Growth of Varicella-Zoster Virus in Human Thyroid Tissue Cultures

Caunt, Anne E.

doi:10.1016/s0140-6736(63)90680-9

Cited by 31 publications

(9 citation statements)

References 5 publications

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“…In addition, mechanisms of disrupting cell integrity (e.g. freeze-thaw, ultrasonication or Dounce homogenisation) result in a progressive loss of infectivity [27][28][29][30]. Even though viral particles are readily observed by transmission electron microscopy (TEM) on the surface of and within VZV-infected cells, these viruses are highly pleomorphic [31][32][33].…”

Section: Vzv Fusion and Cell-to-cell Spreadmentioning

confidence: 99%

Membrane fusion mediated by herpesvirus glycoproteins: the paradigm of varicella‐zoster virus

Cole

Grose

2003

Reviews in Medical Virology

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Varicella-zoster virus (VZV) is well known for its propensity to cause polykaryons (syncytia) in the vesicles within infected skin. Similarly in cultured cells, VZV induces extensive syncytial formation by virus-mediated cell-to-cell fusion. Statistical analyses of fusion parameters demonstrated three-way interactive effects among all three tested variables (incubation temperature, cell type and virus strain). For example, fusion was greatly enhanced at 33 degrees C vs 37 degrees C; also fusion was pronounced in epidermal cells but negligible in fibroblast cells. As with all herpesviruses, VZV gH was a major fusogen. VZV cell fusion was inhibited by antibody to gH, but surprisingly was enhanced by antibody to gE. Other evidence implicating a role for VZV gE in the fusion process was provided by two mutant viruses, in which gE cell surface expression was enhanced. Under transfection conditions, VZV fusion formation occurred after expression of the gH/gL complex; in contrast, pseudorabies virus requires expression of gH, gL and gB, while the herpes simplex virus (HSV) types 1 and 2 require the quartet of gH, gL, gB and gD. VZV has no gD gene and no apparent gD functional homologue. On the other hand, VZV gE exerts a greater effect than HSV gE on membrane fusion. Taken together, the data in this review suggest that VZV has evolved viral glycoprotein machinery more geared toward cell-to-cell fusion (fusion-from-within) than toward virus-to-cell fusion (entry/fusion-from-without), as a means for syncytium formation within the human epidermis.

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Section: Vzv Fusion and Cell-to-cell Spreadmentioning

confidence: 99%

Membrane fusion mediated by herpesvirus glycoproteins: the paradigm of varicella‐zoster virus

Cole

Grose

2003

Reviews in Medical Virology

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“…The infective/total particle ratio ofvirus propagated in cell monolayers derived from human skin is less than 1 in 109 yet virus propagated in the same tissue in the skin of a human being, or in skin maintained as organized cultures of fragments of whole skin with a similar total count, may have a free virus infective titre as high as 105 infective particles per ml, corresponding to an infective/total ratio of about 1 in 104. Thus varicella seems to be a virus sometimes strongly cell-associated and sometimes productive of considerable amounts of free infective virus, depending perhaps on the organization of the cells in which it is grown (Caunt, 1963;Caunt and Taylor-Robinson, 1964;Caunt, 1969). Whether non-infective virions are present during the period of latency in the cells of human sensory ganglia is not known, since no report of any electron microscopical study of such ganglia has appeared.…”

Section: The Mechanism Of Latencymentioning

confidence: 99%

Varicella-zoster and related viruses

McCarthy¹

1972

Journal of Clinical Pathology

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The phenomenal expansion in the study of latent phage infection has meant that there has been no shortage of ideas and hypotheses to explain experimental latent infections of animal cell cultures in vitro; but the greater complexity of the intact animal imposes a more complex pattern on the relationship between animal and virus so that phenomena explicable in the test tube may have scant or at best indirect relevance to the events in the intact animal. Unfortunately because of its strong cell association 'in-vitro' Varicella is a disease of the highest infectivity and nearly everyone contracts it by the age of 10 years. There seems to be only one serotype and second attacks in normal individuals are extremely rare. Zoster occurs in about half of those who have had varicella and second attacks are quite common; indeed a history of zoster does not seem to alter materially the chance of a further attack in the future.Those who suffer zoster have always, it is believed, had varicella in the past (Hope-Simpson, 1965).That a single virus causes both conditions is no longer questioned but the communicability of the two conditions is a matter of considerable interest, particularly in respect of the kind of disease produced in the recipient. Varicella can unquestionably result from exposure to varicella or zoster cases. The question continues to be asked (Seiler, 1949;Berlin and Campbell, 1970) whether zoster can follow as the direct and immediate consequence of exposure to varicella and also whether zoster can follow consequent upon exposure to zoster. There are of course reports of such sequential events but in present circumstances the question of causality must go unanswered until more is known about the pathogenesis of both diseases. Suffice it to say that temporal association of events which are not themselves rare is bound to occur occasionally. If on occasions this association is a causal one we lack the evidence to prove it or refute it. In this connexion Thomas and Robertson (1971) have suggested a reasonable explanation of how zoster might arise from implantation of virus into the skin and cutaneous nerves of a varicella-immune subject and be channelled to the ganglion along a protected pathway. Nevertheless the three cases of zoster they describe following exposure to varicella or zoster were not closely related in time, and one of them was on treatment which might have been immunosuppressive and could have played a provocative role. This suggested explanation of causation was put to the test many years ago by Kundratitz andLipschutz (1925) andBruusgaard (1932). They vaccinated normal and immune subjects with varicella vesicle fluid. Varicella followed in susceptible subjects but no zoster occurred in the immune subjects.

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“…How ever, some complement-fixing viral antigens have been detected in the fluids as well as in extracts of infected cells (27). Occasionally, with filtration experiments, a small amount of infectious virus has been separated from the cells (28)(29)(30). Unfortunately, many of these studies lack quantitation and it is often not possible to determine whether a few intact cells were responsible for the virus transmission observed.…”

Section: Herpesvirusesmentioning

confidence: 99%

Defective Dna Animal Viruses

Rapp¹

1969

Annu. Rev. Microbiol.

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Growth of Varicella-Zoster Virus in Human Thyroid Tissue Cultures

Cited by 31 publications

References 5 publications

Membrane fusion mediated by herpesvirus glycoproteins: the paradigm of varicella‐zoster virus

Membrane fusion mediated by herpesvirus glycoproteins: the paradigm of varicella‐zoster virus

Varicella-zoster and related viruses

Defective Dna Animal Viruses

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