Showing papers on "Virus published in 1979"
TL;DR: Both the clinical picture and animal studies suggested that the patient's diabetes was virus induced.
Abstract: A healthy 10-year-old boy was admitted to the hospital in diabetic ketoacidosis within three days of onset of symptoms of a flu-like illness. He died seven days later and post-mortem examination showed lymphocytic infiltration of the islets of Langerhans and necrosis of beta cells. Inoculation of mouse, monkey and human cell cultures with homogenates from the patient's pancreas led to isolation of a virus. Serologic studies revealed a rise in the titer of neutralizing antibody to this virus from less than 4 on the second hospital day to 32 on the day of death. Neutralization data showed that the virus was related to a diabetogenic variant derived from Coxsackievirus B4. Inoculation of mice with the human isolate produced hyperglycemia, inflammatory cells in the islets of Langerhans and beta-cell necrosis. Staining of mouse pancreatic sections with fluorescein-labeled antiviral antibody revealed viral antigens in beta cells. Both the clinical picture and animal studies suggested that the patient's diabetes was virus induced.
987 citations
735 citations
TL;DR: An adenovirus type 5(Ad5) early gene function located in early region 1 which is required for the production of early cytoplasmic mRNAs corresponding to early regions 2, 3, and 4 is identified.
Abstract: We have identified an adenovirus type 5(Ad5) early gene function located in early region 1 which is required for the production of early cytoplasmic mRNAs corresponding to early regions 2, 3, and 4. Mutant dl312 (lacks the segment between 1.5 and 4.5 map units) grows as well as wild-type virus in 293 cells (Ad5-transformed human embryonic kidney cells), but its growth is severely restricted in HeLa cells. We detect no viral RNAs in the cytoplasm of dl312-infected HeLa cells. Viral RNA sequences are present, however, in dl312-infected HeLa cell nuclei.
685 citations
TL;DR: In this article, a protein with an apparent molecular weight of 53,000 in extracts of transformed BALB/c cells was detected in normal adult mouse fibroblasts, lymphoid cells, or hematopoietic cells or in mouse embryo cells.
Abstract: Antisera prepared against BALB/c Meth A sarcoma in syngeneic or compatible F1 mice recognize a protein with an apparent molecular weight of 53,000 in extracts of [35S]methionine-labeled transformed BALB/c cells. This component, designated p53, was not detected in normal adult mouse fibroblasts, lymphoid cells, or hematopoietic cells or in mouse embryo cells or 3T3 cells. An extensive variety of antisera, including alloantisera and heterologous antisera directed against structural antigens of murine leukemia viruses, was tested for reactivity with p53; other than Meth A antisera, only comparably prepared antisera against another BALB/c sarcoma, CMS4, had anti-p53 activity. All transformed mouse cells tested were found to express p53; these tests included chemically induced sarcomas, leukemias, spontaneously transformed fibroblasts, and cells transformed by simian virus 40 and murine sarcoma virus. The presence of p53 in tumors of no known viral etiology indicates coding by resident cellular genes; this does not exclude endogenous viruses as the source of coding sequences or the possibility that transforming viruses code directly for p53.
678 citations
TL;DR: A composite DNA sequence of regions of hepatitis B virus, determined from a series of recombinant plasmids, reveals the genes for the surface antigen and the core antigen of the virus.
Abstract: A composite DNA sequence of regions of hepatitis B virus, determined from a series of recombinant plasmids, reveals the genes for the surface antigen and the core antigen of the virus. The sequence of the core antigen shows it to be a DNA binding protein. The core antigen gene is expressed in Escherichia coli and when injected into rabbits the bacterial product induces antibodies which react with core antigen isolated from human sources.
566 citations
TL;DR: Infectious pancreatic necrosis virus of fish, infectious bursal disease virus of chickens, Tellina virus and oyster virus of bivalve molluscs, and drosophila X virus of Drosophila melanogaster are naked icosahedral viruses with an electron microscopic diameter of 58 to 60 nm as mentioned in this paper.
