Cell‐mediated Immune Response to Ross River Virus in Mice: Evidence for a Defective Effector Cell Response

Aaskov, J. G.; Da, Dalglish; Davies, Cea; Tucker, M.; Donaldson,

doi:10.1038/icb.1983.50

Cited by 5 publications

(3 citation statements)

References 3 publications

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“…Additionally, an early report on RRV infection in mice showed virus-specific T cell proliferation when exposed to virus ex vivo (77), and a recent report on CHIKV infection in mice demonstrated that spleen and footpad-infiltrating T cells could produce IFN-γ after ex vivo stimulation with virus (32). Additionally, several studies have shown virus-specific T cell responses following immunization with different CHIKV vaccines in mouse and macaque models (36, 78), indicating an expansion and activation of virus-specific T cells.…”

Section: Discussionmentioning

confidence: 99%

CD8+ T Cells Control Ross River Virus Infection in Musculoskeletal Tissues of Infected Mice

Burrack

Montgomery

Homann

et al. 2015

The Journal of Immunology

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Ross River virus (RRV), chikungunya virus (CHIKV), and related alphaviruses cause debilitating polyarthralgia and myalgia. Mouse models of RRV and CHIKV have demonstrated a role for the adaptive immune response in the control of these infections. However, questions remain regarding the role for T cells in viral control, including the magnitude, location, and dynamics of CD8+ T cell responses. To address these questions, we generated a recombinant RRV expressing the H-2b-restricted gp33 determinant derived from the glycoprotein (gp) of lymphocytic choriomeningitis virus (LCMV) (“RRV-LCMV”). Utilizing tetramers, we tracked gp33-specific CD8+ T cells during RRV-LCMV infection. We found that acute RRV infection induces activation of CD8+ T cell responses in lymphoid and musculoskeletal tissues that peak from 10 to 14 days post-inoculation (dpi), suggesting that CD8+ T cells contribute to control of acute RRV infection. Mice genetically deficient for CD8+ T cells or wild-type mice depleted of CD8+ T cells had elevated RRV loads in skeletal muscle tissue, but not joint-associated tissues, at 14 dpi, suggesting that the ability of CD8+ T cells to control RRV infection is tissue-dependent. Finally, adoptively transferred T cells were capable of reducing RRV loads in skeletal muscle tissue of Rag1−/− mice, indicating that T cells can contribute to the control of RRV infection in the absence of B cells and antibody. Collectively, these data demonstrate a role for T cells in the control of RRV infection and suggest that the antiviral capacity of T cells is controlled in a tissue-specific manner.

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Section: Discussionmentioning

confidence: 99%

CD8+ T Cells Control Ross River Virus Infection in Musculoskeletal Tissues of Infected Mice

Burrack

Montgomery

Homann

et al. 2015

The Journal of Immunology

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show abstract

“…We found that Sindbis virus-primed NW-enriched T cells from C3H mice responded well to homologous but not to VEE virus stimulation (unpublished observation). Aaskov et al (1983) observed a virus-specific lymphoproliferative response with the alphaviruses Ross River, Getah and Sindbis, all antigenically unrelated. When we used a battery of antigenically related VEE subtype viruses to stimulate VEE TC-83 virus-primed T cells, the magnitude of the lymphoblastogenic response correlated with the antigenic classification scheme proposed by Young & Johnson (1969) based on kinetic HI using spiny rat antisera.…”

Section: Discussionmentioning

confidence: 97%

“…A virus-specific proliferative response was noted in a limited study with Getah, Ross River and Sindbis viruses (Aaskov et al, 1983).…”

Section: Introductionmentioning

confidence: 99%

Specificity of the Murine T Helper Cell Immune Response to Various Alphaviruses

Mathews

Roehrig

1989

Journal of General Virology

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SUMMARYWe investigated the specificity of the T helper (Th) cell immune response to three alphaviruses: Venezuelan equine encephalomyelitis (VEE), eastern equine encephalitis (EEE) and western equine encephalitis (WEE). Single cell suspensions were prepared from spleens of virus-primed C3H mice, and T lymphocyte populations were enriched by nylon wool chromatography. T cells were incubated in vitro with irradiated, syngeneic splenic stimulator cells previously exposed to purified virus. Cellular proliferation was measured by [3H]thymidine uptake 5 days post-stimulation. The predominant proliferating cell type secreted interleukin-2 and was of the Th cell phenotype Thy-I +, Lyt-l+,2 -, L3T4 ÷. Stimulation of VEE, EEE and WEE virusprimed Th cells with homologous and heterologous virus resulted primarily in a proliferative response specific for the immunizing virus. The corresponding antibody response, as measured by ELISA using purified virus as antigen, was also specific for the immunizing virus. The magnitude of the blastogenic response of VEE TC-83 virusprimed lymphocytes to a battery of VEE subtype viruses was remarkably similar to schemes of antigenic classification. The results indicate that the dominant Th cell epitopes on these alphaviruses represent regions largely virus-specific and lead to a virus-specific B cell response which does not change over time after primary inoculations of mice with VEE and WEE viruses and multiple inoculations of mice with EEE virus.

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Immunogens of encephalitis viruses

Roehrig¹

1993

Veterinary Microbiology

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Cell‐mediated Immune Response to Ross River Virus in Mice: Evidence for a Defective Effector Cell Response

Cited by 5 publications

References 3 publications

CD8+ T Cells Control Ross River Virus Infection in Musculoskeletal Tissues of Infected Mice

CD8+ T Cells Control Ross River Virus Infection in Musculoskeletal Tissues of Infected Mice

Specificity of the Murine T Helper Cell Immune Response to Various Alphaviruses

Immunogens of encephalitis viruses

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