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PubMed1998

Coinfection by hepatitis B virus and hepatitis C virus.

Coinfection by hepatotropic viruses can occur due to the fact that hepatitis B virus (HBV) and hepatitis C virus (HCV) share similar routes of transmission. Different clinical features of liver disease can be observed in infected patients, ranging from fulminant, acute and chronic hepatitis to hepatocellular carcinoma (HCC). The relative role of the infecting viruses in determining the final clinical picture is not yet well defined. Several reports indicate that clinical and pathological severity of liver disease among coinfected patients is increased and in patients with HCC, co-occurrence of both viruses is a common event. The potential mechanism of tumour development still remains speculative, although direct and indirect roles for both HBV and HCV have been proposed. At the molecular level, reciprocal interference of virus replication has been repeatedly described and the extent of interference is influenced by the infecting HCV genotype, genotype 1 of HCV having more efficient inhibitory activity on HBV than genotype 2. Sequence similarities between an arginine-rich nucleocapsid motif of both viruses could support these clinical observations. Concerning response rates to interferon therapy, no satisfactory results have been achieved to date, although identification of effective therapeutic schemes, based on virological status of both viruses are warranted.

Age Factors↗
PubMed2004

Herpes simplex virus 2 virion host shutoff protein interferes with type I interferon production and responsiveness.

The herpes simplex virus 2 (HSV-2) virion host shutoff (vhs) protein is a ribonuclease contained in the virion tegument. vhs-deficient mutants of HSV-2 are profoundly attenuated in vivo, and we have previously shown that replication and virulence of vhs-deficient HSV-2 are largely restored to levels of wild-type virus in mice lacking the interferon alpha/beta receptor (IFNalphabetaR(-/-)). This result demonstrated that HSV-2 vhs interferes with the type I IFN response, but whether vhs inhibits production of type I IFN or synthesis or function of key mediators of the IFN-induced antiviral state was not clear. Here we address these questions using primary murine embryonic fibroblasts (MEFs), which produce and respond to IFNalphabeta. The vhs-deficient HSV-2 strain 333d41 replicated similarly to wild-type virus (333 clone SB5) and vhs rescue virus (333d41(R)) after infection of MEFs at high moi, but at low moi, 333d41 replication was severely attenuated, recapitulating the attenuated phenotype of vhs-deficient HSV-2 in vivo. Replication of 333d41 at low moi was restored to levels of wild-type virus in MEFs lacking the IFNalphabeta receptor or when IFNalphabeta was neutralized, thus establishing the IFNalphabeta response as the sole mechanism attenuating vhs-deficient HSV-2 replication in MEFs. MEFs infected with 333d41 produced >50-fold more IFNalphabeta than cells infected with 333 and 333d41(R). Pretreatment of MEFs with type I IFN inhibited replication of 333d41 more than 333 and 333d41(R), indicating that vhs also interferes with activation of the IFNalphabeta-induced antiviral response. We therefore examined vhs interference with PKR and RNase L, two key mediators of the IFNalphabeta response. 333d41 replication was restored to wild-type levels after low moi infection of PKR(-/-) and RNase L(-/-) MEFs, and was not inhibited in PKR(-/-) MEFs pretreated with IFNalpha. Together, these observations indicate that HSV-2 vhs is a broad and potent countermeasure to the IFN-mediated antiviral response in IFN-naïve and -sensitized MEFs.

Animals↗
PubMedDate not supplied

[Interrelationships between the interfering capacity of an "incomplete" virus and its infectivity].

A comparative analysis of UV inactivation curves of the interfering activity of "incomplete" influenza virus and infectivity showed certain differences in the structures responsible for these functions. All the data exclude the role of virus protein and virus-induced interferon of "incomplete" influenza virus and suggest that RNA is responsible for this interference. The size of the "target" of the "incomplete" virus interfering capacity calculated on the basis of sensitivity to UV-light is approximately 40 times as small as that of the "target" responsible for infectivity. The analogous pattern of UV inactivation in the standard influenza virus and the so-called Magnus virus suggests that in the latter the infectivity is due to the presence of complete virions in the preparation.

