Varicella Virus

Taylor-Robinson, D.; Caunt, Anne E.

doi:10.1007/978-3-7091-3427-6

Cited by 25 publications

(14 citation statements)

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“…During primary infection, VZV accesses sensory neurons located within spinal ganglia, where it has the ability to initiate a productive infection, as demonstrated by the presence of productive viral transcripts and proteins (9,16,68,69,77). However, at some point after this infection, the virus establishes latency in these cells.…”

Section: Discussionmentioning

confidence: 99%

Varicella-Zoster Virus-Infected Human Sensory Neurons Are Resistant to Apoptosis, yet Human Foreskin Fibroblasts Are Susceptible: Evidence for a Cell-Type-Specific Apoptotic Response

Hood

Cunningham

Slobedman

et al. 2003

J Virol

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The induction of apoptosis or programmed cell death in virus-infected cells is an important antiviral defense mechanism of the host, and some herpesviruses have evolved strategies to modulate apoptosis in order to enhance their survival and spread. In this study, we examined the ability of varicella-zoster virus (VZV) to induce apoptosis in primary human dorsal root ganglion neurons and primary human foreskin fibroblasts (HFFs). Three independent methods (annexin V, TUNEL [terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling] staining, and electron microscopy) were used to assess apoptosis in these cells on days 1, 2, and 4 postinoculation. By all three methods, apoptosis was readily detected in VZV-infected HFFs. In stark contrast, apoptosis was not detected during productive VZV infection of neurons. The low-passage clinical isolate Schenke and the tissue culture-adapted ROka strain both induced apoptosis in HFFs but not in neurons, suggesting that this cell-type-specific apoptotic phenotype was not VZV strain specific. These data show that the regulation of apoptosis differs markedly between HFFs and neurons during productive VZV infection. Inhibition of apoptosis during infection of neurons may play a significant role in the establishment, maintenance, and reactivation of latent infection by promoting survival of these postmitotic cells.

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Section: Discussionmentioning

confidence: 99%

Varicella-Zoster Virus-Infected Human Sensory Neurons Are Resistant to Apoptosis, yet Human Foreskin Fibroblasts Are Susceptible: Evidence for a Cell-Type-Specific Apoptotic Response

Hood

Cunningham

Slobedman

et al. 2003

J Virol

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“…In contrast to the broad host range of most alphaherpesviruses in cultured cells, productive VZV infection in vitro is restricted almost exclusively to cells derived from humans and other primates (64). Reported exceptions are guinea pig embryonic fibroblasts (62, 64), rabbit kidney cells (64,68), and cotton rat fibroblasts (54). For many viruses, restriction in cultured cells is determined by specific cellular receptors that must be engaged for virus binding and entry.…”

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confidence: 99%

Postentry Events Are Responsible for Restriction of Productive Varicella-Zoster Virus Infection in Chinese Hamster Ovary Cells

Finnen¹,

Mizokami²,

Banfield

et al. 2006

J Virol

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Varicella-zoster virus (VZV) is a human alphaherpesvirus that causes chicken pox (varicella) upon primary infection and shingles (zoster) upon reactivation of the virus from latently infected sensory neurons. In contrast to the broad host range of most alphaherpesviruses in cultured cells, productive VZV infection in vitro is restricted almost exclusively to cells derived from humans and other primates (64). Reported exceptions are guinea pig embryonic fibroblasts (62, 64), rabbit kidney cells (64,68), and cotton rat fibroblasts (54). For many viruses, restriction in cultured cells is determined by specific cellular receptors that must be engaged for virus binding and entry. After successfully entering a cell, viruses can encounter other blocks to productive infection (20,36). In studies using rats, cotton rats, or mice as in vivo models of VZV latency, viral DNA (1,6,27,[51][52][53][54]69), viral transcripts (6,27,51,54,69), and immediate early viral proteins (18,27,51) were detected in infected cells, primarily neurons, indicating that VZV is capable of entering rodent cells and initiating early events in the infectious cycle. Cultured rat neurons and the mouse neuroblastoma cell line neuro-2A also permitted VZV entry, but productive infection was blocked in both cases (4, 37). Thus, the restriction of productive VZV infection in cultured nonprimate cells may be governed primarily by postentry events.Much of our understanding of alphaherpesvirus entry comes from studies of herpes simplex virus type 1 (HSV-1) (60, 61). HSV-1 envelope glycoproteins gB and/or gC mediate binding of virus to cell surface glycosaminoglycans, predominantly heparan sulfate (59, 63). Following virus binding, gD engages one of several entry receptors (19,40,58,60). Fusion of viral and cellular membranes then ensues, either directly at the cell surface (15, 16) or following endocytosis (38,42,43) by a mechanism that requires the participation of gB, gD, a heterodimer of gH and gL, and a gD entry receptor (5,44,47,65). The emerging picture of entry from HSV-1 studies is one that involves multiple entry receptors and multiple entry pathways. This versatility likely contributes to the wide host range observed for HSV-1 in vitro and the success of this virus as a pathogen.Much less is known about the binding and entry of VZV, largely due to the difficulty in obtaining high titers of cell-free (CF) virus. An entry process similar to that described for HSV-1 has been proposed for VZV, commencing with binding of virions to heparan sulfate via gB (25, 70), followed by interaction of viral glycoproteins with an entry receptor (7, 70). The interaction of mannose-6-phosphate (M6P) groups found on at least four VZV glycoproteins (gB, gE, gH, and gI) with the cation-independent mannose-6-phosphate receptor (CI-MPR) is believed to facilitate virus entry (7,17,70). While the exact consortium of VZV proteins needed for virus-cell fusion has not been defined, results from cell-cell fusion assays (9,11,12,46), blocking assays with antiglycoprotein antibo...

