scholarly journals Efficacy of HER2 retargeted herpes simplex virus as therapy for high-grade glioma in immunocompetent mice

2012 ◽  
Vol 19 (11) ◽  
pp. 788-795 ◽  
Author(s):  
E Reisoli ◽  
E Gambini ◽  
I Appolloni ◽  
V Gatta ◽  
M Barilari ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
High Grade Glioma ◽  
High Grade ◽  
Immunocompetent Mice ◽  
Simplex Virus

scholarly journals HG-08ONCOLYTIC HERPES SIMPLEX VIRUS: AN ANTI-INVASIVE THERAPEUTIC STRATEGY FOR PAEDIATRIC HIGH GRADE GLIOMA AND DIFFUSE INTRINSIC PONTINE GLIOMA

2016 ◽  
Vol 18 (suppl 3) ◽  
pp. iii49.3-iii49
Author(s):  
Julia Cockle ◽  
Elizabeth Ilett ◽  
Anke Brüning-Richardson ◽  
Jill Thompson ◽  
Tim Kottke ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Therapeutic Strategy ◽  
High Grade Glioma ◽  
Diffuse Intrinsic Pontine Glioma ◽  
High Grade ◽  
Pontine Glioma ◽  
Simplex Virus

scholarly journals Replication-competent Herpes Simplex Virus Retargeted to HER2 as Therapy for High-grade Glioma

2012 ◽  
Vol 20 (5) ◽  
pp. 994-1001 ◽  
Author(s):  
Eleonora Gambini ◽  
Elisa Reisoli ◽  
Irene Appolloni ◽  
Valentina Gatta ◽  
Gabriella Campadelli-Fiume ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
High Grade Glioma ◽  
High Grade ◽  
Simplex Virus

scholarly journals Adenovirus-mediated delivery of herpes simplex virus thymidine kinase administration improves outcome of recurrent high-grade glioma

Oncotarget ◽  
2015 ◽  
Vol 7 (4) ◽  
pp. 4369-4378 ◽  
Author(s):  
Nan Ji ◽  
Danhui Weng ◽  
Cang Liu ◽  
Zheng Gu ◽  
Shizhang Chen ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Thymidine Kinase ◽  
High Grade Glioma ◽  
High Grade ◽  
Simplex Virus

scholarly journals Effect of prior exposure to herpes simplex virus 1 on viral vector-mediated tumor therapy in immunocompetent mice

Gene Therapy ◽  
1999 ◽  
Vol 6 (10) ◽  
pp. 1751-1758 ◽  
Author(s):  
A Chahlavi ◽  
S D Rabkin ◽  
T Todo ◽  
P Sundaresan ◽  
R L Martuza
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Viral Vector ◽  
Tumor Therapy ◽  
Prior Exposure ◽  
Herpes Simplex Virus 1 ◽  
Immunocompetent Mice ◽  
Simplex Virus

Chlamydia pneumoniae, Herpes simplex virus and Cytomegalovirus in symptomatic and asymptomatic high-grade internal carotid artery stenosis. Does infection influence plaque stability?

VASA ◽  
2005 ◽  
Vol 34 (3) ◽  
pp. 163-169 ◽  
Author(s):  
Müller ◽  
Huber ◽  
Henrich ◽  
Adams ◽  
Berns ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Chlamydia Pneumoniae ◽  
Internal Carotid ◽  
Internal Carotid Artery Stenosis ◽  
High Grade ◽  
Asymptomatic Patients ◽  
Simplex Virus

Background: Current debates are focused on inflammatory processes in atherosclerotic lesions as a possible pathomechanism for destabilization and thrombembolism. In this prospective study the role of systemic and local infection in patients with high-grade internal carotid artery stenosis (ICA) was evaluated. Patients and methods: Serum antibody titers of 109 consecutive patients, who underwent surgery for ICA stenosis (asymptomatic n = 40, symptomatic n = 69) were prospectively measured for Chlamydia pneumoniae (Cpn) (IgA and IgG), Herpes simplex virus (HSV) (IgG, IgM) and Cytomegalovirus (CMV) (IgG, IgM) respectively. 53 carotis plaques of this group (asymptomatic n = 17, symptomatic n = 36) could be analyzed by polymerase chain reaction (PCR) for Cpn-, HSV- and CMV-DNA presence. Results: Seropositivity was found in 61,5% for Cpn, 91,7% for HSV and 72,5% CMV respectively. No significant relation was found between symptomatic and asymptomatic patients as well as no difference was seen for presence of IgA antibodies against Cpn comparing both groups. Plaque-PCR revealed Cpn in 7 cases (13,2%), HSV in 2 cases (3,8%) and no CMV had been detected. Again, no significant relationship was found concerning symptomatic and asymptomatic patients. All 9 PCR-positive plaques displayed lesions of "complicated atherosclerosis" as central fibrous necrosis and calcification or plaque bleeding and surface thrombosis. Conclusions: Our results do not support the hypothesis that systemic Cpn, HSV or CMV- infection or evidence of Cpn-, HSV- or CMV-DNA in carotid plaques causes plaque destabilization and cerebral thromboembolism. Plaque infection could only be observed in cases with advanced atherosclerosis.