Animals↗
PubMed1972

Transient inhibition of polyoma virus synthesis by sendai virus (parainfluenza I). II. Mechanism of the interference by inactivated virus.

The mechanism of the transient inhibition of polyoma virus synthesis by betapropiolactone-inactivated Sendai virus was studied. Polyoma virus early functions did not appear to be affected, although deoxyribonucleic acid (DNA) and structural protein synthesis were inhibited 60 and 35% respectively. The inhibition of macromolecular synthesis was not sufficient to account for the 90% inhibition of infectious progeny formation. Encapsidation of polyoma DNA into mature virions appears to be completely inhibited after superinfection by beta-propiolactone-inactivated Sendai virus. Ultraviolet irradiation of live or beta-propiolactone-inactivated Sendai virus preparations abolishes the interfering capacity, indicating that a functional Sendai virus ribonucleic acid molecule is the interfering component.

Animals↗
PubMed1983

Homologous interference by avian infectious bronchitis virus, inhibition of plaque formation of the Beaudette-42 strain by mixed inoculation with the KH strain.

Inhibition of plaque formation by avian infectious bronchitis virus (IBV) Beaudette-42 (Be-42) strain occurred in chick kidney cells with the inoculation of the same cell culture with the KH strain of IBV. For the complete inhibition of approximately 10(2) plaque-forming units (pfu) of the Be-42 strain, at least 10(5) pfu of the KH strain was required. The KH strain would inhibit plaque formation by the Be-42 strain if used as long as six hours after the inoculation of the Be-42 strain. The inactivated KH strain did not inhibit the plaque formation of the Be-42 strain.

Animals↗
PubMedDate not supplied

Identification of infectious bronchitis virus by interference with the B-1 isolant of Newcastle disease virus. Waxing and waning of interference.

The Massachusetts and the Connecticut types of infectious bronchitis virus (IBV) were identified by interference in embryonating chicken eggs (ECE) with the production of hemagglutinin by the B-1 isolant of Newcastle disease virus (NDV). This interference test appears to be specific because the above interference was eliminated by adding type-specific anti-IBV serum to the IBV-NDV system; however, interference was not detectable when fowlpox virus (FPV) and infectious laryngotracheitis virus (LTV) were substituted for IBV. Specificity of the interference test was dependent upon a system involving IBV, NDV, FPV, and LTV. The test can be done in 3 days and requires minimum laboratory facilities. Most of the experiments were done with the Massachusetts type of IBV. Only a few were with the Connecticut type. The interfering action of the above two types of IBV over the B-1 isolant of NDV waxed between the 24th and 54th hr after inoculation of NDV; it was waning at the 54th-60th hr postinoculation and was undetectable by the 66th-72nd hr.

Animals↗
PubMed1979

The physico-chemical characterization of bovine ephemeral fever virus as a member of the family Rhabdoviridae.

This study of the physico-chemical properties of bovine ephemeral fever virus was initiated to establish whether or not it should be classified as a rhabdovirus. In contrast to the regular bullet-shaped morphology of some rhabdoviruses the virus particles are often cone-shaped or slight variants from bullet-shaped. The virion contains single-stranded RNA sedimenting at 42S and six proteins with mol. wt. of 164, 101, 64, 53, 43 and 29 x 10(3). The protein P101 is located on the surface of the virus and is glycosylated. It is removed by treatment of the virus particles with trypsin. Protein P64, the nucleoprotein, was found to be a phosphoprotein, like the N protein of rabies virus, whereas in vesicular stomatitis virus NS is the phosphorylated protein. Virus harvests contain defective-interfering particles. The particles are short cone-shaped forms about one-third the length of the infectious virion and similar in morphology to defective-interfering particles of vesicular stomatitis virus. These particles interfere with the replication of bovine ephemeral fever virus but not with the Indiana serotype of vesicular stomatitis virus. They contain single-stranded RNA sedimenting at 18 to 20S. The particles appear to have a protein composition identical to that found in the virus particle. The physico-chemical properties of bovine ephemeral fever virus justify its inclusion in the family Rhabdoviridae. The protein composition differs in detail from that found for vesicular stomatitis and rabies viruses, but is similar to that found for Obodhiang and kotonkan, two rabies serogroup viruses isolated from insects in Africa.