Abstract: Infectious pancreatic necrosis virus of fish, infectious bursal disease virus of chickens, Tellina virus and oyster virus of bivalve molluscs, and drosophila X virus of Drosophila melanogaster are naked icosahedral viruses with an electron microscopic diameter of 58 to 60 nm. The genome of each of these viruses consists of two segments of double-stranded RNA (molecular weight range between 2.6 x 10(6) and 2.2 x 10(6), and the virion, capsid proteins fall into three size class categories (large, medium, and small; ranging from 100,000 to 27,000) as determined by polyacrylamide slab gel electrophoresis. The hydrodynamic properties of the five viruses are similar as determined by analytical ultracentrifugation and laser quasi-elastic, light-scattering spectroscopy. The calculated particle weights range between 55 x 10(6) and 81 x 10(6). Tryptic peptide comparisons of 125I-labeled virion proteins showed that five viruses are different from each other, although there was considerable overlap in the peptide maps of the three aquatic viruses, indicting a degree of relatedness. Cross-neutralization tests indicated that drosophila X, infectious pancreatic necrosis, and infectious bursal disease viruses were different from each other and from oyster and Tellina viruses. The same test showed oyster and Tellina viruses to be related. The biochemical and biophysical properties of the five viruses cannt be included in the family Reoviridae or in any of the present virus genera.
534 citations
TL;DR: Results are not consistent with negative control of late transcription through the action of a repressor and, taken together with other data, suggest that T antigen has an active role in late RNA synthesis.
Abstract: We have examined the discrete species of simian virus 40 (SV40) RNA present very early in infection of monkey cells with wild-type virus, with mutant tsA58 virus, and with the corresponding DNAs to distinguish between two classes of models for control of late transcription: (i) positive control mediated by large-T antigen and (ii) negative control mediated by a repressor protein associated with viral DNA in the virion. Total cytoplasmic or nuclear polyadenylated RNAs from infected cells were denatured with glyoxal, separated by electrophoresis on agarose gels, and transferred to diazobenzyloxymethyl paper. The positions of specific early and late RNA species were determined with region-specific SV40 DNA probes. The technique can detect individual RNAs present at the level of less than one copy per cell. After 9.5 h at 37 degrees C, appreciable amounts of two early RNAs (2.6 kilobases [kb] and 2.9 kb) were present in the cytoplasm of cells infected with wild-type virus or DNA, along with much smaller amounts of two late RNAs, 1.6 kb (16S) and 2.5 kb (19S). The amounts of the late RNAs were reduced, but they were still synthesized in the presence of cytosine arabinoside, an inhibitor of DNA synthesis. In comparable infections with tsA58 virus or DNA at nonpermissive temperature (41 degrees C), substantial amounts of the two early RNAs were again present, but the two late RNAs could not be detected. However, small amounts of the late RNAs were found when infections with tsA58 virus or DNA were prolonged to 30 h at 41 degrees C. These results are not consistent with negative control of late transcription through the action of a repressor and, taken together with other data, suggest that T antigen has an active role in late RNA synthesis. Specific early and late viral RNAs were also detected in the nuclear poly(A)(+) fractions and were similar in size to the RNA species found in the cytoplasmic polyadenylated fractions. The late nuclear RNAs (1.8 and 2.9 kb) were significantly larger than the late cytoplasmic species, possibly because they are precursors. The 2.6- and 2.9-kb early RNAs found in the cytoplasm are probably the messengers for large-T and small-t antigens, respectively.
517 citations
TL;DR: It is reported that this drug inhibits growth and cytopathology of several unrelated DNA and RNA viruses, while not affecting cell activity and ability to replicate, and inactivates herpes simplex virus particles irreversibly.
Abstract: Screening investigations in antiviral action of plant extracts have revealed that a component of Glycyrrhiza glabra roots, found to be glycyrrhizie acid, is active against viruses. We report here that this drug inhibits growth and cytopathology of several unrelated DNA and RNA viruses, while not affecting cell activity and ability to replicate. In addition, glycyrrhizic acid inactivates herpes simplex virus particles irreversibly.
