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At least 397 records · Page 22Linked to original sources
PubMed1975

Replication of reticuloendotheliosis viruses in cell culture: chronic infection.

After an initial acute infection with cell killing, chicken or duck embryo fibroblasts infected in culture with reticuloendotheliosis viruses set up a chronic infection with no cell killing or morphological transformation. Essentially all of the chronically infected cells produced virus. The virus production was not sensitive to cytosine arabinoside or mitomycin C as was virus production in an acute infection. The chronically infected cells had a strong group-specific resistancto the c.p.e. of superinfecting reticuloendotheliosis viruses. However, they were sensitive to vesicular stomatitis virus and avian leukosis-sarcoma viruses. After double infection, single cells produced reticuloendotheliosis virus and avian leukosis-sarcoma virus.

Alpharetrovirus↗
PubMed1975

The production of a temperature-sensitive persistent measles virus infection.

A persistent infection of measles virus was established in HEp2 cells. All cells contained virus antigen when tested by specific immunofluorescence and approx. 50% were positive by haemadsorption. Infectious virus released into the supernatant medium was usually equivalent to no more than 0-001 p.f.u./cell, but between 10 and 40% of the infected cells produced plaques when plated on Vero cells. Passage of persistently infected cultures in the presence of measles antibody had no effect on the proportion of antigen-positive cells. Virus obtained from the supernatant medium of persistently infected cultures was temperature sensitive at 39-5 degrees C when tested on Vero cells whereas the original non-persistent virus produced infections on Vero cells at 39-8 degrees C. On passage of the persistently infected culture at 39-5 degrees C most of the surface antigens disappeared within 24 h whereas the intracellular virus antigens had not totally disappeared until the 5th passage.

Antigens, Viral↗
PubMed1976

Morphogenesis of picornaviruses: characterization and assembly of bovine enterovirus subviral particles.

Bovine enterovirus-I (BEV-I) infection results in the production of a low amount of infective virus. A large number of non-infectious virus particles can be detected in BEV-I lysates by haemagglutination. Attempts to isolate DI particles that might be responsible for this effect failed. However, infected cells were shown to contain large amounts of 80S particles as well as lesser amounts of 160S, 130S, 45S, 14S and 5S particles. The proportion of these subviral particles detectable by density gradient sedimentation depended on the ionic strength of the gradient buffer. At high ionic strength 130S particles were transformed into 160S particles, and 45S into 80S particles. The polypeptide composition of each virus particle was examined. Pulse-chase experiments confirmed that 80S particles were the predominant virus particles accumulating. No precursor-product relationship could be established for the 80S particle, although 5S and 14S particles were shown to be precursors of mature virus particles.

Animals↗
PubMed1979

Effect of undiluted passage on the polypeptides of measles virus.

Measles virus induces a large polypeptide (L; mol. wt. 180 K), a large glycopolypeptide (H; mol. wt. 80 K), a nucleocapsid associated polypeptide (P; mol. wt. 70 K), a nucleocapsid polypeptide (N; mol. wt. 60 K), a second glycopolypeptide (F0; mol. wt. 60 K), a matrix or membrane polypeptide (M; mol. wt. 37 K) and a small polypeptide (S; mol. wt. 15 K). The second glycopolypeptide (F0) appears to be cleaved in purified measles virus. Defective interfering particles accumulate during passage of measles virus leading to a decrease in the amounts of virus-specific protein synthesized in infected cells. Even in the best preparations of purified measles virus, host proteins are always detected and these become more predominant in preparations with low infectivity.

Carcinoma, Squamous Cell↗
PubMed1979

Regulation of imm gene expression in bacteriophage T4-infected cells.