Animals↗
PubMed1977

Mechanism of restriction of ecotropic and xenotropic murine leukemia viruses and formation of pseudotypes between the two viruses.

Ecotropic and xenotropic murine leukemia viruses (MuLV's) constitute separate interference groups; within each group there is cross-interference, but between the groups there is no detectable interference. Interference is manifest against pseudotypes in which the vesicular stomatitis virus genome is contained within the coat of one of the murine leukemia viruses. The pseudotypes display the cell specificity of the leukemia viruses: pseudotypes with an ecotropic MuLV coat infect mouse cells but not rabbit or mink cells; pseudotypes with a xenotropic MuLV coat infect rabbit or mink cells well but mouse cells very poorly. Efficient pseudotype formation also occurs between the two MuLV classes, and both the interference patterns and the cell specificity of these pseudotypes are entirely determined by their envelope. Using these pseudotypes, ecotropic MuLV infection could be established in xenogeneic cells, and the resulting progeny could be scored by using a conventional XC cell assay. Also, xenotropic MuLV infection could be established in a mouse cell, showing that no absolute intracellular barrier against xenotropic virus growth exists in murine cells. The major barriers against both xenotropic and ecotropic MuLV therefore are cell surface barriers. Xenogeneic cells probably lack receptors for ecotropic MuLV, but murine cells may either lack receptors for xenotropic MuLV or have receptors that are blocked by endogenous expression of the glycoprotein of endogenous xenotropic MuLV.

Cell Line↗
PubMed1988

Interference between influenza A viruses with a cleavable and a noncleavable hemagglutinin; pH-stability after mixed infection.

The infectivity of influenza A viruses like fowl plague virus (FPV) with a cleaved hemagglutinin (HA) is highly sensitive to treatment at pH 5, while strains like PR 8 or virus N with a noncleaved HA survive under this condition. After double infection of chick embryo cells with FPV and PR 8 or virus N, the yield of virus with the HA gene of FPV is greatly reduced. However, it can now survive treatment at pH 5, and the surviving FPV particles form plaques only in the presence of trypsin, indicating that they were coated by the HA of PR 8 or virus N, depending on the coinfecting virus. The results are discussed with respect to the build-up and maintenance of a large reservoir of nonpathogenic influenza A viruses with noncleavable HA in water fowl.

Animals↗
PubMed1992

Adeno-associated virus type 2-mediated inhibition of human immunodeficiency virus type 1 (HIV-1) replication: involvement of p78rep/p68rep and the HIV-1 long terminal repeat.

Microinjection of wild-type adeno-associated virus type 2 (AAV-2) DNA and infectious human immunodeficiency virus type 1 (HIV-1) proviral DNA into the nuclei of human epithelioid SW480 cells leads to specific inhibition of HIV-1 replication. Mutational analysis of the AAV genome showed that this negative interference can be assigned to a functional AAV-2 rep gene. Moreover, the p78rep/p68rep proteins are sufficient for the anti-HIV-1 effects. The rep gene also inhibits the expression of a chloramphenicol acetyl-transferase (CAT) gene driven by the U3/R portion of the HIV-1 long terminal repeat (LTR) in the absence of tat expression. This suggests that the U3/R portion of HIV-1 contains elements responsible for the AAV-2 rep-mediated inhibition of HIV-1 LTR-driven CAT gene expression and, probably, also of HIV-1 replication. The results add support for the general significance of AAV-2 and specifically the rep gene as tools for down-regulating heterologous gene expression.

Base Sequence↗
PubMed1984

Defective interfering Semliki Forest virus populations are biologically and physically heterogeneous.