424 citations
TL;DR: The demonstration of antibody dependence of dengue virus infection in subhuman primates--a complex, outbred experimental host--supports the hypothesis that the severity of d Dengue in humans is regulated by antibody.
Abstract: Five pairs of juvenile, dengue virus-susceptible rhesus monkeys were given normal or dengue-immune human cord-blood serum injected intravenously to a final dilution of 1:300. The pool of immune human cord-blood serum had a titer of antibody to dengue type 2 virus (D2V) of 1:140 in the plaque-reduction neutralization test and a titer of human monocyte infection enhancement of greater than 1:2,000,000. Fifteen minutes after inoculation of serum, animals were infected with D2V (strain no. 16681). Daily titers of viremia were always higher in the animals that had received antiserum to D2V than in animals that had received normal cord-blood serum. Ratios of infection enhancement ranged from 2.7 to 51.4. The demonstration of antibody dependence of dengue virus infection in subhuman primates--a complex, outbred experimental host--supports the hypothesis that the severity of dengue in humans is regulated by antibody.
424 citations
TL;DR: The biological and physicochemical characteristics of the PPR virus indicate that it is closely related to measles, rinderpest and canine distemper viruses, but is sufficiently distinct from these 3 viruses to justify considering it as the fourth member of the Morbillivirus genus.
Abstract: Peste des petits ruminants (PPR) is a virus disease of sheep and goats in West Africa. When first described, the virus was considered a variant of rinderpest virus. The biological and physicochemical characteristics of the virus indicate that it is closely related to measles, rinderpest and canine distemper viruses. These three viruses form the genus Morbillivirus of the Paramyxoviridae. PPR virus is sufficiently distinct from these 3 viruses to justify considering it as the fourth member of the Morbillivirus genus.
393 citations
TL;DR: n-Butyrate was found to increase the number of virus producer cells to a dramatic extent in the Epstein-Barr virus-carrying P3HR-1 and B95-8 lines, raising interesting questions on the mechanism of EBV induction, and its possible relationship to the known differentiation inducing ability of n-butyrate.
TL;DR: The results indicate that DLVs represent recombinants between a common ‘vector’ related to a chicken endogenous virus and one of three types of cellular gene possibly involved in haematopoietic differentiation.
Abstract: The RNAs of seven replication-defective leukaemia virus (DLV) strains contain three types of unique sequences, which correlate with the capacity of a given virus strain to transform erythroblasts, macrophage-like cells and myeloblasts, respectively. These sequences, termed erb, mac and myb, have their counterparts in the normal DNA of avian and mammalian species. Our results indicate that DLVs represent recombinants between a common 'vector' related to a chicken endogenous virus and one of three types of cellular gene possibly involved in haematopoietic differentiation.
TL;DR: These studies represent the first reliable propagation of human hepatitis A virus in vitro and point the way to the eventual means for detection and quantification of live virus in vivo and of production in cell culture of virus for diagnostic antigen and vaccine preparation.
Abstract: SummaryHuman hepatitis A virus was reliably and repeatedly propagated in primary explant cell cultures of marmoset livers and in the normal fetal rhesus kidney cell line (FRhK6). Identity of virus ...
TL;DR: Inhibition of haemagglutination by specific antiserum prepared in specific-pathogen-free beagles provided a convenient method for viral identification and protected dogs against challenge with virulent canine parvo-like virus.
Abstract: A newly recognised canine parvo like virus was isolated from faeces of dogs with haemorrhagic enteritis. Cell cultures from several species were susceptible to it. Virus infected cells could be demonstrated by staining with fluorescent antibody reagents (prepared against canine virus or feline panleucopenia virus) or by haemagglutination with pig or rhesus monkey red blood cells. Inhibition of haemagglutination by specific antiserum prepared in specific-pathogen-free beagles provided a convenient method for viral identification. Experimental inoculation of specific-pathogen-free beagles resulted in elevated body temperatures and caused lymphopenia lasting one to three days. Feline panleucopenia virus vaccines protected dogs against challenge with virulent canine parvo-like virus.
