Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q07644 (polypeptide)
 72,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The infectivity of most rotaviruses is enhanced by treatment with trypsin. We studied the mechanism of enhancement of examining the effect of trypsin on rotavirus infectivity, aggregation, early interactions with host cells, and structure. The results indicated that trypsin does not increase levels of infectious virus by dispersion of aggregates or affect the efficiency or rate of attachment of virus to cells. A fraction of virus that was not infections without trypsin treatment was found to attach to cells, but did not initiate antigen synthesis. When cells were infected with labeled, purified virus, increased levels of uncoated particles were found in cells infected with trypsin-treated virus. Infection of cells with trypsin-treated virus also led to greater levels of RNA synthesis early in the infection. The results suggest that trypsin converts a noninfectious fraction of virus into infectious virus by allowing this fraction to uncoat in the infected cell. Trypsin was found to cleave an 88,000-dalton structural polypeptide of bovine rotavirus generating 67,000- and 20,000-dalton cleavage products.
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PMID:Trypsin enhancement of rotavirus infectivity: mechanism of enhancement. 616 41

Infection of a human lymphoblastoid cell line (F-365 line containing Epstein-Barr viral capsid antigen, derived from an individual without overt signs of lymphoma, infectious mononucleosis, or leukemia) with herpes simplex virus (HSV), maintained and observed for 15 months, was characterized by the continuous production of infectious extracellular virus. By the 5th day postinfection 75% of the cells produced HSV antigen as detected by fluorescent antibody, and by the 10th day 90% did so; production continued through the 15th month. Only 11% of single isolated cells produced detectable infectious virus. HSV produced after the 3rd month formed smaller plaque in monolayer cell culture than did the parental virus. No antigenic or polypeptide change in the HSV was detected by crossed immunoelectrophoresis and sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis over the 15-month cultivation in F-365 cells. Cell susceptibility and HSV virulence did not appear to change. The HSV-lymphoblastoid cell culture provided a useful model in which to study long-term virus-cell interactions.
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PMID:Analysis and characterization of herpes simplex virus after its persistence in a lymphoblastoid cell line for 15 months. 626 Jun 56

Mouse cells are fully nonpermissive for simian virus 40 (SV40). Infection does not lead to detectable virus replication. In this report, it was shown, first, that spliced 16S and 19S SV40 late mRNA were present in cytoplasmic and polysomal polyadenylated acid+ RNA preparations from SV40-infected baby mouse kidney cells. The 16S and 19S SV40 late mRNA's produced in infected baby mouse kidney cells were identical to or similar to the 16S and 19S SV40 late mRNA's produced in permissive monkey cells as judged by their S1 mapping patterns performed with the late strand of HpaII-BamHI fragment B and by their sedimentation patterns in a sucrose gradient. It was also shown that the 16S late mRNA from infected baby mouse kidney cells could be translated into a polypeptide which was identical to or similar to virion protein VP1 in every aspect examined, including the patter of peptide mapping by limited proteolysis. Second, we reported that mouse kidney cells produced detectable, although low, levels of SV40 virion protein VP1, as shown by the sodium dodecyl sulfate-polyacrylamide gel autoradiogram of [35S]methionine-labeled proteins immunoprecipitated by a rabbit antiserum directed against SV40 virion proteins. Third, it was reported that infected baby mouse kidney cells produced late mRNA's either (i) when the infection was done at a restrictive temperature with the nonleaky tsA58 mutant or (ii) in cells treated with 100 microgram of cycloheximide per ml, in which large T antigen synthesis was inhibited by more than 99.9%. This suggested that large T antigen was not required for the synthesis of late mRNA in mouse cells.
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PMID:Ability of nonpermissive mouse cells to express a simian virus 40 late function(s). 626 64