This study demonstrates that populations of defective interfering Semliki Forest virus (DI SEV) are heterogeneous particularly in respect of their interference properties. Interference was quantified by two assays, one measuring inhibition of the yield of infectious progeny virus, and the other measuring reduction in virus-directed RNA synthesis; for 11 different DI SFV preparations a ratio of the two interference titres was calculated. These ratios varied up to 46-fold indicating that each DI virus preparation contained an interference activity that varied independently of the other. However, sister stocks made from the same parental inoculum had similar properties. The effects of different DI virus preparations on other parameters (virus polypeptide synthesis, yield of DI virus and yield of infectious virus) were investigated using inocula with interference titres standardized by either assay. Co-inoculation of L929 cells with 50 p.f.u. SFV showed that these parameters varied independently of each other and of the DI virus inoculum. There was no correlation with the number of undiluted passages each DI stock had received. Direct evidence of physical heterogeneity was demonstrated by metrizamide density gradient centrifugation. Although infecting virus sedimented as a narrow band, DI SFV was distributed over a broad region of the gradient. Its position on the gradient indicated that DI SFV has a higher nucleic acid: protein ratio than standard virus. DI virus progeny obtained by using fractions of the gradient as inoculum were as heterogeneous as the unfractionated parent, confirming that DI viruses retain heterogeneity on passage.

Animals↗
PubMed1974

Properties of Corynebacterium acnes bacteriophage and description of an interference phenomenon.

Nine virulent bacteriophages of the anaerobe Corynebacterium (Propionibacterium) acnes, the P-a series, are DNA phages, with long, curved nonretractile tails (130 nm) without tail plates or fibers. They have isometric heads (420 by 460 nm), and are placed in Bradley's group B-1. There is permanent plaque suppression at highest phage concentrations. After 100- to 1,000-fold dilution, plaques are evident. The latent period is 1 h and burst size 25. Cross-neutralization data of antisera for the nine phages are similar. There is an unexplained precipitous drop in plaque-forming units during the first 5 min of neutralization, after which the rate is linear for 2 h. They are sensitive to pH extremes but are partially protected even at pH 4 or 9 by storage at 4 C. They are resistant to ether and chloroform and are inactivated within 10 min at 70 C.

Antigens, Bacterial↗
PubMed1991

The genes associated with trans-dominance of the influenza A cold-adapted live virus vaccine.

Segment 7 (M) of the cold-adapted live influenza A virus vaccine plays a primary role in the ability of this virus to interfere with the replication of wild-type influenza A viruses. This conclusion is based on several lines of evidence. Single gene reassortant viruses derived by crossing influenza A/Ann Arbor/6/60 (H2N2) cold-adapted donor virus with an epidemic wild-type strain, A/Korea/1/82 (H3N2), were tested for their ability to interfere with wild-type parental virus in the Madin-Darby line of canine kidney cells and embryonated eggs. It was apparent in both hosts that the single gene reassortant carrying segment 7 (M) derived from the cold-adapted virus was dominant over wild-type virus. Additional confirmation of the role of segment 7 (M) in trans-dominance of the cold-adapted vaccine virus was derived from the analysis of reassortants produced by mixed infection by a wild-type virus and its cold-adapted reassortant vaccine strain. After three serial passages, the virus yield contained a high proportion of reassortants carrying segment 7 (M) of the cold-adapted parental strain. When used in mixed infections, these reassortants were dominant over the replication of the parental wild-type virus.

Animals↗
PubMed1993

NF kappa B upstream regulatory sequences of the HIV-1 LTR are involved in the inhibition of HIV-1 promoter activity by the NS proteins of autonomous parvoviruses H-1 and MVMp.

To investigate parvoviral interference with human immunodeficiency virus type 1 (HIV-1) in human cells that are normally susceptible to HIV-1 infection, nonstructural (NS) proteins of the parvoviruses H-1 virus and minute virus of mice were studied for their effect on the activity of the HIV-1 promoter in a variety of CD4+ cells. Transient cotransfection assays revealed a reduced HIV-1 promoter activity in the presence of parvoviral NS proteins. Stimulation of the HIV-1 promoter by phorbol 12-myristate 13-acetate (PMA) led to an increase in its sensitivity to NS-induced suppression. The inhibitory effect of NS polypeptides depended, at least in part, on the presence of the NF kappa B motifs of the HIV-1 long terminal repeat, suggesting an interaction of the parvoviral products with PMA-inducible cellular factors binding to these elements of the HIV-1 promoter.

