamma, interleukin 4 (IL-4), and, to a lesser extent, IL-2 were detectable after stimulation. The levels of IFN-gamma, but not IL-2 or IL-4, were augmented in response to viral antigen, and this specificity was detectable in the CD4+ compartment. When tested for the ability to survive both immunization and challenge with PYF virus, GKO and CD8 knockout mice did not differ from parental mice (80 to 85% survival), although GKO mice exhibited a defect in virus clearance. In contrast, CD4 knockout and Igh-6 mice were unable to resist challenge. The data implicate antibody in conjunction with CD4+ lymphocytes bearing a Th1 phenotype as the critical factors involved in virus clearance in this model.
Author Thomas J. Chambers
Ting Liu
AuthorAffiliation Department of Molecular Microbiology and Immunology, St. Louis University Health Sciences Center, St. Louis, Missouri 63104
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/11160715$$D View this record in MEDLINE/PubMed
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Corresponding author. Mailing address: Department of Molecular Microbiology and Immunology, St. Louis University Health Sciences Center, 1402 S. Grand Blvd., St. Louis, MO 63104. Phone: (314) 577-8447. Fax: (314) 773-3403. E-mail: chambetj@slu.edu.
Present address: Dept. of Pathology, Hahnemann Hospital, Philadelphia, PA.
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Viral encephalitis caused by neuroadapted yellow fever 17D virus (PYF) was studied in parental and gamma interferon (IFN-gamma)-deficient (IFN-gamma knockout...
ABSTRACT Viral encephalitis caused by neuroadapted yellow fever 17D virus (PYF) was studied in parental and gamma interferon (IFN-γ)-deficient (IFN-γ knockout...
Viral encephalitis caused by neuroadapted yellow fever 17D virus (PYF) was studied in parental and gamma interferon (IFN-γ)-deficient (IFN-γ knockout [GKO])...
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SourceType Open Access Repository
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StartPage 2107
SubjectTerms Animals
Brain - immunology
Brain - virology
CD4-Positive T-Lymphocytes
Cytokines - biosynthesis
Encephalitis, Viral - immunology
Encephalitis, Viral - virology
Female
Immunization
Interferon-gamma - genetics
Lymphocyte Activation
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Pathogenesis and Immunity
T-Lymphocytes - immunology
T-Lymphocytes - metabolism
Virus Replication
Yellow Fever - immunology
Yellow Fever - virology
Yellow fever virus - immunology
Title Yellow Fever Virus Encephalitis: Properties of the Brain-Associated T-Cell Response during Virus Clearance in Normal and Gamma Interferon-Deficient Mice and Requirement for CD4+ Lymphocytes
URI http://jvi.asm.org/content/75/5/2107.abstract
https://www.ncbi.nlm.nih.gov/pubmed/11160715
https://search.proquest.com/docview/70643348
https://pubmed.ncbi.nlm.nih.gov/PMC114795
Volume 75
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