Complement Depletion Facilitates the Infection of Multiple Brain Tumors by an Intravascular, Replication-Conditional Herpes Simplex Virus Mutant

Ikeda, Keiro; Wakimoto, Hiroaki; Ichikawa, Tomotsugu; Jhung, Sarah; Hochberg, Fred H.; Louis, David N.; Chiocca, E. Antonio

doi:10.1128/jvi.74.10.4765-4775.2000

Cited by 138 publications

(120 citation statements)

References 67 publications

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“…Two reports from another group are supportive of this concept, as complement depletion improved intravascular delivery of replication-conditional Herpes virus to human xenograft tumors growing in rat brain. 25,26 While Ikeda et al utilized a different virus and model system, their findings of improved delivery of virus to the brain xenografts following complement inhibition is consistent with reduced opsonization and reduced liver sequestration. Less inactivation and removal of virus would make more available to target the xenograft brain tumors.…”

Section: Complement and Liver Transduction By Adenovirus Kr Zinn Et Almentioning

confidence: 99%

Bioluminescence imaging reveals a significant role for complement in liver transduction following intravenous delivery of adenovirus

et al. 2004

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The effect of complement on transgene expression was evaluated in vivo and in vitro using mice lacking complement components. Complement component 3 (C3) deficient mice (C3 À/À) and appropriate wild-type controls were intravenously injected with a replication incompetent, luciferaseexpressing normal Ad5 (Ad5Luc1), or fibritin-fiber Ad5 (Ad5FFLuc1). Repeated, noninvasive bioluminescence imaging was conducted over 35 days. Our data show for the first time that C3 facilitates both short-and long-term hepatic expression of luciferase following systemic delivery. C3 À/À and wildtype mice was 99-fold difference at 3 days for the 2.3 Â 10 9 v.p. dose (Ad5Luc1), 35-fold at 13 days for the 4.0 Â 10 9 v.p. dose (Ad5Luc1), and 22-fold at 13 days for the 4.0 Â 10 9 v.p. dose (Ad5FFLuc1). Preincubation of Ad5Luc1 with wild-type, C1q À/À , or factor B (FB) deficient mouse sera for 5 min significantly (Po0.05) increased transduction of mouse liver cells, as compared to preincubation with C3 À/À sera or PBS. These results suggest the classical or alternate complement pathway enhances Ad5-mediated liver transduction.

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Section: Complement and Liver Transduction By Adenovirus Kr Zinn Et Almentioning

confidence: 99%

Bioluminescence imaging reveals a significant role for complement in liver transduction following intravenous delivery of adenovirus

et al. 2004

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“…50 Depletion of complement via cobra venom factor (CVF) treatment also facilitated in vivo viral propagation and improved antitumor activity of hrR3. 146 As mentioned above, ICP34.5 enables HSV-1 to replicate in neurons and has been described as a specific neurovirulence factor. 43,46,47,147 There are two copies of ICP34.5 gene, because this gene is present in the inverted repeat region flanking the unique long segment.…”

Section: Single Gene Deletionmentioning

confidence: 99%

Herpes simplex virus 1 (HSV-1) for cancer treatment

2006

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Cancer remains a serious threat to human health, causing over 500 000 deaths each year in US alone, exceeded only by heart diseases. Many new technologies are being developed to fight cancer, among which are gene therapies and oncolytic virotherapies. Herpes simplex virus type 1 (HSV-1) is a neurotropic DNA virus with many favorable properties both as a delivery vector for cancer therapeutic genes and as a backbone for oncolytic viruses. Herpes simplex virus type 1 is highly infectious, so HSV-1 vectors are efficient vehicles for the delivery of exogenous genetic materials to cells. The inherent cytotoxicity of this virus, if harnessed and made to be selective by genetic manipulations, makes this virus a good candidate for developing viral oncolytic approach. Furthermore, its large genome size, ability to infect cells with a high degree of efficiency, and the presence of an inherent replication controlling mechanism, the thymidine kinase gene, add to its potential capabilities. This review briefly summarizes the biology of HSV-1, examines various strategies that have been used to genetically modify the virus, and discusses preclinical as well as clinical results of the HSV-1-derived vectors in cancer treatment.

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“…Previous studies have suggested that systemic therapy with oncolytic herpes viruses may be problematic due to inhibitory immune effects. In a rat model, circulating IgM antibody and complement have been shown to impede the intravascular efficacy of an oncolytic herpes virus (25,26). Suppression of IgM antibody with cyclophosphamide and inhibition of rodent plasma complement with cobra venom factor reversed these effects, enhancing viral survival and propagation.…”

Section: Discussionmentioning

confidence: 99%

Effective Intravenous Therapy of Murine Pulmonary Metastases with an Oncolytic Herpes Virus Expressing Interleukin 12

Wong

Chan

et al. 2004

Clinical Cancer Research

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Complement Depletion Facilitates the Infection of Multiple Brain Tumors by an Intravascular, Replication-Conditional Herpes Simplex Virus Mutant

Cited by 138 publications

References 67 publications

Bioluminescence imaging reveals a significant role for complement in liver transduction following intravenous delivery of adenovirus

Bioluminescence imaging reveals a significant role for complement in liver transduction following intravenous delivery of adenovirus

Herpes simplex virus 1 (HSV-1) for cancer treatment

Effective Intravenous Therapy of Murine Pulmonary Metastases with an Oncolytic Herpes Virus Expressing Interleukin 12

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