Recombinant Monoclonal Antibody Recognizes a Unique Epitope on Varicella-Zoster Virus Immediate-Early 63 Protein

Mueller, Niklaus H.; Bos, Nathan; Seitz, Scott; Wellish, Mary; Mahalingam, Ravi; Gilden, Don; Cohrs, Randall J.

doi:10.1128/jvi.06814-11

Cited by 4 publications

(3 citation statements)

References 27 publications

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“…We observed the diffuse presence of VZV IE63 throughout the virus-infected cell but particularly in the nucleus, consistent with previous reports of VZV IE63 localization in the nucleus (Mueller et al 2010; Ambagala et al 2009). Nuclear functions attributed to VZV IE63 include regulation of viral and cellular gene transcription (Jackers et al 1992; Zuranski et al 2005; Habran et al 2007; Khalil et al 2013), perhaps by modulating the host anti-silencing factor (Ambagala et al 2009), by enhancing the function of VZV IE62, the major virus immediate-early regulator of gene transcription (Lynch et al 2002), or by modifying how cellular RNA polymerase II recognized virus and cell gene promoters (Di Valentin et al 2005).…”

Section: Discussionsupporting

confidence: 92%

Varicella zoster virus infection of human fetal lung cells alters mitochondrial morphology

et al. 2016

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Varicella zoster virus (VZV) is a ubiquitous alphaherpesvirus that establishes latency in ganglionic neurons throughout the neuraxis after primary infection. Here, we show that VZV infection induces a time-dependent significant change in mitochondrial morphology, an important indicator of cellular health, since mitochondria are involved in essential cellular functions. VZV immediate-early protein 63 (IE63) was detected in mitochondria-rich cellular fractions extracted from infected human fetal lung fibroblasts (HFL) by Western blotting. IE63 interacted with cytochrome c oxidase in bacterial 2-hybrid analyses. Confocal microscopy of VZV-infected HFL cells at multiple times after infection revealed the presence of IE63 in the nucleus, mitochondria, and cytoplasm. Our data provide the first evidence that VZV infection induces alterations in mitochondrial morphology, including fragmentation, which may be involved in cellular damage and/or death during virus infection.

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Section: Discussionsupporting

confidence: 92%

Varicella zoster virus infection of human fetal lung cells alters mitochondrial morphology

et al. 2016

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“…VZV plaques were identified by immunostaining. Briefly, monolayers were blocked for 60 minutes in 3% blocked for 60 minutes in 3% BSA in TBS, incubated for 60 minutes with primary antibody (rabbit anti-IE63: 1:1,000 dilution) [23] followed by 60 minutes incubation with alkaline phosphatase conjugated secondary antibody (goat anti-rabbit IgG; 1:10,000 dilution; Abcam, Cambridge, MA). Immunostaining was visualized with NBT/BCIP (Pierce, Rockford IL).…”

Section: Methodsmentioning

confidence: 99%

International Archives of Medicine

Shahzad

Cohrs²

2015

Int Arch Med

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Objectives The aim of this study was to determine the in vitro anti-viral effect of honey on varicella zoster virus. Methods Manuka and clover honeys were used at concentrations ranging from 0-6% wt/vol. A clinical VZV isolate was obtained from a zoster vesicle and used at low passage. Various concentrations of manuka and clover honey were added to the tissue culture medium of VZV-infected human malignant melanoma (MeWo) cells. Results Both types of honey showed antiviral activity against varicella zoster virus with an approximate EC50 = 4.5 % (wt/vol). Conclusions Our results showed that honey has significant in vitro anti-VZV activity. As, honey is convenient for skin application, is readily available and inexpensive, honey may be an excellent remedy to treat zoster rash in developing countries where antiviral drugs are expensive or not easily available.

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“…While, in general, the published sequence is correct, the SVV genomic sequences may need correction in certain regions. In summary, since very few SVV-specific antibodies have been available so far (18,55,56), our MAbs will facilitate the analysis of SVV in nonhuman primate models and provide novel insights into SVV pathogenesis.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive Analysis of Varicella-Zoster Virus Proteins Using a New Monoclonal Antibody Collection

Roviš

Bailer

Pothineni

et al. 2013

J Virol

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i Varicella-zoster virus (VZV) is the etiological agent of chickenpox and shingles. Due to the virus's restricted host and cell type tropism and the lack of tools for VZV proteomics, it is one of the least-characterized human herpesviruses. We generated 251 monoclonal antibodies (MAbs) against 59 of the 71 (83%) currently known unique VZV proteins to characterize VZV protein expression in vitro and in situ. Using this new set of MAbs, 44 viral proteins were detected by Western blotting (WB) and indirect immunofluorescence (IF); 13 were detected by WB only, and 2 were detected by IF only. A large proportion of viral proteins was analyzed for the first time in the context of virus infection. Our study revealed the subcellular localization of 46 proteins, 14 of which were analyzed in detail by confocal microscopy. Seven viral proteins were analyzed in time course experiments and showed a cascade-like temporal gene expression pattern similar to those of other herpesviruses. Furthermore, selected MAbs tested positive on human skin lesions by using immunohistochemistry, demonstrating the wide applicability of the MAb collection. Finally, a significant portion of the VZV-specific antibodies reacted with orthologs of simian varicella virus (SVV), thus enabling the systematic analysis of varicella in a nonhuman primate model system. In summary, this study provides insight into the potential function of numerous VZV proteins and novel tools to systematically study VZV and SVV pathogenesis. V aricella-zoster virus (VZV) belongs to the alphaherpesvirus subfamily and is the only member of the genus Varicellovirus that can infect humans (1, 2). Primary infection causes chickenpox and typically occurs in early childhood with a prominent, highly contagious vesicular rash (3). During primary infection, VZV establishes latency in sensory trigeminal and dorsal root ganglia. Reactivation from latency results in a secondary disease called herpes zoster (HZ), or shingles, that is more common in elderly people (4). HZ most frequently occurs in the thoracic or lumbar nerve segments and the distribution area of the trigeminal nerve, causing a painful rash in the corresponding dermatome. While the molecular mechanism for reactivation from latency is not well characterized, it is more frequent in immunocompromised patients (5). The most common sequela of HZ is postherpetic neuralgia (PHN). In addition, VZV reactivation can lead to zoster ophthalmicus, acute retinal necrosis, meningitis, and vasculopathy (6).The seroprevalence of VZV differs significantly between countries, but the majority of individuals are seropositive by the time of adolescence (7). While in otherwise healthy children and adolescents, primary VZV infection mostly resolves spontaneously without sequelae, severe symptoms may occur in immunocompromised people and during pregnancy (6). Vertical transmission of VZV during the first trimester causes congenital varicella syndrome (CVS), which is characterized by skin lesions, hypoplasia, low birth weight, and neurological dis...

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Recombinant Monoclonal Antibody Recognizes a Unique Epitope on Varicella-Zoster Virus Immediate-Early 63 Protein

Cited by 4 publications

References 27 publications

Varicella zoster virus infection of human fetal lung cells alters mitochondrial morphology

Varicella zoster virus infection of human fetal lung cells alters mitochondrial morphology

International Archives of Medicine

Comprehensive Analysis of Varicella-Zoster Virus Proteins Using a New Monoclonal Antibody Collection

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