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At least 271 records · Page 15Linked to original sources
PubMed1990

Successful competition in translation by the flavivirus Kunjin with poliovirus during co-infections in Vero cells.

Infection with poliovirus effectively inhibited the translation of Vero cell messengers (carrying type 1 or type 2 caps at the 5' end) and of influenza virus messengers (type 1 caps) in co-infections. In contrast, Kunjin virus RNA (type 1 caps) and Semliki Forest virus RNA (a togavirus, with type 0 caps) continued to be translated in the presence of co-infecting poliovirus. Translation of Kunjin virus RNA was also unaffected during co-infections with either influenza virus or Semliki Forest virus. Guanidine treatment effectively blocked poliovirus replication only, but the inhibitory effect on translation of cell messengers and influenza virus messengers was still observed, indicating that this effect was not caused by competition in translation with poliovirus messengers. It was therefore concluded that the observed inhibition was most likely caused by cleavage of the p220 subunit of the cap binding protein (CBP) complex of the cell normally required for translation of capped messengers, as reported by others. However, Kunjin virus RNA could be efficiently translated apparently in the absence of a functional CBP complex, except when its secondary structure was stabilized by hypertonic salt in the culture medium.

Animals↗
PubMed1990

Viral protein production in homogeneous and mixed infections of cytopathic and noncytopathic BVD virus.

Experiments were conducted to examine dual infection of cultured cells with cytopathic and noncytopathic bovine viral diarrhea virus (BVDV). Cell monolayers infected with a noncytopathic BVDV isolate and subsequently superinfected with a cytopathic BVDV isolate were refractive to the cytopathic effects of the cytopathic BVDV isolate, as reported in the literature. Immunofluorescence staining of superinfected cultures with monoclonal antibodies specific for the cytopathic or the noncytopathic viral isolate, demonstrated that cells in superinfected cultures contained both viral biotypes. Immunoprecipitation was used to compare the temporal detection of viral induced polypeptides in superinfected cultures to that of cultures infected with a single viral biotype. In single cytopathic viral infections, viral induced polypeptides of 80 kDa and 53-56 kDa are detected simultaneously, but in superinfections a 4 h gap occurred between detection of the 53-56 kDa polypeptide and detection of the 80 kDa polypeptide.

Animals↗
PubMed1984

Biological and macromolecular properties of murine cells persistently infected with MHV-JHM.

A persistently-infected neuroblastoma culture [Neuro-2A( JHMV )] was established with the murine hepatitis virus JHM [MHV-JHM]. After 100 days of passage, the endogenous virus [Neuro-2A( JHMV ) end] released by this culture was unable to induce the syncytia typical of MHV-JHM and the endogenous virus was not temperature-sensitive. The Neuro-2A( JHMV ) culture was cured of virus production by passage under neutralizing antibody [Neuro-2A( JHMV )Ab]. The Neuro-2A( JHMV ) and the Neuro-2A ( JHMV ) Ab cultures were as susceptible to heterologous infection with mengovirus and vesicular stomatitis virus as the uninfected Neuro-2A culture. However, the Neuro-2A ( JHMV ) and Neuro-2A( JHMV ) Ab cultures were partially resistant to homologous superinfection by MHV-JHM and the closely related MHV-A59. Virus related to MHV-JHM was rescued from the antibody-cured cells by cell fusion. The synthesis of MHV-JHM specific antigens by Neuro-2A( JHMV ) cells, Neuro-2A( JHMV ) Ab cells and 17 Cl-1 cells infected by Neuro-2A( JHMV ) end was studied by SDS-PAGE. The genomic RNAs of MHV-JHM and Neuro-2A( JHMV ) end were compared by oligonucleotide mapping. The results of the protein and RNA studies indicated that the genome of Neuro-2A( JHMV ) end was substantially modified from the genome of MHV-JHM, but the modifications did not significantly alter the molecular size of the viral-specific proteins.

Animals↗
PubMed1983

Characterization of four cell lines persistently infected with measles virus.

Persistently infected cell lines were established by infecting Vero cells with four different strains of measles virus: Edmonston "wild type", Schwarz vaccine strain passaged at high multiplicity of infection, Hallé SSPE strain, and a temperature sensitive mutant of Edmonston strain, designated ts 841. The four cell lines have continued to produce virus at a constant low level over a period of more than two years, although cytopathology and hemagglutinating ability have varied with cell passage. Only virus from cells originally infected with ts 841 appears to be temperature sensitive. In each of the cell lines a sizable population of low density, interfering virus particles was generated, indicating that this is an important mechanism for these four cell lines in maintenance of the measles virus persistent infection.