Tissue distribution of radiation leukemia virus (RadLV) was examined after its inoculation into normal C57BL/6J (B6) mice, B6 mice bearing a transplantable, non-virus-producing thymic lymphoma (RL12-NP), and B6 mice bearing a transplanted non-virus producing, Harvey murine sarcoma virus-transformed fibrosarcoma. Virus expression was determined by competition radioimmunoassay for murine leukemia virus (MuLV) p30 (predominant group-reactive antigen of MuLV) and for RadLV p12 (a highly type-specific MuLV polypeptide) and by membrane immunofluorescence for cell surface gp71 (predominant envelope glycoprotein of MuLV). Normal adult B6 mice were given three sequential iv injections of RadLV and were examined several times up to 200 days later for the appearance of neoplastic disease or expression of virion antigens. No clinical abnormalities were noted, and animals remained healthy for greater than 200 days. Significant levels of MuLV p30 and RadLV p12 were detected only in the thymuses. Organs and tumors from RL12-NP-inoculated animals contained low or nondetectable levels of virion antigens. Inoculation of mice with RL12-Rad, a cell line derived by in vitro infection of RL12-NP cells with RadLV, produced widespread, discrete metastatic tumors and infiltrated the lymphoid organs of B6 mice in a pattern identical to that observed after administration of RL12-NP cells. Lymphoid organs of RL12-Rad-inoculated animals expressed variable levels of virion antigens reflecting differences in the extent of tumor cell infiltration as opposed to virus spread from tumor to host cells. Administration of infectious RadLV systemically into RL12-NP tumor-bearing animals converted these tumors to viron antigen expressors with levels in superinfected tumors equivalent to those found in RL12-Rad-induced tumors. Infection was highly selective, and host tissues were minimally contaminated by the inoculated virus. Part of this selectivity was explained by the thymotropic property of RadLV. A rapidly dividing murine fibrosarcoma was not infected by RadLV, but this same non-virus-expressing tumor could be infected by common fibrotropic MuLV isolates.
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PMID:In vivo antigenic modification of tumor cells. III. Metastatic thymic lymphoma specifically infected by thymotropic retrovirus. 626 78

We have used simian virus 40 (SV40) DNA as a vector for expression of functional activity of a cloned influenza viral DNA segment in primate cells. Cloned full-length DNA sequences coding for the hemagglutinin of influenza A virus (Udorn/72/[H3N2]) were inserted into the late region of a viable deletion mutant of SV40, and the hybrid DNA was propagated in the presence of an early SV40 mutant (tsA28) helper. Infection of primate cells with the hybrid virus produced a polypeptide similar in molecular size to the hemagglutinin of influenza virus, as shown by immunoprecipitation and gel electrophoresis. The polypeptide was glycosylated, as shown by incorporation of radioactive sugars. The putative hemagglutinin exhibited functional activity, as shown by agglutination of erythrocytes. In addition, an indirect immunofluorescence assay showed that the hemagglutinin polypeptide of the hybrid virus could be detected on the surface of infected cells.
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PMID:Functional expression in primate cells of cloned DNA coding for the hemagglutinin surface glycoprotein of influenza virus. 627 5

We obtained DNA sequences coding for the nucleoprotein (NP) of an influenza A virus by reverse transcription of virion RNA with synthetic oligonucleotide primers. Terminal sequence analysis showed that the cloned gene contained a full-length copy of the virion RNA segment. The NP-specific DNA was inserted into the late region of a simian virus 40 vector, and the DNA recombinant was propagated in the presence of an early simian virus 40 temperature-sensitive mutant helper. Infection of African green monkey kidney cells with the recombinant produced a polypeptide immunoprecipitable with NP-specific antisera. The polypeptide product had a molecular weight of 56,000, identical to that of the nucleoprotein of influenza virus as estimated on polyacrylamide gels. The putative NP was detected in the nucleus of infected primate cells by an immunofluorescence assay. This nuclear localization of NP from recombinant DNA was similar to that seen during influenza virus infection.
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PMID:The influenza virus nucleoprotein synthesized from cloned DNA in a simian virus 40 vector is detected in the nucleus. 629 49

