Herpes viruses and chromosomal alterations seen with light and whole-mount electron microscopy

Wahrén, Britta; Lampert, F.; Goetz, O

doi:10.1016/0014-4827(72)90547-2

Cited by 8 publications

(4 citation statements)

References 14 publications

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“…The possibility that the differences in the susceptibility of PBLs to HSV-induced damage might be donor specific is supported by the observations of Wahren et al [40], who found that when PBLs from two different donors were infected at a low MOI with HSV-1, one donor's cells had only a 2-fold increase in breaks, gaps, and what were 26 Several studies have tried to define when and what type of damage first appears in HSV-infected cells. In one study [41], Hep-2 cells were infected with HSV-1 or -2 at an MOI of 5 and followed for the first 5 hpi.…”

Section: Herpes Simplex Interactions With the Cellular Genomementioning

confidence: 80%

Viral induction of site‐specific chromosome damage

Fortunato

Spector

2002

Reviews in Medical Virology

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The advent of advanced cell culture and cytogenetics techniques in the 1950s opened a new avenue for research on the pathogenic interactions between animal viruses and their hosts. Studies of many viruses revealed their ability to nonspecifically induce cytogenetic damage to their host cell's chromosomes. However, only three viruses, the oncogenic adenoviruses, herpes simplex virus (HSV) and human cytomegalovirus (HCMV), have been found to cause non-random, site-specific chromosomal damage. Adenovirus (Ad) type 12 induces fragility at four distinct loci (RNU1, RNU2, RN5S and PSU1) in many different types of human cells. A common feature of these loci is that they contain a repeated array of transcriptionally active genes encoding small structural RNAs. Site-specific induction of breaks also requires the virally encoded E1B protein of M(r) 55000 and the C-terminus of the cellular p53 protein. Analysis of the induction of damage by HSV and HCMV necessitates consideration of several factors, including the strain of virus used, the timing of infection, the type of cell used, and the multiplicity of infection. Both HSV strains 1 and 2 are cytotoxic, although the former seems to be more proficient at inducing damage. At early times post infection, HSV induces breaks and specific uncoiling of the centromeres of chromosomes 1, 9 and 16. This is followed at later times by a more complete severing of all of the chromosomes, termed pulverisation. Damage by HSV requires viral entry and de novo viral protein synthesis, with immediate early viral proteins responsible for the induction of breaks and uncoiling and early gene products (most likely nucleases) involved in the extensive pulverisation seen later. HCMV has been studied primarily in permissive human fibroblasts. Its ability to induce specific damage in chromosome 1 at two loci, 1q21 and 1q42, was only recently revealed as the cells must be in S-phase when they are infected for the breaks to be observed. In contrast to adenovirus and HSV, HCMV induction of specific breakage requires only viral entry into the cell and not de novo viral protein expression. This latter point may be a factor in its ability to cause damage in the developing fetal brain, where the most severe clinical manifestations of congenital infection are observed.

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Section: Herpes Simplex Interactions With the Cellular Genomementioning

confidence: 80%

Viral induction of site‐specific chromosome damage

Fortunato

Spector

2002

Reviews in Medical Virology

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“…Our findings are also in agreement with those of studies in which breakage has been investigated in cells infected in vitro with herpes sitnplex viruses. Increased breakage and other aberrations have been found in Chinese hamster cells (11,12), in monkey kidney cells (13), in human cell lines HeLa and Hep-2 (14), in human embryo kidney cells (15), in human leukocytes (16,17), and in human diploid fibroblasts (18); also, in human embryo lung cells (15,19) and in human embryo kidney cells and leukocytes (15) after infection with herpes simplex virus Type 2 (HSV-2). On the contrary, in a few studies no damage has been found in human embryo lung cells and in phytohaemagglutinin-stimulated peripheral blood leukocytes aftter infection with HSV-1 (15).…”

Section: Discussionmentioning

confidence: 99%

Chromosomal breaks and sister chromatid exchanges (SCE) in patients with herpetic stomatitis