TL;DR: Austrian strains of enterovirus 71 regularly caused paralysis in monkeys and morphological poliomyelitis-like lesions in their CNS, and paralysis and myositis with Zenker necrosis in newborn white mice, cotton rats, Syrian hamsters, and 3-week-old cotton rats.
Abstract: Virological and serological studies of an epidemic disease in Bulgaria, 1975, were carried out. Epidemiologically, clinically and pathomorphologically, the disease simulated almost all known forms of poliomyelitis, acute stem encephalitis, encephalomyocarditis and aseptic meningitis. The studies completely rules out the participation of polioviruses and provided comprehensive evidence for the etiological role of a peculiar enterovirus subsequently identified as enterovirus (EV) type 71 known in the literature since 1974. Altogether, in 1975 and 1976 from 65 cases of poliomyelitis-like disease (PLD) 92 strains of EV71 were isolated, including 37 strains from the brain and medulla, 1 from the cerebrospinal fluid, 10 from mesenterial lymph nodes and tonsils and 44 from faeces. In addition, in 282 convalescent cases of the disease, diagnostic seroconversion or high titers of antibody to this virus were demonstrated. The most successful virus isolation was achieved by inoculation of green monkey kidney cell cultures and newborn white mice. Bulgarian strains of enterovirus 71 regularly caused paralysis in monkeys and morphological poliomyelitis-like lesions in their CNS, and paralysis and myositis with Zenker necrosis in newborn white mice, cotton rats, Syrian hamsters, and 3-week-old cotton rats. The diseased rodents had much more virus in their mucles than in brains.
TL;DR: Data indicate that during infectious mononucleosis, EBV causes polyclonal activation of B cells, reflected by hypergammaglobulinemia and increased circulating immunoglobulin-secreting cells.
Abstract: Infectious mononucleosis is caused by the Epstein-Barr virus (EBV), an unusual human pathogen because it preferentially infects B lymphocytes and consequently activates them to produce immunoglobulins. When cultures of lymphocytes from patients with infectious mononucleosis were stimulated with polyclonal activators, unseparated cells failed to produce immunoglobulins, whereas purified B cells responded normally. Cocultures demonstrated profound suppressor T-cell activity in blood from patients with infectious mononucleosis. Early in this disease, circulating immunoglobulin-secreting cells were elevated, but during the second week their number was strikingly depressed. These data indicate that during infectious mononucleosis, EBV causes polyclonal activation of B cells, reflected by hypergammaglobulinemia and increased circulating immunoglobulin-secreting cells. Next, suppressor T cells become activated and inhibit further B-cell activation. Thus, activation of suppressor T cells in infectious mo...
TL;DR: The results obtained permit the conclusion that in naturally occurring avian influenza viruses the structure of the hemagglutinin, that is its susceptibility to proteolytic cleavage in a broad spectrum of host cells, is the determining factor for pathogenicity.
TL;DR: It is suggested that respiratory syncytial virus may readily infect neonates, but the disease may be atypical and may be overlooked.
Abstract: Respiratory syncytial virus infections are thought to be uncommon in the first month of life. During a community outbreak, we prospectively studied such infection in our neonatal units. Of 82 neonates studied, 66 were hospitalized for six days or longer, and 23 (35 per cent) acquired this virus. Four infants died, two unexpectedly. Infected infants had a significantly shorter gestation and birth weight. Illness was often atypical, with nonspecific signs, especially in infants under three weeks of age, who had significantly less lower-respiratory-tract involvement and lower quantities of virus in their nasal washes. The titer of virus shed correlated with the infants' postnatal, but not gestational, age. Infection was also acquired by 34 per cent of the staff, who appeared to be important in the spread of the virus. These findings suggest that respiratory syncytial virus may readily infect neonates, but the disease may be atypical and may be overlooked.
TL;DR: Treatment of Ehrlich ascites tumour cells with highly purified interferon results in the accumulation of a particular mRNA and the corresponding protein within the cells, but the function of the induced protein is not yet identified.
