Herpesvirus Saimiri-induced Proteins in Lytically Infected Cells. I. Time-ordered Synthesis

Modrow, Susanne; Wolf, Hans

doi:10.1099/0022-1317-64-1-37

Cited by 19 publications

(16 citation statements)

References 24 publications

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“…We did not confirm previous claims that TPA treatment shortened the cycle of virus replication (Modrow & Wolf, 1983) and infection of cells at different stages of the cell-cycle had no consistent effects on the asynchronous expression of the IE 52K protein. Because differences in the rates of many cellular processes would be expected to occur throughout the cell-cycle, we were surprised by the latter result.…”

Section: Discussioncontrasting

confidence: 53%

“…It has been suggested that the growth cycle of HVS is advanced in TPA-treated relative to untreated cultures of O M K cells (Modrow & Wolf, 1983). We therefore examined the effects of TPA treatment on the time course of protein synthesis both by an analysis of labelled polypeptides separated from infected cultures by SDS-gel electrophoresis (Fig.…”

Section: Asynchronous Expression Of Hvs Ie 52k In Populations Of Tpa-mentioning

confidence: 99%

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Asynchronous Expression of the Immediate-Early Protein of Herpesvirus Saimiri in Populations of Productively Infected Cells

Randall¹,

Newman²,

Honess³

1985

Journal of General Virology

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SUMMARYThe time course of virus replication in cultures of permissive cells infected with high multiplicities of herpesvirus saimiri (HVS), a gammaherpesvirus, is protracted relative to the replication of herpes simplex virus (HSV), an alphaherpesvirus, under similar conditions. The basis for this difference was investigated by quantitative immunofluorescence microscopy exploiting monoclonal antibodies specific to the HVS 52000 mol. wt. immediate-early polypeptide (IE 52K) and to delayed-early (DE 51K, DE 110K) and late (130K and capsid proteins) gene products to measure the timing of gene expression in individual cells of infected cultures. The timing of the transitions from IE to DE and from DE to late protein synthesis occurred at proportionately different intervals in the growth cycle of HVS, relative to that of HSV. In particular, the DE to late transition occurred relatively later in HVS infections. However, asynchrony in the events leading to the expression of the first class of virus proteins (IE 52K) was the main source of the extended course of HVS replication in populations of infected cells. This asynchrony was not modified significantly by infection at different stages of the host cell-cycle and was reduced, but not overcome, by very high applied multiplicities of infection. Double-antibody staining revealed a positive correlation between the accumulation of high concentrations of parental virus particles at perinuclear sites and early detection of HVS IE 52K gene expression. Both of these events remained sensitive to a microtubule poison (colcemid) for many hours after infection with HVS, whereas the rapid and synchronous expression of the IE 175K protein (ICP4) in HSV-1-infected cells was insensitive to post-infection exposures to this drug. We conclude that significant differences in early stages of virus entry and intracellular processing which precede immediate-early gene expression are largely responsible for differences between the replicative cycles of these representatives of gamma-and alphaherpesviruses in cultures of permissive cells.

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Section: Discussioncontrasting

confidence: 53%

Section: Asynchronous Expression Of Hvs Ie 52k In Populations Of Tpa-mentioning

confidence: 99%

Asynchronous Expression of the Immediate-Early Protein of Herpesvirus Saimiri in Populations of Productively Infected Cells

Randall¹,

Newman²,

Honess³

1985

Journal of General Virology

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“…2a), although it can not be excluded that their presence may simply be due to leakage from nuclei during the subcellular fractionation procedure. A relatively slow and inefficient shut-down of host protein synthesis is also observed following infection by herpesvirus sylvilagus (Patick & Hinze, 1984) and herpesvirus saimiri (Modrow & Wolf, 1983;Randall et al, 1983), the disadvantages of which in the latter case have been partly overcome by the use of phorbol esters (Modrow & Wolf, 1983). Since our major interest has been a description of the nuclear DBPs we have not tried this approach, although a more complete investigation of CTHV-specific protein synthesis may well require such a procedure.…”

Section: Discussionmentioning

confidence: 99%

“…Although we have not exhaustively investigated various parameters that might influence optimal growth, the use of various cell types, media, serum concentrations or incubation temperatures did not markedly shorten the growth cycle (unpublished data). The slow growth of CTHV resembles the growth properties of herpesvirus sylvilagus (Patick & Hinze, 1984) and herpesvirus saimiri (Modrow & Wolf, 1983;Randall et al, 1983) in tissue culture. total cell extracts (not shown).…”

Section: Single Cycle Growth: Production Of Infectious Virus and Appementioning

confidence: 99%

DNA-binding Proteins Induced by the Cottontail Rabbit Herpesvirus CTHV

Cajean-Feroldi

Laithier²,

Foulon³

et al. 1988

Journal of General Virology

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SUMMARYSeveral new polypeptides were detected in cells infected with CTHV, a cottontail rabbit herpesvirus. All of them (Mr 150K, ll0K, 93K, 83K, 75K and 35K) accumulated in the nucleus during the infectious cycle, and all except the 150K species bound to DNA-cellulose affinity columns in low-salt buffers. Polyclonal antisera prepared against the 35K DNA-binding protein also recognized the 75K species. Although the 75K protein could be detected earlier in infection than the 35K protein, late in the infectious cycle the latter increased to an abundance approaching that of cellular histones. Treatment of partially purified virions with a non-ionic detergent indicated that the 35K protein, but not the 75K protein, is a component of capsid/ tegument structures. The anti-35K/75K serum did not cross-react with herpesvirus sylvilagus virion proteins, which, in an electrophoretic comparison, exhibited both similarities to and differences from the virion proteins of CTHV. Labelling of CTHVinfected cells with [32p]orthophosphate revealed the presence of phosphoproteins electrophoretically comigrating with the 93K, 83K, 75K and 35K proteins.

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“…The specificity of antibodies in the various experimental and natural hosts (Saimiri scireus) was determined by immunoprecipitation of viral polypeptides obtained fiom owl monkey kidney (OMK) cells infected with H. saimiri in the presence of labeled preCursors. Whereas we describe the unglycosylated virus-induced proteins involved in another report [9], we include in this report the description of the glycoproteins in H. saimiri-infected cells.…”

Section: S Modrow H Schmidt and H Wolfmentioning

confidence: 99%

Characterization of Proteins Induced by Herpesvirus saimiri: Comparative Immunoprecipitation and Analysis of Glycosylation

Modrow¹,

Ha²,

Wolf³

1983

Haematology and Blood Transfusion / Hämatologie Und Bluttransfusion

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Herpesvirus Saimiri-induced Proteins in Lytically Infected Cells. I. Time-ordered Synthesis

Cited by 19 publications

References 24 publications

Asynchronous Expression of the Immediate-Early Protein of Herpesvirus Saimiri in Populations of Productively Infected Cells

Asynchronous Expression of the Immediate-Early Protein of Herpesvirus Saimiri in Populations of Productively Infected Cells

DNA-binding Proteins Induced by the Cottontail Rabbit Herpesvirus CTHV

Characterization of Proteins Induced by Herpesvirus saimiri: Comparative Immunoprecipitation and Analysis of Glycosylation

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