Herpes Simplex Virus Type 1 Evades the Effects of Antibody and Complement In Vivo

Lubinski, John M.; Jiang, Ming; Hook, Lauren M.; Chang, Yueh J.; Sarver, C. E.; Mastellos, Dimitrios C.; Lambris, John D.; Cohen, Gary H.; Eisenberg, Roselyn J.; Friedman, Harvey M.

doi:10.1128/jvi.76.18.9232-9241.2002

Cited by 92 publications

(89 citation statements)

References 51 publications

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“…The lipid envelope contains at least 11 virus-encoded glycoproteins that participate in many aspects of the virus life cycle including attachment and entry, [3][4][5] cell-to-cell spread, 6 and immune evasion. [7][8][9] Proteins residing in the underlying tegument are responsible for initiating gene expression from the viral genome, 10,11 shutting off host cell protein synthesis, 12,13 and assist in virion maturation and egress. [14][15][16][17][18] The virion proteins VP5, VP19c, VP23, and VP26 [19][20][21][22] form the icosadeltahedral capsid that encases the double-stranded DNA genome.…”

Section: Introductionmentioning

confidence: 99%

HSV trafficking and development of gene therapy vectors with applications in the nervous system

et al. 2005

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Herpes simplex virus type 1 (HSV-1) is a neurotropic doublestranded DNA virus that causes cold sores, keratitis, and rarely encephalitis in humans. Nonpathogenic HSV-1 gene transfer vectors have been generated by elimination of viral functions necessary for replication. The life cycle of the native virus includes replication in epithelial cells at the site of initial inoculation followed by retrograde axonal transport to the nuclei of sensory neurons innervating the area of cutaneous primary infection. In this review, we summarize the current understanding of the molecular basis for HSV cell entry, nuclear transport of the genome, virion egress following replication, and retrograde and anterograde axonal transport in neurons. We discuss how each of these properties has been exploited or modified to allow the generation of gene transfer vectors with particular utility for neurological applications. Recent advances in engineering virus entry have provided proof of principle that vector targeting is possible. Furthermore, significant and potentially therapeutic modifications to the pathological responses to various noxious insults have been demonstrated in models of peripheral nerve disease. These applications exploit the natural axonal transport mechanism of HSV, allowing transgene expression in the cell nucleus within the inaccessible trigeminal ganglion or dorsal root ganglion, following the noninvasive procedure of subcutaneous vector inoculation. These findings demonstrate the importance of understanding basic virology in the design of vector systems and the powerful approach of exploiting favorable properties of the parent virus in the generation of gene transfer vectors. Gene Therapy (2005) 12, 891-901.

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Section: Introductionmentioning

confidence: 99%

HSV trafficking and development of gene therapy vectors with applications in the nervous system

et al. 2005

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“…Further in vivo research by this group using deletion mutants lacking one or both domains of gC1 involved in modulating complement activation indicated that the C3b-binding domain of gC1 was much more important during complement evasion than the domain responsible for blocking properdin binding to C3b (Lubinski et al, 1999). Interestingly, it was shown recently that an HSV mutant carrying mutations in the C3b-binding domain of gC as well as in the IgG-binding domain of gE (see above) was much more sensitive to antibody and complement attack than the single mutated strains, suggesting synergistic effects by acting at multiple steps in the complement cascade (Lubinski et al, 2002).…”

Section: Herpesviridaementioning

confidence: 99%

“…Thus, gC1 has two structural domains that are involved in modulating complement activation: one binds C3b and is located in the central region of the molecule from residues 124 to 366 and the other which is required for blocking properdin binding to C3b and is located near the NH 2 terminus from residues 33 to 133 (Hung et al, 1994). The C3b-binding capacity of gC1 has been demonstrated to mediate complement evasion of the virus in vivo (Lubinski et al, , 1999(Lubinski et al, , 2002. Further in vivo research by this group using deletion mutants lacking one or both domains of gC1 involved in modulating complement activation indicated that the C3b-binding domain of gC1 was much more important during complement evasion than the domain responsible for blocking properdin binding to C3b (Lubinski et al, 1999).…”

Section: Herpesviridaementioning

confidence: 99%

“…To this end, an HSV mutant was constructed in which four amino acids were inserted into the immunoglobulin-like domain of gE, abolishing gE Fc receptor function without affecting other gE functions. Comparing this mutant in mice to wild-type HSV revealed that the Fc receptor activity of gE enables HSV to evade antibody and complement attack in vivo (Nagashunmugam et al, 1998;Lubinski et al, 2002).…”

Section: Herpesviridaementioning

confidence: 99%

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Virus complement evasion strategies

Favoreel

Walle

Nauwynck

et al. 2003

Journal of General Virology

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The immune system has a variety of tools at its disposal to combat virus infections. These can be subdivided roughly into two categories: 'first line defence', consisting of the non-specific, innate immune system, and 'adaptive immune response', acquired over time following virus infection or vaccination. During evolution, viruses have developed numerous, and often very ingenious, strategies to counteract efficient recognition of virions or virus-infected cells by both innate and adaptive immunity. This review will focus on the different strategies that viruses use to avoid recognition by one of the components of the immune system: the complement system. Complement evasion is of particular importance for viruses, since complement activation is a crucial component of innate immunity (alternative and mannan-binding lectin activation pathway) as well as of adaptive immunity (classical, anti body-dependent complement activation)

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“…41,42 The gC-null virus has also been shown to be less virulent than the wildtype virus in animals. 43 It would be interesting to examine the immune responses after the MG11-pCON-GA-Luc and its equivalent control amplicon viral vectors in the tumor microenvironment. Depending on the findings, it may be possible to further manipulate the MG11-gC fusion for improved retention of the viruses in glioma cells after infection.…”

Section: Pconga4-lucmentioning

confidence: 99%

Targeting human glioma cells using HSV-1 amplicon peptide display vector

Miao

Sia

et al. 2009

Gene Ther

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Targeting cell infection using herpes simplex virus type 1 (HSV-1) vectors is a complicated issue as the process involves multiple interactions of viral envelope glycoproteins and cellular host surface proteins. In this study, we have inserted a human glioma-specific peptide sequence (denoted as MG11) into a peptide display HSV-1 amplicon vector replacing the heparan sulfate-binding domain of glycoprotein C (gC). The modified MG11:gC envelope recombinant vectors were subsequently packaged into virions in the presence of helper virus deleted for gC. Our results showed that the tropism of these HSV-1 recombinant virions was increased for human glioma cells in culture as compared with wild-type virions. The binding of these recombinant virions could also be blocked effectively by preincubating the cells with the glioma-specific peptide, indicating that MG11 peptide and the recombinant virions competed for the same or similar receptor-binding sites on the cell surface of human glioma cells. Furthermore, preferential homing of these virions was shown in xenograft glioma mouse model following intravascular delivery. Taken together, these results validated the hypothesis that HSV-1 binding to cells can be redirected to human gliomas through the incorporation of MG11 peptide sequence to the virions.

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Herpes Simplex Virus Type 1 Evades the Effects of Antibody and Complement In Vivo

Cited by 92 publications

References 51 publications

HSV trafficking and development of gene therapy vectors with applications in the nervous system

HSV trafficking and development of gene therapy vectors with applications in the nervous system

Virus complement evasion strategies

Targeting human glioma cells using HSV-1 amplicon peptide display vector

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