Abstract: INTERFERONS are glycoproteins which are synthesised by various vertebrate cells in response to virus infection or some other stimuli. They are secreted and then interact with other cells and convert these into an antiviral state, in which the multiplication of viruses is impaired1. It is thought that transcription and translation are required for the establishment of the antiviral state as actinomycin D or inhibitors of protein synthesis, suitably administered, prevent or delay the effect2,3. Results with enucleated cells also support this idea4. We show here that treatment of Ehrlich ascites tumour (EAT) cells with highly purified interferon results in the accumulation of a particular mRNA and the corresponding protein within the cells. However, we have not yet identified the function of the induced protein.
TL;DR: A comparison of the efficacy of 5-iodocytosine analogue 7e against HSV-1 with other known nucleoside antiviral agents indicates that further in vitro and in vivo evaluation of 7e is warranted.
Abstract: A series of 5-substituted 1-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl)cytosines 7a-d and their corresponding uracils 9a-d,f were prepared by condensation of 3-O-acetyl-5-O-benzoyl-2-deoxy-2-fluoro-D-arabinosyl bromide (5) with appropriately trimethylsilylated pyrimidines followed by saponification of the protected nucleosides 6 or 8. 1-(2-Deoxy-2-fluoro-beta-D-arabinofuranosyl)-5-iodocytosine (7e) was obtained by iodination of 7a. Iodination of 8a followed by removal of the protecting acyl-protecting groups afforded the 5-iodo nucleoside 9e. Several of these 2'-fluoro-substituted nucleosides completely obviated replication of herpes simplex virus type 1 (HSV-1) in monolayers of Vero cells at concentrations of 10-100 microgram/mL. The 5-iodocytosine analogue 7e was the most effective, showing 99.5% suppression of viral replication even at concentrations of 0.1 microgram/mL. The cytotoxicity of 7e to L5178Y or P815 cells in culture was minimal. A comparison of the efficacy of 7e against HSV-1 with other known nucleoside antiviral agents indicates that further in vitro and in vivo evaluation of 7e is warranted.
TL;DR: The antiviral activity of ACG against clinical isolates of HSV-1, HSv-2, and varicella-zoster virus and the lack of toxicity to monkey or human cells in culture at concentrations which markedly inhibited these viruses are demonstrated.
Abstract: Inhibition by acycloguanosine (ACG) of plaque formation by harpes simplex virus types 1 and 2 (HSV-1 and HSV-2), varicella-zoster virus, and cytomegalovirus was studied. Seventeen clinical isolates of HSV-1 were inhibited by ACG at a mean 50% inhibitory dose (ID 50 ) of 0.15 ± 0.09 μM. The mean ID 50 for 10 isolates of HSV-2 was 1.62 ± 0.76 μM, and for four isolates of varicella-zoster virus it was 3.75 ± 1.30 μM. The ID 50 9s for two cytomegalovirus isolates were 100 and 160 μM, and for four additional isolates of cytomegalovirus no end point (ID 50 ) was reached at 200 μM. ACG at a concentration of 200 μM had no effect on deoxyribonucleic acid synthesis in human fibroblast cells and only inhibited thymidine incorporation by Vero cells by one-third. These studies demonstrated the antiviral activity of ACG against clinical isolates of HSV-1, HSV-2, and varicella-zoster virus and the lack of toxicity to monkey or human cells in culture at concentrations which markedly inhibited these viruses. ACG had little effect on cytomegalovirus at concentrations in excess of 100 μM.
TL;DR: Serologic study of healthy schoolchildren showed annual rates of infection that paralleled but greatly exceeded rates of recognized M. pneumoniae pneumonia, and a higher proportion of infections among children aged five to nine years than among adolescents aged 15-19 years resulted in pneumonia.
Abstract: Pneumonia due to Mycoplasma pneumoniae was monitored in a large prepaid medical-care group in Seattle, Washington, between 1963 and 1975. The disease was diagnosed by isolation of M. pneumoniae and/or significant rises in titer of complement-fixing (antilipid) antibody in paired sera. Infection was endemic without significant seasonal fluctuations. Two epidemics occurred: the first peaked in January 1967, the second late in the summer of 1974. Total rates of pneumonia infection in children increased during M. pneumoniae epidemics, but epidemics of infection with respiratory syncytial virus had a greater effect. Age-specific attack rates for M. pneumoniae pneumonia among children aged five to nine years (about six per 1,000) were about twice the rates for younger children and four times those for adults. Serologic study of healthy schoolchildren showed annual rates of infection that paralleled but greatly exceeded rates of recognized M. pneumoniae pneumonia. Infection rates varied from 2% in endemic years to 35% in epidemic periods. A higher proportion of infections among children aged five to nine years than among adolescents aged 15-19 years resulted in pneumonia.
