The varicella-zoster virus (VZV) causes two diseases. The primary VZV infection, known as chickenpox, typically occurs during childhood. Herpes zoster infection results later in life from reactivation of VZV in the dorsal root ganglia. Herpes zoster characteristically results in a rash with a unilateral dermatomal distribution, which usually resolves within 2 to 4 weeks. If the infection does n...

Mink lung cells (MvILu) are highly susceptible to varicella-zoster virus (VZV). The titres of cell-free VZV suspensions reached 1.0 x 10(7) p.f.u./ml at 3 days post-infection, with subsequent cell degeneration, if MvILu cells were infected with a multiplicity of infectious virus of 0.01 p.f.u./cell. In contrast, during the same period and under the same conditions the titres of cell-free VZV we...

Varicella-zoster virus (VZV) can complement temperature-sensitive mutants of herpes simplex virus. Of seven mutants tested, two, carrying mutations in the immediate-early ICP4 and ICP27 proteins, were complemented. This complementation was not seen in coinfections with adenovirus type 5 or cytomegalovirus. Following transfection into CV-1 cells, a DNA fragment containing the VZV short repeat se...

Varicella zoster virus (VZV) pneumonitis and brainstem encephalitis developed in an immunocompetent adult without rash. Chest computed tomography exhibited nodularity; lung biopsy revealed multinucleated giant cells, Cowdry A inclusions, VZV antigen, and DNA. Varicella zoster virus central nervous system disease was verified by cerebrospinal fluid (CSF) anti-VZV IgG antibody with reduced serum/...

Varicella-zoster virus (VZV) glycoprotein I (gI) is dispensable in cell culture; the SCIDhu model of VZV pathogenesis was used to determine whether gI is necessary in vivo. The parental and repaired viruses grew in human skin and thymus/liver implants, but the gI deletion mutant was not infectious. Thus, gI is essential for VZV infectivity in skin and T cells.

IE62, the major transcriptional activator protein encoded by varicella-zoster virus (VZV), locates to the nucleus when expressed in transfected cells. We show here that cytoplasmic forms of IE62 accumulate in transfected and VZV-infected cells as the result of the protein kinase activity associated with VZV open reading frame 66 (ORF66). Expression of the ORF66 protein kinase but not the VZV OR...

Although acyclovir prophylaxis against varicella zoster virus (VZV) infection for ≥1 year is recommended after allogeneic hematopoietic cell transplantation (HCT), the emergence of acyclovir-resistant viruses and adverse drug effects cannot be ignored. We investigated the cumulative incidence of VZV infection after allogeneic HCT in children receiving a shorter duration of acyclovir prophylaxis...

AIMS To study the cutaneous and visceral distribution of herpes simplex virus (HSV) and varicella zoster virus (VZV) in fatal infections. METHODS Standard histology, immunohistochemistry (monoclonal antibodies VL8 and VL2 and polyclonal antibody IE63 directed against VZV; monoclonal antibodies IBD4 and HH2 and polyclonal antibodies directed against HSVI and HSVII) and in situ hybridisation (a...

Although envelope glycoprotein M (gM) is highly conserved among herpesviruses, the varicella-zoster virus (VZV) gM homolog has never been investigated. Here we characterized the VZV gM homolog and analyzed its function in VZV-infected cells. The VZV gM homolog was expressed on virions as a glycoprotein modified with a complex N-linked oligosaccharide and localized mainly to the Golgi apparatus ...