Zoster in Children with Cancer: Radioimmune Precipitation Profiles of Sera Before and After Illness

Grose, Charles

doi:10.1093/infdis/147.1.47

Cited by 22 publications

(9 citation statements)

References 23 publications

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“…Zweerink & Neff (1981) reported immunoprecipitation studies on nine patients; antibodies to 14 polypeptides including three glycosylated ones were described. Grose (1983) detected antibodies to 16 polypeptides, of which three were glycosylated, in sera from five children with zoster. studying sequential sera from 10 patients with VZV infection determined antibodies to four glycoproteins, gp118, gp98, gp66 and gp62 in sera from patients convalescing from chickenpox.…”

confidence: 98%

Antibody Response to Varicella-Zoster Virus Surface Glycoproteins in Chickenpox and Shingles

Larkin

Heckels

Ogilvie

1985

Journal of General Virology

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SUMMARYVaricella-zoster virus (VZV)-infected cell surface proteins were investigated using extrinsic radiolabelling of the cell surface, immunoprecipitation of detergentsolubilized extract of the same cell surface and fractionation of the immunoprecipitates using SDS-PAGE. Glycosylated proteins were identified by their affinity for Ricinus communis lectin. Six glycoproteins with apparent mol. wt. of 170K, 105K, 93K, 81K, 53K and 45K were identified. The 170K glycoprotein was shown to be disulphidelinked since under reducing conditions for SDS-PAGE it was cleaved to a protein of 63K mol. wt. The IgG responses to these glycoproteins during various clinical circumstances are described. In acute sera from all chickenpox patients and in the majority of acute shingles sera, antibodies reactive with glycoproteins could not be detected. In chickenpox convalescence, antibodies reactive with glycoproteins of mol. wt. 170K, 105K, 53K and 45K were identified, whilst during zoster convalescence antibodies to all six were prominent. Antibodies to the disulphide-linked glycoprotein persisted for many years following both the primary disease and its reactivation. Disseminated zoster was associated with significantly low levels of antibodies to these surface glycoproteins.

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confidence: 98%

Antibody Response to Varicella-Zoster Virus Surface Glycoproteins in Chickenpox and Shingles

Larkin

Heckels

Ogilvie

1985

Journal of General Virology

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“…Detection of VZV DNA with a PCR amplification test would be suggestive, although a negative VZV DNA test does not exclude the diagnosis of a stroke related to herpes zoster. Since most patients with stroke do not have a cerebrospinal fluid examination, a diagnosis of recent herpes zoster can be inferred by titration of anti-VZV antibody in peripheral blood during the stroke episode, since there is a marked and prolonged increase in VZV titer after herpes zoster [19]. However, commercial or hospital microbiology laboratories rarely offer this option, so the test may need to be performed in a research laboratory.…”