TL;DR: The data suggest that evolution of oncogenic retroviruses has frequently involved a mechanism whereby incorporation and perhaps modification of different host genes provides each virus with the ability to induce its characteristic tumors.
Abstract: The avian carcinoma virus MC29 (MC29V) contains a sequence of approximately 1,500 nucleotides which may represent a gene responsible for tumorigenesis by MC29V. We present evidence that MC29V has acquired this nucleotide sequence from the DNA of its host. The host sequence which has been incorporated by MC29V is transcribed into RNA in uninfected chicken cells and thus probably encodes a cellular gene. We have prepared radioactive DNA complementary to the putative MC29V transforming gene (cDNA(mc) (29)) and have found that sequences homologous to cDNA(mc) (29) are present in the genomes of several uninfected vertebrate species. The DNA of chicken, the natural host for MC29V, contains at least 90% of the sequences represented by cDNA(mc) (29). DNAs from other animals show significant but decreasing amounts of complementarity to cDNA(mc) (29) in accordance with their evolutionary divergence from chickens; the thermal stabilities of duplexes formed between cDNA(mc) (29) and avian DNAs also reflect phylogenetic divergence. Sequences complementary to cDNA(mc) (29) are transcribed into approximately 10 copies per cell of polyadenylated RNA in uninfected chicken fibroblasts. Thus, the vertebrate homolog of cDNA(mc) (29) may be a gene which has been conserved throughout vertebrate evolution and which served as a progenitor for the putative transforming gene of MC29V. Recent experiments suggest that the putative transforming gene of avian erythroblastosis virus, like that of MC29V, may have arisen by incorporation of a host gene (Stehelin et al., personal communication). These findings for avian erythroblastosis virus and MC29V closely parallel previous results, suggesting a host origin for src (D. H. Spector, B. Baker, H. E. Varmus, and J. M. Bishop, Cell 13:381-386, 1978; D. H. Spector, K. Smith, T. Padgett, P. McCombe, D. Roulland-Dussoix, C. Moscovici, H. E. Varmus, and J. M. Bishop, Cell 13:371-379, 1978; D. H. Spector, H. E. Varmus, and J. M. Bishop, Proc. Natl. Acad. Sci. U.S.A. 75:4102-4106, 1978; D. Stehelin, H. E. Varmus, J. M. Bishop, and P. K. Vogt, Nature [London] 260:170-173, 1976), the gene responsible for tumorigenesis by avian sarcoma virus. Avian sarcoma virus, avian erythroblastosis virus, and MC29V, however, induce distinctly different spectra of tumors within their host. The putative transforming genes of these viruses share no detectable homology, although sequences homologous to all three types of putative transforming genes occur and are highly conserved in the genomes of several vertebrate species. These data suggest that evolution of oncogenic retroviruses has frequently involved a mechanism whereby incorporation and perhaps modification of different host genes provides each virus with the ability to induce its characteristic tumors.
TL;DR: A synthetic fowl plague virus (FPV) haemagglutinin gene has been cloned in bacteria and the complete sequence of the RNA gene deduced.
Abstract: A synthetic fowl plague virus (FPV) haemagglutinin gene has been cloned in bacteria and the complete sequence of the RNA gene deduced. It is 1,742 nucleotides long and the mRNA codes for 563 amino acids in an uninterrupted sequence. The nature of some of the important domains in the haemagglutinin has been established, and their structure is discussed in relation to their function. Extensive amino acid sequence homologies exist between FPV and human influenza haemagglutinins.
TL;DR: It is concluded that the p21 of Ha-MuSV and Ki- MuSV are homologous proteins coded for bv homologueous sequences found in the recombinant genomes of Ha,MuSv and Ki,muSV.