Infection of mammalian cells with either herpes simplex virus (HSV) or vesicular stomatitis virus (VSV) results in a marked inhibition of host protein synthesis. These viruses employ different mechanisms to turn off the host. In previous studies we showed that following infection with HSV, cellular mRNA was degraded and host polyribosomes were dissociated (Nishioka and Silverstein, Proc. Nat. Acad. Sci. USA 74, 2370-2374, 1977; Nishioka and Silverstein, J. Virol. 25, 422-426, 1978a). Degradation required synthesis of an HSV-specified polypeptide whereas dissociation appeared to be mediated by a heat-labile virion associated function (Nishioka and Silverstein, J. Virol. 27, 619-627, 1978b). In contrast, when cells are infected with VSV, host mRNAs are not degraded and polyribosome profiles are not drastically altered (Nishioka and Silverstein, 1978a). We have exploited the properties of these two viruses by infecting cells either simultaneously or sequentially in an effort to test our previous hypotheses. Analyses of the distribution of polyribosomes, stability of mRNA, synthesis of mRNA, and patterns of protein synthesis in coinfected cells permit us to conclude that dissociation of polyribosomes in cells infected with HSV results from expression of a virion associated function, degradation of cellular mRNA requires expression of the HSV genome, and VSV is dominant in doubly infected cells because it inhibits de novo transcription of the HSV genome.
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PMID:Inhibition by vesicular stomatitis virus of herpes simplex virus-directed protein synthesis. 629 58

Infection of 10-day chicken embryos with an avian leukosis virus, RAV-7, resulted in hypothyroidism within 3 weeks posthatching. Histological examination of the thyroids from infected chickens showed an extensive infiltration of lymphoblastoid cells by 7 days posthatching. Areas resembling germinal centers were present in the thyroids of infected chickens by 3 weeks posthatching. Examination of circulating thyroid and pancreas hormones showed a significant reduction in T3 and T4 levels and a trend toward higher insulin levels after 16 days posthatching. T4 supplementation of RAV-7-infected chickens alleviated some aspects of the disease syndrome but did not abrogate all symptoms. Marked involution of both bursa and thymus glands was noted. RAV-7 had an RNA genome of 8.2 kilobases and a polypeptide composition characteristic of an avian leukosis virus. The hypothyroidism followed a dose response to RAV-7 infection.
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PMID:Rapid induction of hypothyroidism by an avian leukosis virus. 630 5

Infection of young turnip leaves with an aphid-transmissible isolate, Cabb B-JI, of cauliflower mosaic virus (CaMV) causes synthesis of an Mr 18 000 polypeptide (p18) which co-purifies with virus inclusion bodies. This polypeptide is not detectable in leaves infected with either of two aphid non-transmissible isolates. Campbell and CM4-184. Construction in vitro, of hybrid genomes between Cabb B-JI and Campbell isolates demonstrates that aphid transmissibility and presence of p18 is dependent on the small genome fragment from the BstEII site to the XhoI site. A deletion made in this fragment within open reading frame (ORF) II causes loss of aphid transmissibility and also terminates production of p18. We conclude that aphid transmissibility and the presence of p18 are related to the expression of ORF II of the CaMV genome.
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PMID:Aphid transmission and a polypeptide are specified by a defined region of the cauliflower mosaic virus genome. 631 74

Infection of BHK cells with foot-and-mouth disease virus (FMDV) causes a thorough change in the electrophoretic profile of whole nuclear histones. It consists in the disappearance of histone H3 and the appearance of a new polypeptide (Pi) which migrates between histones H2A and H4 on SDS-polyacrylamide gels. Protein Pi is detected at 2 hr postinfection (pi), the time in which viral RNA synthesis begins to increase, and reaches equimolecular amounts with the remaining core histones 1 hr later, when the disappearance of histone H3 is almost complete. Labeling of cells prior to infection demonstrates that Pi is not a novo product but the result of a viral-induced processing of a host precursor synthetized beforehand. Protein Pi comigrates with histone H2A/B in acetic acid/urea polyacrylamide gels and it shares common major peptides with histone H3 under controlled proteolysis with protease V8 or trypsin. The mononucleosomal and nucleosomal DNA pattern analysis after micrococcal nuclease treatment of nuclei from infected and mock-infected cells did not show any significant differences even though after 3 hr (p.i.), protein Pi replaces histone H3 in the nucleosomal structure. It was concluded that FMDV infection is responsible for a specific modification in the nucleus of infected cells which leads, after 3 hr (p.i.), to a complete histone H3 protein Pi transition in the nucleosomes.
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PMID:Histone H3 modification in BHK cells infected with foot-and-mouth disease virus. 633 Sep 87


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