Vaccination with a DNA Vaccine Encoding Herpes Simplex Virus Type 1 VP22 Linked to Antigen Generates Long-Term Antigen-Specific CD8-Positive Memory T Cells and Protective Immunity

2004 ◽  
Vol 15 (2) ◽  
pp. 167-177 ◽  
Author(s):  
Tae Woo Kim ◽  
Chien-Fu Hung ◽  
Jeong Won Kim ◽  
Jeremy Juang ◽  
Pei-Jer Chen ◽  
...  
Keyword(s):  
T Cells ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Dna Vaccine ◽  
Herpes Simplex Virus Type ◽  
Protective Immunity ◽  
Memory T Cells ◽  
Simplex Virus

Effect of a combination therapy between IL-12 and soluble IL-4 receptor (sIL-4R) onCandida albicansand herpes simplex virus type 1 infections in thermally injured mice

2002 ◽  
Vol 48 (10) ◽  
pp. 886-894 ◽  
Author(s):  
Makiko Kobayashi ◽  
Hitoshi Takahashi ◽  
David N Herndon ◽  
Richard B Pollard ◽  
Fujio Suzuki
Keyword(s):  
T Cells ◽  
Candida Albicans ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Herpes Simplex Virus Type ◽  
Cell Responses ◽  
Ifn Γ ◽  
Simplex Virus ◽  
Hsv 1

The effectiveness of a combination using IL-12 and soluble IL-4 receptor (sIL-4R) to treat severe infections of herpes simplex virus type 1 (HSV-1) and Candida albicans in thermally injured mice was investigated. Although sIL-4R decreased burn-associated type 2 T-cell responses, the effect of sIL-4R was minimal on the morbidity and mortality of thermally injured mice exposed to 250 times LD50of HSV-1 or 10 times LD50of C. albicans. Compared with 100% mortality in control mice, mortality for HSV-1 and C. albicans was 40 and 20%, respectively, in thermally injured mice that received IL-12 and sIL-4R in combination. After stimulation with anti-CD3 monoclonal antibody, splenic T cells from thermally injured mice exposed to large amounts of HSV-1 or C. albicans did not produce gamma interferon (IFN-γ) into their culture fluids. However, IFN-γ was produced by splenic T cells from thermally injured and infected mice treated with IL-12 and sIL-4R in combination. These results suggest that therapeutic treatment with a combination of IL-12 and sIL-4R may be effective by inducing type 1 T-cell responses in thermally injured mice exposed to large amounts of HSV-1 or C. albicans.Key words: burn, IL-12, soluble IL-4 receptor, herpesvirus, Candida albicans.

Disseminated herpes simplex virus type-1 infection in long-term usage of everolimus

2012 ◽  
Vol 40 (1) ◽  
pp. 84-85 ◽  
Author(s):  
Monji Koga ◽  
Ichiro Nakayama ◽  
Teppei Sakai ◽  
Kaori Koga ◽  
Shinichi Imafuku ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Simplex Virus

scholarly journals CD8+ T cells control corneal disease following ocular infection with herpes simplex virus type 1

2004 ◽  
Vol 85 (7) ◽  
pp. 2055-2063 ◽  
Author(s):  
Patrick M. Stuart ◽  
Brett Summers ◽  
Jessica E. Morris ◽  
Lynda A. Morrison ◽  
David A. Leib
Keyword(s):  
T Cells ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Herpes Simplex Virus Type ◽  
T Cell Subsets ◽  
Trigeminal Ganglia ◽  
Corneal Disease ◽  
Simplex Virus

The role that T cell subsets play in herpetic stromal keratitis (HSK) has been the subject of intense research efforts. While most studies implicate CD4+ T cells as the principal cell type mediating primary corneal disease, recent reports using knockout mice have suggested that both CD4+ and CD8+ T cell subsets may play integral roles in modulating the disease. Furthermore, recent studies suggest that CD8+ T cells are directly involved in maintaining virus latency in infected trigeminal ganglia. This work has addressed these discrepancies by infecting the corneas of mice lacking CD4+ and CD8+ T cells with herpes simplex virus type 1 (HSV-1) and monitoring both corneal disease and latent infection of trigeminal ganglia. Results indicated that mice lacking CD8+ T cells had more severe corneal disease than either BALB/c or B6 parental strains. In contrast, mice lacking CD4+ T cells had a milder disease than parental strains. When mice were evaluated for persistence of infectious virus, only transient differences were observed in periocular tissue and corneas. No significant differences were found in persistence of virus in trigeminal ganglia or virus reactivation from explanted ganglia. These data support the following conclusions. CD4+ T cells are not required for resistance to infection with HSV-1 and probably mediate HSK. Mice lacking CD8+ T cells do not display differences in viral loads or reactivation and thus CD8+ T cells are not absolutely required to maintain latency. Finally, CD8+ T cells probably play a protective role by regulating the immunopathological response that mediates HSK.

Pathogenic potentials of glycoprotein C-negative syncytial mutants from rabbit T cells infected persistently with herpes simplex virus type 1

2005 ◽  
Vol 76 (1) ◽  
pp. 89-97
Author(s):  
Yoshimasa Ishida ◽  
Tomoyuki Okabe ◽  
Yoshimi Azukizawa ◽  
Takahiro Isono ◽  
Akira Seto
Keyword(s):  
T Cells ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Glycoprotein C ◽  
Simplex Virus
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