Two polypeptides (imm-a and imm-b) which are not induced by an immunity mutant T4Dimm2 but by a wild-type strain T4D were identified by sodium dodecyl sulphate (SDS)-polyacrylamide gel electrophoresis. Their mol. wt. were 77 000 and 45 000, respectively. These polypeptides exhibited a similar kinetic pattern of synthesis. Within a few minutes p.i. the primary phage established the system that inhibited imm gene expression of superinfecting phage. This was shown by measuring both the phenotypic expression of immunity and the synthesis of imm gene polypeptides. The expression of two other immediate-early genes, namely genes s and 30, and early gene 33, was not affected by primary infection.

Genes, Viral↗
PubMed1979

Heterogeneity of virus particles in measles virus.

A heterogeneous population of virions is generated by measles virus-infected cells. These particles are partially separable by sucrose density centrifugation into three peaks. Each population is stable and contains infectious particles. The particles of all three populations contain at least six polypeptide species that differ between particle populations only in quantity. All three populations contain a 50S RNA species, and the heaviest density peak also contains an additional species of 43S RNA. The difference between these results and previous studies with measles virions will be discussed.

Animals↗
PubMed1980

Gradual changes of influenza virions during passage of undiluted material.

Defective influenza virions undergo gradual changes during passage of undiluted material: the amount of RNA in virions diminishes, the equimolarity of the RNA segments is lost and the interfering activity of defective virions decreases. Defective virions of early passages have a small deficiency in genetic material and at a high m.o.i. induce the synthesis of the complete set of virus-specific proteins. Defective virions from later passages are characterized by a considerable deficiency in genetic material and a decrease in the amount of high mol. wt. RNA segments. They do not demonstrate complementation and at a high m.o.i. do not induce the synthesis of virus-specific proteins, thus revealing analogous defects in the genome of the majority of defective virions. The characteristics of protein synthesis in cells infected with these virions are similar to those in uninfected cells. During undiluted passage of influenza virus the cyclic production of defective and infectious virions takes place.

Animals↗
PubMed1981

Biochemical composition of lymphocytic choriomeningitis virus interfering particles.

Lymphocytic choriomeningitis (LCM) was interfering particles were enriched relative to infectious virions by ultracentrifugation in a shallow gradient made of Urografin. Electrophoretic analysis revealed that they lacked the small ('S') 23S RNA as well as GP-1 and GP-2 of the infectious virion and also lacked a newly characterized glycoprotein of apparent mol. wt. 85 x 10(3); instead, they contained a novel glycoprotein with mol. wt. 65 x 10(3).

Glycoproteins↗
PubMed1982

Characterization of the Hallé SSPE measles virus isolate.

The Hallé subacute sclerosing panencephalitis (SSPE) measles virus isolate and its plaque-purified progeny were investigated to determine whether any unusual properties could be associated with its ability to cause persistent infection. Three types of plaque-purified progeny were isolated. One population appeared to be similar in biological and biochemical properties to laboratory-adapted measles virus and had the ability to induce syncytia (syn+). A second population (syn-) plaqued more efficiently at 39 degrees C than at 33 degrees C, did not cause normal cell fusion at either temperature, and produced particles that interfered with the replication of other measles virus isolates in vivo and in vitro. This syn- virus was further plaque-purified to eliminate the interfering particles, producing the syn- P2 virus. This virus also plaqued more efficiently at 39 degrees C than at 33 degrees C, but caused cell fusion only at 39 degrees C. Both syn- viruses and the parental virus were significantly less virulent in vivo than the syn+ virus and caused a more prolonged infection. Biochemical analysis showed that the syn- P2 population produced particles that banded at two different densities in potassium tartrate gradients; both densities were less than those of the standard laboratory measles virus and the syn+ virus. Although the syn- P2 virus did not cause cell fusion at 33 degrees C, [35S]methionine labelling demonstrated that the haemolysin/cell fusion protein was present in syn- P2 virions. The production of interfering particles, the inability to cause cell fusion at 33 degrees C, and the cold-sensitive nature of the syn- population appear to play a role in the ability of the Hallé SSPE virus to establish persistent infection.

Animals↗
PubMed1982

Analysis of viral and defective-interfering nucleocapsids in acute and persistent infection by rhabdoviruses.

