Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0268318 (ICP)
 10,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In cells infected with herpes simplex virus a protein associated with the small subunit of ribosomes became phosphorylated. It was not detectably labelled with 14C-amino acids added after infection and is therefore probably a cellular protein. The phosphorylated ribosomal proteins from HSV-1- and HSV-2-infected cells were indistinguishable electrophoretically and had an apparent mol. wt. of about 48 000. Phosphorylation of the 48K protein was detected 2 to 3 h after infection and reached a maximum rate at 4 to 5 h. It was prevented by adding cycloheximide at 2 h, or actinomycin at 1.5 h p.i., or azetidine at the beginning of infection. The phosphorylation did not occur on reversal of a cycloheximide block in the presence of actinomycin, confirming that it is not caused by a virus alpha-polypeptide. Virus that had been irradiated with u.v. light, although still able to suppress synthesis of cellular protein and DNA, did not induce phosphorylation of the 48K ribosomal protein. Therefore the phosphorylation is not responsible for the suppression of host synthesis. The alpha polypeptides ICP 4, 0, 22 and 27 are also phosphorylated but, in contrast to that of the ribosomal protein, their phosphorylation does not depend on the synthesis of beta and gamma polypeptides. It is probably mediated by a host enzyme.
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PMID:Phosphorylation of a ribosomal protein and of virus-specific proteins in cells infected with herpes simplex virus. 23 30

The BamHI-B DNA fragment of herpes simplex virus type-1 (HSV-1) is associated with intraperitoneal pathogenicity. Among the recently mapped RNA transcripts from this fragment (15), one was reported to be associated with latency. To relate the RNA transcripts to virus pathogenicity, the in vitro-transcribed RNAs from BamHI-B fragments of three HSV-1 strains--F (pathogenic), R19, and HFEM (apathogenic), were studied by in vitro translation. When the BamHI-HpaI (0.738-0.755 map units) DNA fragment from HSV-1 strain F was transcribed rightward and translated, three proteins of 70, 63, and 51 kD were detected. The 63 kD protein resembles in size and orientation the protein encoded by the ICP-27 (IE-2) gene (0.740-0.749 mu). The 51 kD polypeptide is assumed to be a prematurely terminated form of this protein. No proteins were obtained from RNA transcribed in the opposite direction. The SalI-NcoI (0.746-0.761 mu) fragment of the three HSV-1 strains yielded two proteins of 25 and approximately 15 kD when transcribed rightward and a 35 kD polypeptide from RNA transcribed in the opposite direction. As a result of the genomic deletion in HFEM, it was possible to obtain the 35 kD protein from the SalI-SalI DNA fragment (0.746-0.761 mu) as well. In vitro transcription and translation of the PstI-SalI (0.778-0.790 mu) DNA fragment (the right-hand side of HpaI-P) did not result in protein synthesis. The possibility that the UL56 gene is connected with the intraperitoneal pathogenicity of HSV-1 is discussed.
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PMID:In vitro transcription and translation of proteins encoded by the BamHI-B genomic fragment of herpes simplex virus-1. 164 66

The water-extractable component of snuff (snuff extract) inhibits the replication of herpes simplex virus (HSV) by suppressing the synthesis of viral DNA. This process probably causes HSV to be oncogenic. To further understand the mechanism of inhibitory action of snuff extract on HSV replication, the effect of snuff extract on the synthesis of viral DNA and proteins in type 1 HSV (HSV-1) infected cells was investigated. Snuff extract inhibited the synthesis of viral DNA and altered the production of certain classes of viral proteins. The syntheses of ICP4, a viral alpha-protein, and ICP8, a beta-protein, were not generally reduced by noncytotoxic concentrations of snuff extract (where ICP = infected cell polypeptide). However, snuff extracts significantly inhibited the production of ICP gC (glycoprotein C), a gamma 2-protein, and the inhibition was in a concentration-dependent fashion: the higher the concentration of snuff extracts, the greater the inhibition. Based on the fact that the production of alpha- and beta-proteins is absolutely necessary for and precedes the viral DNA synthesis and that viral gamma 2-proteins are mostly produced by the newly synthesized viral DNA, it is concluded that snuff extract inhibits HSV-1 DNA replication directly rather than indirectly via the alteration of viral protein synthesis.
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PMID:Effect of snuff extract on the replication and synthesis of viral DNA and proteins in cells infected with herpes simplex virus. 215 33