Animals↗
PubMed1983

Properties of lymphocytic choriomeningitis virus interfering particles.

Lymphocytic choriomeningitis virus (LCM virus) interfering particles (IP) were generated in cultivated cells and their properties determined. Unlike true defective interfering (DI) particles, LCM virus IP did not show the phenomenon of enrichment and, consequently, passaging the virus undiluted did not result in their accumulation; in fact, more IP were produced during dilute passages. Furthermore, the progeny of each of 20 plaques contained high numbers of IP. On the basis of these and previous observations, we consider LCM virus IP not deletion mutants but by-products of virus synthesis.

Animals↗
PubMed1975

Effect of alkaline maintenance medium upon the growth of rabies virus in chick embryo cells.

HEP Flury strain of rabies virus was propagated in chick embryo cells under maintenance media of different pH. It was found that viral growth was better and reached a markedly higher maximum titer when the initial pH of maintenance medium was 8.2 to 9.0 than when it was 7.4. The enhancement of viral growth was not ascribable to mere neutralization of acids produced from infected cells, because the different media became almost equally neutral within an early phase of growth curve. Serial passage of the virus in chick embryo cells using pH 8.2 maintenance medium resulted in altered growth characteristics of the progeny virus; first, the virus so passaged could now grow equally well under alkaline and neutral maintenance media, and, secondly, autointerference observable with the parent virus eventually lowered virus yield when neutral maintenance medium was used, but this effect of undiluted passage was eliminated by the use of pH 8.2 maintenance medium.

Animals↗
PubMed1986

Isolation of a novel type of interfering influenza B virus defective in the function of M gene.

A novel type of interfering influenza B virus which is defective in the function of M gene has been reported. Clone 301, a B type virus clone obtained by successive back-crosses of A/Aichi/2/68 (H 3 N 2) with B/Yamagata/1/73, grew normally in MDCK cells when inoculated at a low multiplicity, but was easily converted to a hemagglutinating but non-infectious form by one cycle of high multiplicity infection. Within MDCK cells infected with infectious clone 301 at a high multiplicity, synthesis of M protein was greatly reduced. The virus particle produced by a high multiplicity infection was devoid of RNA segment 7 (M gene), contained less amount of M protein compared with the standard virus, and interfered with the replication of wild type B/Yamagata, again accompanied by a selective suppression of M protein synthesis within the co-infected cells.

Defective Viruses↗
PubMed1987

Pathogenic and structural properties of wild type infectious bursal disease virus (IBDV) and virus grown in vitro.

Large plaque (LP) and small plaque (SP) variants of Infectious Bursal Disease Virus (IBDV) which are formed in vitro after serial passages in CE-cells at low or high multiplicities of infection were tested for their pathogenic properties in susceptible chickens. LP virus caused clinical manifestations and destruction of the Bursa of Fabricius (BF) without killing the animals. No signs of a disease appeared after infection with SP virus, and only limited necrotic foci developed in the BF. Coinfection with the SP variant and the highly pathogenic wild type (wt) virus reduced mortality and the severity of the disease. In contrast to the SP variant, which forms incomplete particles of low density, with one or the other of the two genomic RNA segments missing, the two RNA segments characteristic for IBDV were present in approximately equal amounts in wt particles with a buoyant density of 1.29 g/ml isolated from the BF. In spite of an almost total replacement of one of the two major structural polypeptides with a molecular weight of 32 kd by a 28 kd protein, infectivity in this low density fraction was only slightly reduced. This finding underlines the importance of the type of post-translational modification in lymphoid cells or fibroblasts.

Animals↗
PubMed1976

Studies on a measles virus variant inducing persistent infections in cultured cells.I. Isolation and characterization of plaque purified virus clones.

Attempts were made to characterized by a plaque assay two variants of the Edmonston strain of measles virus and to obtain plaque purified virus populations. The UP non-cytocidal variant, in all the examined cell systems, mainly produced small but also large plaques; the DP cytocidal variant always large plaques. Three clones, UP-SP4, UP-LP4 and DP-LP4, were derived by plaque purfication respectively of the UP small plaque, UP large plaque and DP large plaque forming particles. The virus populations of the clones could be distinguished by some other biological and physical characters: cytopathic effect in roller tube cultures, growth potential in HeLa cells, thermal stability at 45 degrees C, stability of the properties during serial passages at different input multiplicity. The hypothesis was supported that the typical properties of the UP and DP variants are host-independent and genetically controlled viral markers.

Animals↗
PubMed2005

Viral evasion of the MHC class I antigen-processing machinery.

