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At least 199 records · Page 11Linked to original sources
PubMed1993

Expression of the HN, F, NP and M proteins of Sendai virus by recombinant vaccinia viruses and their contribution to protective immunity against Sendai virus infections in mice.

Recombinant vaccinia viruses (RVVs) expressing each of the haemagglutinin-neuraminidase (HN), fusion (F), nucleocapsid (NP) and matrix (M) proteins of Sendai virus were constructed to investigate their capacities to induce protective immunity against Sendai virus infections. The proteins expressed in cultured cells appeared to be authentic with respect to their antigenicity, electrophoretic mobility, surface expression of the HN and F proteins and, in the case of the HN protein, biological activities. Mice inoculated intranasally with these RVVs developed serum antibodies to the respective Sendai virus proteins, suggesting their in vivo expression. In mice immunized with RVV carrying either the HN or the F gene, growth of the challenging Sendai virus was almost completely suppressed in the lung, indicating their capacities to induce effective protective immunity against Sendai virus infections. In contrast, in mice immunized with RVV carrying the NP or M gene, the challenging virus propagated as well as in the control mice, but the virus titres were significantly lower at the late stage of infection than those in the control mice, suggesting that they can also induce protective immunity especially at the late stage of the challenge infection.

Animals↗
PubMed1993

Influenza virus naked RNA can be expressed upon transfection into cells co-expressing the three subunits of the polymerase and the nucleoprotein from simian virus 40 recombinant viruses.

The functionality of the influenza virus polymerase subunits and the nucleoprotein expressed from simian virus 40 (SV40) recombinants has been tested by their ability to direct the in vivo expression of influenza virus-like RNAs. These RNAs, which contained either the chloramphenicol acetyltransferase (CAT) or haemagglutinin (HA) genes, were synthesized and reconstituted in vitro into viral ribonucleoproteins with a polymerase/nucleoprotein mixture purified from influenza virus-infected cells. Only the coinfection with SV40 recombinant viruses expressing the three polymerase subunits and the nucleoprotein allowed the expression of the transfecting CAT or HA RNAs, confirming that this set of viral genes is the minimal requirement for viral gene expression. Unexpectedly, transfection of the corresponding naked RNAs into SV40 recombinant-infected cells was as effective in directing the synthesis of CAT or HA proteins as the standard reconstituted ribonucleoprotein transfection. These results may be important for the genetic analysis of trans-acting factors involved in influenza virus transcription and replication and may open the way to rescuing influenza viruses in the absence of a helper virus.

Animals↗
PubMed1998

Evaluation of a candidate human immunodeficiency virus type 1 (HIV-1) vaccine in macaques: effect of vaccination with HIV-1 gp120 on subsequent challenge with heterologous simian immunodeficiency virus-HIV-1 chimeric virus.

Human immunodeficiency virus type 1 (HIV-1) envelope vaccines can now be evaluated for efficacy in macaques by challenging with chimeric viruses in which the env, tat and rev genes of simian immunodeficiency virus (SIV) have been replaced by those of HIV-1. Most experiments have so far been conducted using gp120 molecules derived from T-cell-adapted LAI or MN strains of HIV-1, which predominantly use the CXCR-4 co-receptor. These vaccines protect against infection by apathogenic chimeric virus carrying the same envelope sequences. In the experiment described here, four macaques were vaccinated with W61D gp120 derived from a low passage Dutch isolate and capable of inhibiting the binding of MIP1beta to the co-receptor CCR-5. This vaccine was potent, inducing high titres of binding and neutralizing antibodies against the homologous HIV-1 and tenfold lower titres against a heterologous challenge virus (SHIV(SF33)) in which the env, tat and rev genes of SIV had been replaced by those of a San Francisco isolate, HIV-1(SF33). Despite strong immune responses to the vaccine there was no evidence that it protected against challenge with this chimeric virus. The antigenic divergence between vaccine and challenge virus or the increased virulence of the challenge virus may be responsible for the inability of this vaccine to protect against infection by SHIV(SF33).

AIDS Vaccines↗
PubMed2006

Barley stripe mosaic virus-encoded proteins triple-gene block 2 and gammab localize to chloroplasts in virus-infected monocot and dicot plants, revealing hitherto-unknown roles in virus replication.