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“…Varicella-zoster virus (VZV) is a human herpesvirus which causes varicella (chicken pox) and, after a highly variable latency period, may reactivate to produce zoster (shingles) (1). The poor growth of VZV in cell culture and the inherent difficulty in obtaining and purifying sufficient quantities of viral DNA have significantly impeded the detailed molecular characterization ofthe genome.…”

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confidence: 99%

Molecular cloning and physical mapping of varicella-zoster virus DNA.

Straus¹,

Owens²,

Ruyechan³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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Varicella-zoster virus (VZV) DNA was cleaved with restriction endonuclease EcoRI, and most of the resulting fragments were successfully cloned in the phage vector AgtWES-AB. Double digestions ofcloned fragments with EcoRI and BamHI and hybridizations to blot-transferred BamHI digests of VZV DNA were used to construct a physical map of the genome. The molecular termini of the DNA were identified by restriction enzyme analysis after exonuclease HI digestion. The data indicate that VZV DNA exists in two isomeric forms that differ by inversion of one short terminal genome segment. Electron microscopic studies revealed that the short genome segment consists of a terminal sequence of about 3.4 x 106 daltons that is separated from an internal inverted repeat of itself by a 5.8 x 106-dalton unique DNA segment.Varicella-zoster virus (VZV) is a human herpesvirus which causes varicella (chicken pox) and, after a highly variable latency period, may reactivate to produce zoster (shingles) (1). The poor growth of VZV in cell culture and the inherent difficulty in obtaining and purifying sufficient quantities of viral DNA have significantly impeded the detailed molecular characterization ofthe genome. Although early studies suggested that VZV DNA is a double-stranded molecule of 92-110 megadaltons (MDal) (2, 3), more recent estimates indicate that the genome is only about 80 MDal (4, 5). Initial restriction endonuclease-generated cleavage profiles of VZV DNA revealed the presence of submolar genome fragments, suggesting that this genome, like those of other herpesviruses, may exist in multiple conformations (2,(6)(7)(8). Recently, we have shown by quantitative densitometry of gel profiles that endonuclease digestion can generate up to four half-molar fragments, but no quarter-molar fragments. We postulated, therefore, that the genome may exist in either of two isomeric forms that differ by inversion of but one genome segment (5).In this report we describe the molecular cloning ofVZV DNA restriction fragments in a phage A vector and present a physical restriction map of the VZV genome. This map plus electron microscopic analyses reported here demonstrate that VZV DNA exists in two isomeric forms. MATERIALS AND METHODSCells and Viruses. VZV strain Ellen was obtained from the American Type Culture Collection (ATCC VR-586). Other VZV isolates used were recovered from vesicle fluid aspirates from patients with zoster infection. VZV was grown in human embryonic lung fibroblasts as described (5). Phage AgtWES-AB was grown and purified as described (9). Cloning of VZV DNA. Purified VZV DNA was digested with EcoRI and ligated to purified AgtWES-AB vector arms as described (9, 10). The DNA was packaged into phage particles in vitro (15), and the virus was assayed by plaque formation and amplified in Escherichia coli LE 392 (9). This procedure routinely yielded about 106 plaque-forming units/,ug of vector DNA. Recombinant A phage DNA was extracted and prepared as described (10).Electron Microscopy ofVZV DNA. Viral DNAs (0.5-1.0 ...

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Varicella Virus

Cited by 25 publications

References 0 publications

Varicella-Zoster Virus-Infected Human Sensory Neurons Are Resistant to Apoptosis, yet Human Foreskin Fibroblasts Are Susceptible: Evidence for a Cell-Type-Specific Apoptotic Response

Varicella-Zoster Virus-Infected Human Sensory Neurons Are Resistant to Apoptosis, yet Human Foreskin Fibroblasts Are Susceptible: Evidence for a Cell-Type-Specific Apoptotic Response

Postentry Events Are Responsible for Restriction of Productive Varicella-Zoster Virus Infection in Chinese Hamster Ovary Cells

Molecular cloning and physical mapping of varicella-zoster virus DNA.

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