In their adaptation to the immune system in vertebrates, viruses have been forced to evolve elaborate strategies for evading the host's immune response. To ensure life-long persistence in the host, herpes viruses, adenoviruses and retroviruses have exploited multiple cellular pathways for their purpose, including the class I antigen-processing machinery. Attractive and prominent targets for viral attacks are the proteasome complex, the transporter associated with antigen processing, and MHC class I molecules. This review briefly outlines the different mechanisms of viral interference with the antigen-presentation pathway.

ATP-Binding Cassette Transporters↗
PubMed2003

Resistance to superinfection of Vero cells persistently infected with Junin virus.

Two non-virogenic Vero cell lines persistently infected with the arenavirus Junin (JUNV), named V3 and V7, were characterized with respect to their resistance to superinfection with homologous and antigenically related viruses. Both lines were refractory to JUNV multiplication and partially resistant to other arenaviruses. JUNV was able to adsorb and penetrate persistently infected cells and, although V3 and V7 were able to support synthesis of antigenomic sense viral RNA, protein production of superinfecting virus was totally blocked. This resistance was not mediated by defective interfering particles but rather by a "cell-associated factor" that could be cell to cell transmitted. Prolonged thermal treatment of V3 and V7 abrogated expression of the viral nucleoprotein (N) and turned persistently infected cells permissive to JUNV multiplication. Thermal treated cells cultured at 37 degrees C resumed the expression of N in association to the recovery of resistance. Results strongly suggest a correlation between the presence of the viral nucleoprotein and superinfection exclusion.

Animals↗
PubMed1998

Turnover of hepatitis C virus genotypes in hemodialysis patients.

Hepatitis C virus (HCV) genotypes were determined in hemodialysis patients with a high prevalence and incidence of infection. A change of HCV genotype was observed in 6/14 follow-up samples analyzed 13 and 21 months later. The appearance and disappearance of HCV genotypes may be due to either genotype-specific intermittent viremic status or viral interference.

Genotype↗
PubMed2004

HIV accessory proteins and surviving the host cell.

Human immunodeficiency virus generates the accessory proteins Nef, viral infectivity factor (Vif), viral protein R, and viral protein U or viral protein X during viral replication in host cells. Although the significance of these accessory proteins is often lost in vitro, they are essential for viral pathogenesis in vivo. Therefore, these proteins have much potential as antiviral targets. Recent data reveal Vif perturbs an ill-defined antiviral pathway in host cells allowing HIV replication. These data highlight a common feature among HIV accessory proteins in manipulating the host to aid viral pathogenesis. Therefore, these new insights into Vif and other HIV accessory proteins are reviewed, emphasizing host cell interactions and new targets for therapeutic intervention.

HIV Infections↗
PubMed1987

Adenovirus infection reverses the antiviral state induced by human interferon.

HeLa cells treated with human lymphoblastoid interferon do not synthesize poliovirus proteins. The antiviral state against poliovirus is reversed if cells are previously infected with adenovirus type 5. A late gene product seems to be involved in this reversion, since no effect is observed at early stages of infection or in the presence of aphidicolin.

Adenine Nucleotides↗
PubMed1976

On the lack of host-cell reactivation of UV-irradiated phage T5 II. Further characterization of the repair inhibition exerted by T5 infection.

Experiments reported in the preceding paper [4] had shown that host-cell reactivation (HCR) of UV-irradiated phage T1 in excision-repair proficient Escherichia coli cells is inhibited by superinfection with phage T5. Theoretical considerations have led to predictions concerning the dependence of repair inhibition on the multiplicity of superinfecting T5 phage and on the UV fluence to which they were exposed. These predicitions have been supported by experimental results described in this paper. The fluence dependence permitted calculation of the relative UV sensitivity of the gene function responsible for repair inhibition; it was found to be about 2.3% that of the plaque-forming ability of phage T5. The T5-inhibitable step in excision repair occurs early in the infective cycle of T1. Furthermore, experiments involving the presence of 400 mug/ml chloramphenicol showed that HCR inhibition of T1 is caused by a protein produced after the FST segment of T5 (i.e. the first 8% of the T5 genome) has entered the host cell. A previously described minor T1 recovery process, occurring in both excision-repair-proficient and -deficient host cells, is inhibited by T5 infection due to a different substance, which is most likely associated with the "second-step-transfer" region of T5 DNA (involving the remainder of the genome). Superinfection with T4v1 phage resulted in HCR inhibition of T1, resembling that observed after T5 superinfection. The discussion of these results suggests that inhibition of the bacterial excision repair system by T5 or T4 infection occurs at the level of UV-endonucleolytic incision, and that lack of HCR both in T-even phages and in T5 can be explained in the same manner.

Caffeine↗