A gene in equine herpesvirus 1 (EHV-1; equine abortion virus) equivalent to the gB glycoprotein gene of herpes simplex virus (HSV) has been identified by DNA hybridization and nucleotide sequencing. A 4.3 kbp EHV-1 PstI-ClaI sequence (0.40 to 0.43 map units) contained an open reading frame flanked by appropriate control elements and was capable of encoding a polypeptide of 980 amino acids. This had 50 to 60% identity over a 617 amino acid conserved region with the gB gene products of HSV and three other alphaherpesviruses, and 20 to 30% identity with those of human cytomegalovirus and Epstein-Barr virus. Analysis of the amino acid sequence predicts a long signal peptide, hydrophobic and hydrophilic domains and N-glycosylation sites, and has identified a probable internal proteolytic cleavage site. The EHV-1 gB open reading frame appears to be overlapped at its 5' end by 135 nucleotides of the 3' end of an upstream open reading frame the potential translation product of which has approximately 50% identity with HSV gene ICP 18.5 and VZV gene 30 products.
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PMID:Identification and nucleotide sequence of a gene in equine herpesvirus 1 analogous to the herpes simplex virus gene encoding the major envelope glycoprotein gB. 254 44

Five monoclonal antibodies to the alkaline nuclease of herpes simplex virus (HSV) types 1 and 2 have been used in immunoperoxidase tests to demonstrate the nuclear localization of the enzyme within HSV-1- and HSV-2-infected cells and to purify the enzyme from cells infected with either virus by immunoadsorbant chromatography. Affinity chromatography with a 32P-labelled extract of HSV-2-infected cells has enabled us to demonstrate that the nuclease eluting from the immunoadsorbant is a phosphoprotein, hence confirming the nuclease to be identical to the phosphorylated polypeptide previously referred to as ICSP 22 (HSV-2) or ICP 19 (HSV-1). In addition, the results clearly demonstrate that monoclonal antibodies Q1, CC1 and CH2 are directed against HSV type-common epitopes while V1 and T2T1 antibodies are against HSV-2-specific epitopes on the enzyme. Using the type-specific monoclonal antibodies in an immunoperoxidase test, the enzyme specified in cells infected with intertypic recombinants has been typed; correlation of these data with restriction endonuclease maps of the recombinants has enabled us to map the position of the active site of the nuclease gene to map units 0.168 to 0.184 on the genomes of both HSV-1 and HSV-2. Taken with the data mapping the mRNA encoding this enzyme, the nuclease active site can be mapped to 0.168 to 0.175 on the genome. Finally, the use of monoclonal antibodies in immunofluorescence tests on infected cells has demonstrated that the nuclease is synthesized within 2 h post-infection.
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PMID:Studies on the herpes simplex virus alkaline nuclease: detection of type-common and type-specific epitopes on the enzyme. 257 50

Antibody responses to herpes simplex virus (HSV) types 1 and 2, as determined by enzyme-linked immunoabsorbent assay (ELISA), neutralization, and immunoblot, were assessed in sera from newborns with documented HSV infections. The antibody response of the newborns was defined by disease duration and correlated with disease classification and outcome. Three unique observations were made. First, the quantity of total antibodies at presentation, as determined by ELISA and neutralization, was not predictive of disease classification or outcome. Second, the frequency and intensity of antibody responses to immunologically recognized HSV polypeptides in newborns with central nervous system and disseminated infections were greater than those in newborns with infections localized to the skin, eye, and mouth. Third, the long-term outcome in HSV-infected newborns could be predicted by the quantity of antibodies to the immediate-early infected cell polypeptide ICP 4. These data provide insight into host response to individual polypeptides and their potential value in predicting long-term prognosis.
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PMID:Antibody response of the newborn after herpes simplex virus infection. 284 11

We have analyzed the accumulation of herpes simplex virus type 1 RNA of the immediate early (IE; infected cell polypeptide types 4 and 0 [ICP-4 and ICP-0]), early (thymidine kinase), and early late (ICP-5) kinetic classes in the cytoplasm of infected cells in the presence of anisomycin, canavanine, or phosphonoacetic acid and in the course of a normal infection. IE RNAs were overproduced and were the only class of transcript detected in anisomycin-blocked cells. Phosphonoacetic acid treatment resulted in overaccumulation of early RNAs and underaccumulation of early late RNAs. Although low-stringency canavanine treatment resulted in accumulation of RNA from all kinetic classes, high-stringency conditions restricted accumulation of herpes simplex virus type 1 RNAs to the IE class. More importantly, the IE RNAs for ICP-4 and ICP-0 accumulated to a lesser extent under high-stringency canavanine conditions compared with their accumulation in anisomycin-treated cells. Therefore, the absence of newly synthesized viral proteins (anisomysin treatment) and the presence of analog proteins (stringent canavanine treatment) have different consequences with regard to the accumulation of these two IE RNAs. The kinetics of cytoplasmic accumulation for these RNAs was different for each class of RNA. The IE RNAs were detectable at 1 h postinfection and reached a maximum accumulation at ca. 3 h postinfection. The IE RNAs for both ICP-4 and ICP-0 persisted at late times of infection; however, they differed in that the RNA for ICP-4 remained at relatively low levels and the RNA for ICP-0 remained at relatively high levels as compared with their peak levels of accumulation. The 1.4-kilobase RNA for the herpes simplex virus type 1 thymidine kinase was detected by 2 h, with maximum accumulation occurring at ca. 5 h postinfection. After the peak of accumulation, the amount of thymidine kinase RNA declined rapidly from 8 to 14 h postinfection. The early late RNA for ICP-5 was detected between 2 and 3 h, after which accumulation increased to a peak between 8 and 10 h postinfection. The level of ICP-5 RNA remained at close to the peak level until 14 h postinfection. We also compared the accumulation of viral mRNAs in the cytoplasm with the rates of synthesis of their respective polypeptides. Our results suggest that translational controls may be involved in the regulation of IE genes but not early or late genes.
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PMID:Accumulation of herpes simplex virus type 1 RNAs of different kinetic classes in the cytoplasm of infected cells. 298 33