TL;DR: The RNA of infectious bursal disease virus was reexamined in a detailed analysis and it could be established that its genome consists of two segments of double-stranded RNA.
Abstract: The RNA of infectious bursal disease virus was reexamined in a detailed analysis. It could be established that its genome consists of two segments of double-stranded RNA. The RNA is RNase resistant and has a sedimentation coefficient of 14S and a buoyant density of 1.62 g/ml. The purine/pyrimidine ratio is nearly 1; the guanine plus cytosine content is 55.3%; the Tm is 95.5 degrees C. The molecular weights of the two double-stranded segments were determined to be 2.2 x 10(6) and 2.5 x 10(6).
TL;DR: Natural occurrence of inierfer on-mediated 2′–5′ adenine oligonucleotide inhibitors in interferon-treated, EMC virus-infected mouse L cells is reported, consistent with the idea that they play a part in the inhibition of virus growth.
Abstract: Until now the inierfer on-mediated 2′–5′ adenine oligonucleotide inhibitors (2–5A) of cell-free protein synthesis have not been detected in intact cells. Here we report their natural occurrence in interferon-treated, EMC virus-infected mouse L cells in amounts consistent with the idea that they play a part in the inhibition of virus growth.
TL;DR: A series of compounds, representing three classes of tumor-promoting diterpene esters, efficiently induced EBV in persistently infected cells, and prostaglandins, reported to be released after treatment with tumor promoters, were ineffective in virus induction under the conditions tested.
Abstract: The effect of various tumor initiators and promoters on induction of persisting Epstein-Barr virus (EBV) in different lines of lymphoblastoid cells was analyzed. Neither five polycyclic aromatic hydrocarbons, amongst them potent tumor initiators (e.g., 7,12-dimethylbenz[a]anthracene), nor the potent (ultimate) liver carcinogen N-acetoxy-N-2-acetylamino-fluorene induced EBV. A series of compounds, representing three classes of tumor-promoting diterpene esters (e.g., 12-O-tetradecanoylphorbol-13-acetate), efficiently induced EBV in persistently infected cells. The concentration required for maximal induction ranged between 0.5 and 100 nM. Some nonpromoting diterpenes (phorbol, 4α-phorbol-12,13-didecanoate, and ingenol) did not induce EBV. However, the nonpromoters, resiniferatoxin and 12-deoxyphorbol-13-decatrienoate, were effective, whereas anthralin, a tumor promoter, did not induce EBV. In three lines of EBV genome-carrying cells (Raji, NC-37, and RPMI 64-10) only abortive induction was noted, leading exclusively to synthesis of early antigen. In cells of lines with low spontaneous virus release (P3HR-1, B95-8, and QIMR-Wil), upon treatment with tetradecanoylphorbol acetate, approximately 20-40 times more viral DNA was recovered as compared to untreated controls. Viral DNA from tetradeca-noylphorbol acetate-induced cultures revealed the same restriction endonuclease cleavage pattern as viral DNA obtained from noninduced cells. Within 10 days after induction, release of infectious virus increased approximately by one order of magnitude. Prostaglandins, reported to be released after treatment with tumor promoters, were ineffective in virus induction under the conditions tested.
TL;DR: Analysis of nucleotide sequence analysis of the 5' and the 3' terminal of the RNA segments of the genome of fowl plague virus confirms the presence of a common sequence at the 5', 3' terminus of each segment and a complementary sequence which may be important in the control of transcription and replication of the genomes.
Abstract: EXtensive nucleotide sequence analysis of the 5' and the 3' terminal of the RNA segments of the genome of fowl plague virus, an avian strain of influenza virus, confirms the presence of a common sequence at the 5' terminus of each segment and a common sequence at the 3' terminus of each segment. Between the ends of each individual segment there is a complementary sequence which may be important in the control of transcription and replication of the genome. In addition, the probable sites of initiation of translation of fowl plague virus mRNA are indicated along with the corresponding NH2-terminal amino acid sequences of the virus polypeptides.