Zervou-Valvi

Bazopoulou-Kyrkanidou

Angelopoulos

1986

J Oral Pathology Medicine

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Zervou-Valvi F, Biizopoulou-Kyrkanidou E, Angelopoulos AP. Chromosomal breaks and sister chtomatid exchanges (SCE) in patients with herpetie stomatitis. .) Oral Pathol 1986: 15: LS 1-154.Chromosomal breakage and sister-chroniatid exchanges (SCE) were studied in peripheral lymphocytes of 9 patients with primary herpetie stomatitis (PHS). 12 patients with secondary herpetie stomatitis (SnS) and 12 controls. The incidence of chromosomal breakage was signifieantly higher in PHS patients (mean 23%, P.=().0()()2) and in SHS patients (mean 20.25%, P. = 0.0003) compared to the controls (mean 4.2%). The incidence of SCE per 46 chromosomes was significantly higher in SHS patients (mean 16.564) compared with (P.

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“…At about the same time as reports of the effects of Ad12 were published, it was shown that infection of human cells with HSV resulted in limited chromosome breaks in some cells and/or complete severing of all the chromosomes (termed 'pulverization') in others (Stich et al, 1964;Wahren et al, 1972). Virus strain, cell type and time of infection all play a part in determining the outcome of HSV infection.…”

Section: An Historical Perspectivementioning

confidence: 99%

DNA viruses and the cellular DNA-damage response

Turnell

Grand

2012

Journal of General Virology

135

141

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It is clear that a number of host-cell factors facilitate virus replication and, conversely, a number of other factors possess inherent antiviral activity. Research, particularly over the last decade or so, has revealed that there is a complex inter-relationship between viral infection and the host-cell DNA-damage response and repair pathways. There is now a realization that viruses can selectively activate and/or repress specific components of these host-cell pathways in a temporally coordinated manner, in order to promote virus replication. Thus, some viruses, such as simian virus 40, require active DNA-repair pathways for optimal virus replication, whereas others, such as adenovirus, go to considerable lengths to inactivate some pathways. Although there is ever-increasing molecular insight into how viruses interact with host-cell damage pathways, the precise molecular roles of these pathways in virus life cycles is not well understood. The object of this review is to consider how DNA viruses have evolved to manage the function of three principal DNA damage-response pathways controlled by the three phosphoinositide 3-kinase (PI3K)-related protein kinases ATM, ATR and DNA-PK and to explore further how virus interactions with these pathways promote virus replication. IntroductionThe DNA-damage response (DDR) is a general term employed to describe a complex series of cellular pathways that detect DNA damage, initiate cell-cycle arrest so that mutated DNA is not duplicated, and then go on to repair the lesion or, if damage is too great, trigger apoptosis. Infection by many virus species is sufficient to initiate a DDR, activating some or all of the repair pathways. Simplistically, this has been seen as recognition by the host cell of viral DNA as its own damaged DNA, but it is now considered that this could, at least to some extent, be an antiviral response, aimed directly at combating infection. Viruses have a complex series of mechanisms that, in turn, have evolved to combat and inactivate the cellular damage-response pathways.The aim of this review is to consider how and why different viruses affect the balance of these opposing pathways: for example, to what extent is an activated DDR directly required by particular virus species to facilitate or assist virus replication or, conversely, to what extent does the cellular damage response hinder replication. Additionally, it is often not clear whether activation of the DDR is a mere byproduct of infection or a direct result of 'intentional' action of viral protein activity. If DDR activation is an unwanted result of infection, a further point of interest is to understand what measures viruses take to circumvent the deleterious effects of the cellular pathways. Past experience would suggest that viruses are so highly evolved and their primary structures so tightly constrained that the selective activation of DDR pathways by some viruses might prove advantageous to them. Whether this is the case will only become evident after considerable further investigation.The r...

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Herpes viruses and chromosomal alterations seen with light and whole-mount electron microscopy

Cited by 8 publications

References 14 publications

Viral induction of site‐specific chromosome damage

Viral induction of site‐specific chromosome damage

Chromosomal breaks and sister chromatid exchanges (SCE) in patients with herpetic stomatitis

DNA viruses and the cellular DNA-damage response

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