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confidence: 99%

Reassessing the link between herpes zoster ophthalmicus and stroke

Grose

Adams

2014

Expert Review of Anti-infective Therapy

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This editorial will assess a proposed link between herpes zoster ophthalmicus and subsequent stoke. Herpes zoster (also called shingles) is caused by varicella-zoster virus (VZV), one of the 9 human herpesviruses. When children contract their primary VZV infection, virus often travels to the trigeminal ganglia and establishes latency. Upon reactivation in late adulthood, the same virus travels anterograde to cause herpes zoster ophthalmicus. In some people, the virus also traffics from the same trigeminal ganglion along afferent fibers around the carotid artery and its branches. Subsequently VZV-induced inflammation within the affected cerebral arteries leads to occlusion and stroke. In one retrospective analysis of people with herpes zoster ophthalmicus, there was a 4.5 fold higher risk of stroke than in a control group. Two other studies found a less compelling association.The potential links between herpes zoster and subsequent stroke are receiving increasing attention. Varicella-zoster virus (VZV) is the well-known agent of varicella or chickenpox, an exanthematous disease common to children around the world (FIGURE 1) [1]. The vesicular exanthem is caused by the virus exiting the capillaries and replicating in the epidermis. Stroke was known to occur in a very small number of children during or shortly after the primary infection varicella [2]. Since VZV can cause a generalized encephalomyelitis, the low incidence of stroke was not considered to be highly unusual. Furthermore, the widespread use of varicella vaccination has markedly decreased the prevalence of varicella in many countries, with a further decrease in varicella-related stroke [3].During primary varicella infection, the virus frequently establishes latency in the trigeminal ganglia on the surface of the petrous bones (FIGURE 1); virus also commonly enters other cranial nerves as well as the dorsal root ganglia and autonomic ganglia. Decades later, the latent virus reactivates and travels anterograde from the ganglion to the skin, to cause a dermatomal exanthem known as herpes zoster (shingles) [4,5]. A common location of zoster is along the lower chest, representing reactivation from several lower thoracic (dorsal) ganglia. Another common site for reactivation is in the ophthalmic division of the trigeminal nerve, which provides sensation to the eye and forehead. The resultant infection is diagnosed as herpes zoster ophthalmicus (HZO) [6]. Herpes zoster ophthalmicus & strokeThe major points about the pathogenesis of herpes zoster are well known. Herpes zoster is a reactivation of a latent VZV genome within a ganglion. The VZV DNA genome is approximately 125,000 base pairs; the genome is not integrated within the human genome [7]. The most common explanation for reactivation is waning immunity in the elderly [4]. Herpes zoster can also be precipitated earlier in adults who receive chemotherapy or other immunosuppressive regimens, for example, for treatment of diseases such as systemic lupus. The emergent virus travels anterograde in the axon of ...

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“…"and was to the broadest complement of viral proteins," which is in agreement with our observations. That many of the most reactive bands detected by IgG immunoblotting, notably between 57 and 114 kDa, represent viral glycoproteins is supported by the results obtained by €UP [Grose, 1983;Larkin et al, 1985;Weigle and Grose, 1984;Zweerink and Neff, 19811. All of these groups reported glycoproteins corresponding to at least some of the bands reported herein.…”

Section: Discussionmentioning

confidence: 71%

“…The analysis of these responses is an important step in the development of a subunit vaccine and may provide valuable information about the pathogenesis of VZV infections. Work to date using radioimmunoprecipitation [Grose, 1983;Weigle and Grose, 1984;Zweerink and Neff, 19811 has identified the viral glycoproteins and the major capsid antigen as the main targets for IgG antibodies. What little information is available about the targets for IgM class antibodies is concerned only with the primary response [Palumbo et al, 19841.…”

Section: Introductionmentioning

confidence: 99%

Serological responses in varicella and zoster assayed by immunoblotting

Harper

Kangro

Heath

1988

Journal of Medical Virology

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Acute and convalescent zoster sera taken from 11 patients with varicella and 12 patients with zoster were assayed using immunoblotting for the presence of IgG- and IgM-class antibodies to proteins present in varicella-zoster virus-infected cells. All patients exhibited a detectable virus-specific response with both antibody classes. The IgG responses involved up to 28 protein bands between 28 and 255 kilodaltons (kDa). The reactivity was particularly strong in the 78-114-kDa region, with additional bands observed with all patients at 32, 35, 66, and 220 kDa. This pattern of reactivity typically developed more slowly and was weaker and more variable in patients with varicella compared to those with zoster. The reactivity of IgM antibodies in immunoblotting was similar after varicella and after zoster. Individual sera showed up to 25 bands, with the major reactivity being directed against the 78-96-kDa region and two bands at 32 and 35 kDa. Some differences were apparent between the primary and anamnestic responses with both IgG and IgM antibodies, but this did not allow reliable discrimination of the two types of infection.

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Zoster in Children with Cancer: Radioimmune Precipitation Profiles of Sera Before and After Illness

Cited by 22 publications

References 23 publications

Antibody Response to Varicella-Zoster Virus Surface Glycoproteins in Chickenpox and Shingles

Antibody Response to Varicella-Zoster Virus Surface Glycoproteins in Chickenpox and Shingles

Reassessing the link between herpes zoster ophthalmicus and stroke

Serological responses in varicella and zoster assayed by immunoblotting

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