Animals↗
PubMed1977

Heterotypic exclusion between vesicular stomatitis viruses of the New Jersey and Indiana serotypes.

Co-infection of cells with vesicular stomatitis viruses of the Indiana and New Jersey serotypes results in interference. Using specifically-labelled immunofluorescent antibodies, it was demonstrated that within any one co-infected cell, one virus serotype replicated to the relative exclusion of the other serotype. This result was further substantiated by an examination of the virus serotypes released by infectious centres co-infected with both viruses. Dominance of one serotype over the other was shown to be a function of the relative multiplicity of the two viruses. Superinfection by the second serotype at a higher multiplicity resulted in dominance by the second virus during the early period (up to 1-5 h) post-infection. After this time, the minority virus was able to overcome this dominance. Dominance of the majority virus was also abolished by u.v; inactivation. Cell protein synthesis appeared to be less affected in cells infected with both serotypes than when infection was with a single serotype.

Fluorescent Antibody Technique↗
PubMed1995

Intracellular interference of tick-borne flavivirus infection by using a single-chain antibody fragment delivered by recombinant Sindbis virus.

A single-chain antibody fragment that identifies a neutralizing epitope on the envelope protein of louping ill and some other tick-borne flaviviruses was previously expressed in soluble form from bacteria and shown to be functionally active in vitro. To see whether or not the single-chain antibody could bind and inactivate infectious virus in vivo, we have used recombinant Sindbis virus as a delivery vehicle for intracellular expression of the antibody fragment. The variable genes and interchain linker encoding the single-chain antibody were cloned into a double subgenomic Sindbis virus expression vector to generate recombinant Sindbis virus. Infection with this recombinant Sindbis virus provided high-level cytoplasmic expression of the antibody fragment in mammalian cells. We demonstrate (i) that the antibody fragment was antigen binding and (ii) that louping ill virus infectivity was significantly reduced in the presence of intracellular antibody expressed by the superinfecting recombinant Sindbis virus.

Animals↗
PubMed1979

The role of temperate bacteriophage SP beta in prophage-mediated interference in Bacillus subtilis.

Virulent bacteriophage phi 1 grows on a variety of Bacillus subtilis strains, mutants of this virus which abortively infect the transformable bacillus. B. subtilis 168, while retaining the ability to productively infect related bacteria have been found. In the present study, we demonstrate that the inability of one such variant, phi 1m, to develop normally in strain 168 is mediated by cryptic prophage SP beta. The latter is a temperate bacteriophage which is carried by B. subtilis 168 and most strains derived from this bacterium. Phi 1 m infection of SP beta lysogens begins with apparently normal adsorption, penetration, and inititaion of virus-directed syntheses. At about the 20th min of the latent period, however, there is an abrupt cessation of nucleic acid synthesis and cellular respiration, accompanied by a change in cell permeability. This course of events can be altered to a permissive infection by mutation in the mpi gene of SP beta, by mutation in the spoOA gene of the host, or by growing SP beta lysogens at high temperature. In addition, we found a second class of phi 1 mutants which abortively infect B. subtilis 168 derivatives even in the absence of the SP beta prophage.

Bacillus subtilis↗
PubMed2003

RNA interference for treating cancers caused by viral infection.

The newly discovered phenomenon of RNA interference (RNAi) offers the dual facility of selective viral gene silencing coupled with ease of tailoring to meet genetic variation within the viral genome. Such promise identifies RNAi as an exciting new approach to treat viral-induced diseases, including viral-induced cancers (e.g. cervical carcinoma, hepatocellular carcinomas and haematopoietic and lymphoid malignancies). Cervical cancer is the second most common cancer in women worldwide and is caused by human papilloma virus (HPV). Silencing of HPV gene expression by RNAi induces apoptosis of cervical carcinoma cells in culture, and the effect is apparent within 3 days. The RNAi process is triggered by double-stranded RNA (dsRNA), and a single dose is sufficient to maintain RNAi for several days in vitro (cell culture) and in vivo (experimental animal models). Thus, the stage is set for the development of novel antiviral and anticancer therapies based upon selective gene silencing by RNA interference.

Animals↗