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<sup>+</sup>Lymphocytes

Liu, Ting; Chambers, Thomas J.

doi:10.1128/jvi.75.5.2107-2118.2001

Cited by 79 publications

(76 citation statements)

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“…In our study, the vaccination induced the activation of CD8 + T cells, as could be observed on the significant increase of the CD8 + CD38 + T cells in all volunteers. CD4 + T cells are involved in several steps in the mechanics of immune response, as antibodies and cytokine production, among other events during the type-2 immune response, through B cells activation and posterior plasma cell differentiation (Mills et al 2000, Liu & Chambers 2001. As was observed in this study, all first-time vaccinees have presented a significant increase in their numbers of B cells (data not shown) and in the CD4 + T cell subsets.…”

Section: Discussionsupporting

confidence: 66%

Lymphocyte subset analyses in healthy adults vaccinated with yellow fever 17DD virus

Santos¹,

Bertho

Dias³

et al. 2005

Mem. Inst. Oswaldo Cruz

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In this study the kinetics of humoral and cellular immune responses in first-time vaccinees and re-vaccinees with the yellow fever 17DD vaccine virus was analyzed. Flow cytometric analyses were used to determine percentual values of T and B cells in parallel to the yellow fever neutralizing antibody production. All lymphocyte subsets analyzed were augmented around the 30th post vaccination day, both for first-time vaccinees and re-vaccinees. CD3 + T cells increased from 30.8% (SE ± 4%) to 61.15% (SE ± 4.2%), CD4 + T cells from 22.4% (SE ± 3.6%) to 39.17% (SE ± 2%) with 43% of these cells corresponding to CD4 + CD45RO + T cells, CD8 + T cells from 15.2% (SE ± 2.9%) to 27% (SE ± 3%) with 70% corresponding to CD8 + CD45RO + T cells in first-time vaccinees. In revaccinees, the CD3 + T cells increased from 50.7% (SE ± 3%) to 80% (SE ± 2.3%), CD4 + T cells from 24.9% (SE ± 1.4%) to 40% (SE ± 3%) presenting a percentage of 95% CD4 + CD45RO + T cells, CD8 + T cells from 19.7% (SE ± 1.8%) to 25% (SE ± 2%Key words: yellow fever -vaccine -flow cytometry -neutralizing antibodies -lymphocyte subsets Yellow fever (YF) is a viral illness transmitted by infected mosquitoes (Aedes and Haemagogus genus) with yellow fever virus (YFV), which belongs to the Flavivirus genus, Flaviviridae family (Monath & Heinz 1996). It remains a serious health problem in endemic areas of tropical and subtropical Africa and South America (Vasconcelos 2003). Since the 19th century, studies about YF immunization have been accomplished (WHO 2001a). The YF 17D vaccine virus strain is one of the most effective and safe vaccines available. Immunization with the 17D vaccine strain induces a long-term neutralizing antibody response and provides excellent protection against infection with the virulent YFV (Wisseman & Sweet 1962). In 1937, the production of the YF 17DD vaccine virus substrain was started in Brazil, and has been in continuous use for 60 years (Post et al. 2001). The YFV 17DD vaccine is highly immunogenic and induces neutralizing antibody persistent at least 10 years and in some individuals up to 30 years or more (WHO 2001b).Although the YF 17D virus strain and the 17DD substrain are the most successful vaccines developed to date, recently, rare cases of postvaccinal neurological disorders have been recorded (Chan et al. 2001, Martin et al. 2001, Vasconcelos et al. 2001 .Despite the large literature on the humoral immune response to the YF vaccine virus, few works of the evaluation of cellular immune response, in particular T cell responses have been published (Reinhardt et al. 1998, Co et al. 2002, van der Most et al. 2002. The capacity of vaccines to activate the cellular immune system and induce T cell memory is an important mechanism of protection against wild-type viral infection. T cells often recognize more conserved epitopes that do not change due to antibody mediated selection pressure (Whitton & Oldstone 1996, Reinahrdt et al. 1998. Co and collaborators (2002) studying the T cell responses to YFV 17D in four volunteers could observ...

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Section: Discussionsupporting

confidence: 66%

Lymphocyte subset analyses in healthy adults vaccinated with yellow fever 17DD virus

Santos¹,

Bertho

Dias³

et al. 2005

Mem. Inst. Oswaldo Cruz

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“…4). Similar immune cell infiltrates have been observed in hamsters and mice infected with YFV-17D, a neurovirulent DENV isolate, WNV and other neurotropic flaviviruses (Dominguez & Baruch, 1963;Hase et al, 1990;Klein et al, 2005;Liu & Chambers, 2001;Mateo et al, 2007;Wang et al, 2004).…”

Section: Discussionmentioning

confidence: 52%

Spectrum of disease outcomes in mice infected with YFV-17D

Erickson

Pfeiffer

2015

Journal of General Virology

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“…IFN-␥ has been implicated in control of some viral CNS infections (52-54), although it is not always essential (55). In a model of another flaviviral encephalitis, IFN-␥ deficiency was associated with impaired recruitment of inflammatory cells to the CNS and with increased viral titers, although no survival difference was noted (56). In the present study, we have shown: 1) IFN-␥-deficient animals are more susceptible to infection, 2) ␥␦ T cells produce IFN-␥ early following infection, and 3) this is one of their essential effector functions as cells from TCR␤ Ϫ/Ϫ IFN-␥ Ϫ/Ϫ mice were unable to transfer protection.…”

Section: Discussionmentioning

confidence: 99%

IFN-γ-Producing γδ T Cells Help Control Murine West Nile Virus Infection

Wang

Scully

Yin

et al. 2003

The Journal of Immunology

171

187

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West Nile (WN) virus causes fatal meningoencephalitis in laboratory mice, thereby partially mimicking human disease. Using this model, we have demonstrated that mice deficient in γδ T cells are more susceptible to WN virus infection. TCRδ−/− mice have elevated viral loads and greater dissemination of the pathogen to the CNS. In wild-type mice, γδ T cells expanded significantly during WN virus infection, produced IFN-γ in ex vivo assays, and enhanced perforin expression by splenic T cells. Adoptive transfer of γδ T cells to TCRδ−/− mice reduced the susceptibility of these mice to WN virus, and this effect was primarily due to IFN-γ-producing γδ T cells. These data demonstrate a distinct role for γδ T cells in the control of and prevention of mortality from murine WN virus infection.

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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

Abstract: Viral encephalitis caused by neuroadapted yellow fever 17D virus (PYF) was studied in parental and gamma interferon (IFN-␥)-deficient (IFN-␥

Cited by 79 publications

References 70 publications

Lymphocyte subset analyses in healthy adults vaccinated with yellow fever 17DD virus

Lymphocyte subset analyses in healthy adults vaccinated with yellow fever 17DD virus

Spectrum of disease outcomes in mice infected with YFV-17D

IFN-γ-Producing γδ T Cells Help Control Murine West Nile Virus Infection

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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

Abstract: Viral encephalitis caused by neuroadapted yellow fever 17D virus (PYF) was studied in parental and gamma interferon (IFN-␥)-deficient (IFN-␥

Cited by 79 publications

References 70 publications

Lymphocyte subset analyses in healthy adults vaccinated with yellow fever 17DD virus

Lymphocyte subset analyses in healthy adults vaccinated with yellow fever 17DD virus

Spectrum of disease outcomes in mice infected with YFV-17D

IFN-γ-Producing γδ T Cells Help Control Murine West Nile Virus Infection

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Product

Resources

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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