We have isolated and characterized the RNA of intracellular virus nucleocapsids recovered from a number of cell cultures persistently infected with rabies virus or vesicular stomatitis virus (VSV). VSV persistent infections in BHK21, L cells and Aedes albopictus (mosquito) cells generally showed the presence of large amounts of defective-interfering (DI) nucleocapsid RNA and much smaller amounts of standard (B) nucleocapsid RNA. Persistent infections of BHK21 cells by two rabies virus strains, challenge virus standard (CVS-11) or HEP-Flury, were followed for several months during which time the ratio of DI to B nucleocapsid RNA cycled dramatically. We also observed coordinated fluctuations in the absolute amount of incorporation of [3H]uridine into virus nucleocapsid RNA. Total incorporation was generally highest following a decrease in the relative amount of DI nucleocapsid RNA synthesis. At no time were DI nucleocapsids absent in any of the persistently infected cultures.

Aedes↗
PubMed1982

Translation of capped virus mRNA in encephalomyocarditis virus-infected cells.

The pattern of protein synthesis in HeLa cells simultaneously infected with encephalomyocarditis virus (EMCV) and Semliki Forest virus (SFV) has been analysed throughout the time course of the infection. The ratio of the picornavirus protein gamma versus the togavirus late protein C increased when the m.o.i. of EMCV was raised, and the ratio of C/gamma increased with higher multiplicities of SFV. Under some conditions, the co-infected cells simultaneously synthesized the picornavirus and togavirus proteins, and the cells exclusively translated the capped 26S mRNA from SFV at the end of the co-infection experiment. The influence of the time of addition of the second virus on the relative translation of the capped and uncapped mRNAs was also studied. When HeLa cells were co-infected with 5 p.f.u./cell of EMCV and 200 p.f.u./cell of SFV, only the synthesis of SFV proteins was apparent, whereas if SFV was added 1 to 3 h later during the course of EMCV infection the cells synthesized picornavirus and togavirus proteins. If the cells were superinfected with SFV 1 h after EMCV addition, host protein synthesis was drastically inhibited after 3 h of EMCV infection. By 5 h post-infection both kinds of virus proteins were synthesized and at 7 h post-infection the cells preferentially translated the capped 26S mRNA from SFV. If cells were first infected with SFV (10 p.f.u./cell) and co-infected or superinfected at 1 h with EMCV (50 p.f.u./cell), shut-off of host protein synthesis occurred 3 h after infection and the cells synthesized both kinds of virus proteins. However, 9 h after infection the cells synthesized SFV proteins only. When double-infected HeLa cells were placed in a hypotonic medium, they mainly synthesized the togavirus late proteins, whereas under hypertonic conditions, they translated the picornavirus RNA exclusively. These results suggest that the two kinds of mRNAs (SFV 26S mRNA and EMCV 35S mRNA) are present in the infected cells and that the relative translation of each of them depends on the external ionic conditions.

Encephalomyocarditis virus↗
PubMed1982

Ultraviolet-irradiated vesicular stomatitis virus and defective-interfering particles are similar non-specific inhibitors of virus infection.

The way in which ultraviolet-irradiated vesicular stomatitis virus (VSV) inhibits the early events in VSV infection has been further characterized. Comparison of several different u.v.-irradiated thermolabile, temperature-sensitive mutants before and after heat inactivation established a requirement for inhibitory activity of functional G, N and L proteins, but not M protein. Defective-interfering (DI) particles, whether irradiated or not, inhibited VSV primary transcription as efficiently as UV-VSV, suggesting that virus proteins rather than transcription products are responsible for inhibition. Addition of inhibitory UV-VSV at different times after infection established that inhibition results from an action at an intracellular site, rather than at the cell surface or in the process of internalization. A similar inhibition by UV-VSV of infection by Sendai virus, Semliki Forest virus, Sindbis virus and influenza virus suggests that UV-VSV is acting by inducing a general change in the intracellular environment.

Animals↗