Replication of Barley stripe mosaic virus (BSMV), genus Hordeivirus, is thought to be associated with vesicles in proplastids and chloroplasts, but the molecular details of the process and identity of virus proteins involved in establishing the virus replication complexes are unknown. In addition, BSMV encodes a triple-gene block of movement proteins (TGBs) that putatively share functional roles with their counterparts in other hordei-, pomo- and pecluviruses, but detailed information on the intracellular locations of the individual TGBs is lacking. Here, the subcellular localizations of BSMV-encoded proteins TGB2 and gammab fused to green or red fluorescent proteins were examined in epidermal cells of Nicotiana benthamiana and barley (Hordeum vulgare 'Black Hulless'). The fusion proteins were expressed from a BSMV vector or under the control of the cauliflower mosaic virus 35S promoter. The subcellular localizations were studied by confocal laser-scanning microscopy (CLSM). CLSM studies showed that both proteins were recruited to chloroplasts in the presence of viral RNA and that virus RNA, coat protein and gammab protein were detected in plastid preparations from infected leaves. Electron microscope images of thin sections of virus-infected leaves revealed abnormal chloroplasts with cytoplasmic inclusions containing virus-like particles. In addition, cellular localizations of BSMV TGB2 suggest subtle differences in function between the hordei-like TGB2 proteins. The results indicate that TGB2 and gammab proteins play a previously unknown functional role at the site of virus replication.

Artificial Gene Fusion↗
PubMed1988

Herpes simplex viruses lacking glycoprotein D are unable to inhibit virus penetration: quantitative evidence for virus-specific cell surface receptors.

Herpes simplex virus (HSV) glycoprotein D (gD) plays an essential role in the entry of virus into cells. HSV mutants unable to express gD were constructed. The mutants can be propagated on VD60 cells, which supply the viruses with gD; however, virus particles lacking gD were produced in mutant-infected Vero cells. Virus particles with or without gD adsorbed to a large number (greater than 4 x 10(4] of sites on the cell surface; however, virions lacking gD did not enter cells. Cells pretreated with UV-inactivated virions containing gD (approximately 5 x 10(3) particles per cell) were resistant to infection with HSV type 1 (HSV-1) and HSV-2. In contrast, cells pretreated with UV-inactivated virions lacking gD could be infected with HSV-1 and HSV-2. If infectious HSV-1 was added prior to UV-inactivated virus particles containing gD, the infectious virus entered cells and replicated. Therefore, virus particles containing gD appear to block specific cell surface receptors which are very limited in number. Particles lacking gD are presumably unable to interact with these receptors, suggesting that gD is an essential receptor-binding polypeptide.

Adsorption↗
PubMed1989

Mice immunized with recombinant vaccinia virus expressing dengue 4 virus structural proteins with or without nonstructural protein NS1 are protected against fatal dengue virus encephalitis.

We have constructed vaccinia virus recombinants expressing dengue virus proteins from cloned DNA for use in experimental immunoprophylaxis. A recombinant virus containing a 4.0-kilobase DNA sequence that codes for three structural proteins, capsid (C), premembrane (pre-M), and envelope (E), and for nonstructural proteins NS1 and NS2a produced authentic pre-M, E, and NS1 in infected CV-1 cells. Mice immunized with this recombinant were protected against an intracerebral injection of 100 50% lethal doses of dengue 4 virus. A recombinant containing only genes C, pre-M, and E also induced solid resistance to challenge. Deletion of the putative C-terminal hydrophobic anchor of the E glycoprotein did not result in secretion of E from recombinant-virus-infected cells. Recombinants expressing only the E protein preceded by its own predicted N-terminal hydrophobic signal or by the signal of influenza A virus hemagglutinin or by the N-terminal 71 amino acids of the G glycoprotein of respiratory syncytial virus produced glycosylated E protein products of expected molecular sizes. These vaccinia virus recombinants also protected mice.

Animals↗
PubMed1986

LAV/HTLV-III gag gene product p24 shares antigenic determinants with equine infectious anemia virus but not with visna virus or caprine arthritis encephalitis virus.