scholarly journals Pathogenesis of Herpes Simplex Virus-Induced Ocular Immunoinflammatory Lesions in B-Cell-Deficient Mice

2000 ◽  
Vol 74 (8) ◽  
pp. 3517-3524 ◽  
Author(s):  
Shilpa P. Deshpande ◽  
Mei Zheng ◽  
Massoud Daheshia ◽  
Barry T. Rouse
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
B Cell ◽  
Corneal Stroma ◽  
Chain Gene ◽  
Herpetic Encephalitis ◽  
Immunocompetent Mice ◽  
Virus Expression ◽  
Simplex Virus ◽  
Deficient Mice

ABSTRACT The role of B cells and humoral immunity in herpes simplex virus (HSV) ocular infections was studied in immunoglobulin μ chain gene-targeted B-cell-deficient mice (μK/O). At doses of virus well tolerated by immunocompetent mice, heightened susceptibility of μK/O mice to herpetic encephalitis as well as to herpetic stromal keratitis (HSK) was observed. An explanation was sought for the increased severity of HSK in the μK/O mice. First, the lack of antibody responses in μK/O mice resulted in longer viral persistence and dissemination to the corneal stroma, the site of inflammation. Prolonged virus expression in the corneal stroma was suggested to cause bystander activation of Th1-type CD4+ T cells, further contributing to the severity of HSK lesion expression in μK/O mice. Second, μK/O mice generated minimal Th2 cytokine responses compared to wild-type mice. Such responses might serve to downregulate the severity of Th1-mediated HSK lesions.

Herpes simplex virus type 1 (HSV-1) UL56 gene is involved in viral intraperitoneal pathogenicity to immunocompetent mice

1994 ◽  
Vol 134 (1-2) ◽  
pp. 73-83 ◽  
Author(s):  
C. Berkowitz ◽  
M. Moyal ◽  
A. R�sen-Wolff ◽  
G. Darai ◽  
Y. Becker
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Immunocompetent Mice ◽  
Simplex Virus ◽  
Hsv 1

scholarly journals Virus-Encoded B7-2 Costimulation Molecules Enhance the Protective Capacity of a Replication-Defective Herpes Simplex Virus Type 2 Vaccine in Immunocompetent Mice

2008 ◽  
Vol 83 (2) ◽  
pp. 953-960 ◽  
Author(s):  
Sri P. Vagvala ◽  
Lydia G. Thebeau ◽  
Saydra R. Wilson ◽  
Lynda A. Morrison
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Immune Responses ◽  
Progeny Virus ◽  
Vaginal Mucosa ◽  
Protective Capacity ◽  
Challenge Virus ◽  
Immunocompetent Mice ◽  
Simplex Virus ◽  
Defective Virus

ABSTRACT Herpes simplex virus 2 (HSV-2) and, to a lesser extent, HSV-1 cause the majority of sexually transmitted genital ulcerative disease. No effective prophylactic vaccine is currently available. Replication-defective HSV stimulates immune responses in animals but produces no progeny virus, making it potentially useful as a safe form of live vaccine against HSV. Because it does not replicate and spread in the host, however, replication-defective virus may have relatively limited capacity to solicit professional antigen presentation. We previously demonstrated that in mice devoid of B7-1 and B7-2 costimulation molecules, replication-defective HSV-2 encoding B7-1 or B7-2 induces stronger immune responses and protection against HSV-2 challenge than immunization with replication-defective virus alone. Here, we vaccinated wild-type mice fully competent to express endogenous B7 costimulation molecules with replication-defective HSV-2 or replication-defective virus encoding B7-2 and compared their capacities to protect against vaginal HSV-2 infection and disease. Replication-defective virus encoding B7-2 induced more IFN-γ-producing CD4 T cells than did replication-defective virus alone. Immunization with B7-2-expressing virus decreased challenge virus replication in the vaginal mucosa, genital and neurological disease, and mortality more effectively than did immunization with the parental replication-defective virus. Prior immunization with B7-expressing, replication-defective virus also effectively suppressed infection of the nervous system compared to immunization with the parental virus. Thus, B7 costimulation molecules expressed at the site of HSV infection can enhance vaccine efficacy even in a fully immunocompetent host.

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