We have used an in vitro nuclear run-off assay to measure the levels of transcription of specific herpes simplex virus genes at different times during a lytic infection. We analyzed the effects of inhibition of DNA replication and of defects in two herpes simplex virus regulatory proteins on the transcription of these genes. We present evidence that the transcription of the alpha ICP4 gene is negatively regulated during a lytic infection. The regulation of ICP4 gene transcription requires the beta protein ICP8 (where ICP = infected cell polypeptide). Transcription of the beta ICP8, gamma 1 ICP5, and gamma 2 glycoprotein C (gC) genes was dependent on ICP4, and transcription of the gamma 2gC gene was strongly inhibited when DNA replication was blocked. Defects in ICP8 also resulted in increased levels of transcription of the ICP4, ICP8, ICP5, and gC genes from parental viral genomes. Our results suggest that ICP8 may be important in maintaining the highly ordered cascade of viral gene expression.
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PMID:Transcriptional control of herpesvirus gene expression: gene functions required for positive and negative regulation. 300 29

The viral polypeptide ICP 4 (or Vmw 175) is synthesized during the immediate early phase of infection by herpes simplex virus (HSV) and is required during the viral reproductive cycle for efficient transcription of delayed early viral genes. Replication of mutant strains of HSV-1 such as tsLB 2 that encode a temperature-sensitive variant of ICP 4 does not proceed beyond the immediate early phase in cells that are infected and maintained at the nonpermissive temperature (NPT). Under these conditions, the immediate early viral polypeptides accumulate to levels that are 10 to 100 fold greater than normal. We have investigated the use of tsLB 2-infected cells maintained at the NPT as a source for substantial amounts of ICP 4 for further characterization. Extraction of ICP 4 from tsLB 2-infected cells requires 0.5 M NaCl and yields aggregates that contain ICP 4, ICP 6, ICP 27, and lesser amounts of other proteins. These large aggregates cannot be disrupted under nondenaturing conditions and thus are not a suitable source for native ICP 4. We have used this overproduced ICP 4 as an antigen to generate ICP 4-specific antibody and for characterization of the primary structure of ICP 4. Analysis of acid-hydrolysed 32P-labeled ICP 4 revealed that the major phosphorylated residues in ICP 4 are phosphoserine and phosphothreonine.
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PMID:Characterization of a herpes simplex virus regulatory protein: aggregation and phosphorylation of a temperature-sensitive variant of ICP 4. 302 82

We have shown that a latent infection of herpes simplex virus type 2 (HSV-2) can be established in a human neuroblastoma cell line IMR-32 if the infected cells are cultured at 40 degrees C. In the present study, viral polypeptides and cellular heat-shock proteins which were synthesized in HSV-2 infected IMR-32 cells cultured at 40 degrees C were analyzed by polyacrylamide gel electrophoresis. It was found that the synthesis of late viral polypeptide ICP 5 was markedly reduced in the infected cells at 40 degrees C as compared with those at 37 degrees C. Although infection of IMR-32 cells with HSV-2 at 40 degrees C resulted in shutoff of cellular protein synthesis, it was found that some cellular heat-shock proteins (90, 72 and 70 kd polypeptides) were synthesized and accumulated intracellularly. These findings suggest that modification of cascade regulation of HSV-2 polypeptide synthesis and/or accumulation of heat-shock proteins may be involved in the incomplete arrest of virus growth and in survival of the infected cells, leading to the establishment of HSV-2 latency in IMR-32 cells.
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PMID:Macromolecular synthesis at the early stage of herpes simplex virus type 2 (HSV-2) latency in a human neuroblastoma cell line IMR-32: repression of late viral polypeptide synthesis and accumulation of cellular heat-shock proteins. 303 46


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