Antigenic cross-reactivity of the human acquired immunodeficiency disease syndrome virus LAV/HTLV-III with the lentiviruses visna virus, caprine arthritis encephalitis virus (CAEV), and equine infectious anemia virus (EIAV) was determined with indirect enzyme-linked immunosorbent assays, immunoblot analysis, and virus-specific polyclonal antisera. Nonreciprocal cross-reactivity was seen between the gag gene products p24 of LAV/HTLV-III and p28 of EIAV. Reciprocal cross-reactivity was seen between the gag gene product p28 of visna virus and CAEV. No cross-reactivity was detected between visna virus (or CAEV) and EIAV (or LAV/HTLV-III). This suggests a closer relationship of LAV/HTLV-III with EIAV than with visna virus or CAEV.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Relationship of lychnis ringspot virus to barley stripe mosaic virus and poa semilatent virus.

Barley stripe mosaic virus (BSMV), poa semilatent virus (PSLV), and lychnis ringspot virus (LRSV) have previously been assigned to the hordeivirus group because of similarities in their particle morphology, physicochemical properties and serological analyses. However, the serological relationships of the three viruses have not been determined by direct comparison. The present study evaluated the relatedness of these viruses by Western and dot immunoblotting and by nucleic acid hybridizations. Serological analyses of the coat proteins separated by gel electrophoresis and of intact virus particles bound to nitrocellulose membranes revealed that BSMV and PSLV are distantly related, but that they are more closely related to each other than to LRSV. The genomic RNAs of the viruses failed to cross-hybridize in northern hybridization tests conducted at different temperatures. These comparisons showed that BSMV, PSLV and LRSV are distinct viruses with little nucleotide sequence relatedness. Thus our data provide additional support for their inclusion as separate members of the hordeivirus group.

Antigens, Viral↗
PubMed1992

Coat protein properties suggest that azuki bean mosaic virus, blackeye cowpea mosaic virus, peanut stripe virus, and three isolates from soybean are all strains of the same potyvirus.

The interrelationship of a number of potyviruses infecting legumes has been investigated by comparing molecular properties of their coat proteins. Comparison of the coat proteins by the techniques of amino acid analysis and PAGE was inadequate to distinguish strains from distinct potyviruses. However, high-performance liquid chromatographic peptide profiles of tryptic digests of coat proteins of these legume-infecting potyviruses enabled such assignments to be made. These data indicate that amino acid sequences of coat proteins of azuki bean mosaic virus, the Type and W strains of blackeye cowpea mosaic virus, three isolates (74, PM, PN) of a potyvirus obtained from soybean in Taiwan, and the Blotch and Mild Mottle strains of peanut stripe virus (PStV) may be very similar to the known sequence of PStV Stripe coat protein. In contrast, peptide profiles of coat proteins from soybean mosaic virus, clover yellow vein virus, bean yellow mosaic virus, potato virus Y, and tobacco etch virus were dissimilar to each other and to the profile of PStV Stripe, suggesting that their coat protein sequences were also quite different. Based on observations of the coat protein structure of many potyviruses, the results suggest that the potyvirus isolates with similar coat proteins are strains of the same potyvirus.

Amino Acid Sequence↗
PubMed1975

Continuous replication of Friend virus complex (spleen focus-forming virus-lymphatic leukemia-inducing virus) in mouse embryo fibroblasts. Retention of leukemogenicity and loss of immunosuppressive properties.

Exposure of NIH Swiss mouse embryo fibroblasts (MEF) to infectious Friend virus (FV) complex [containing defective spleen focus-forming virus (SFFV) and endogenous NB-tropic leukemia-inducing helper virus (LLV-F)] resulted in the productive infection of these cells by both SFFV and LLV-F. Stocks of SFFV derived after extensive growth in this Swiss MEF cell culture system are fully leukemogenic in adult mice for the induction of erythroleukemia and spleen foci. In addition, in vitro-derived LLV-F, when isolated free of SFFV, is fully leukemogenic for the induction of lymphatic leukemia when inoculated into susceptible newborn BALB/c mice. The host range of in vitro-derived FV complex (i.e., FV-TC) for focus formation in vivo is NB-tropic. Unlike in vivo-derived FV complex, FV-TC does not suppress the responsiveness of murine thymocytes to concanavalin A (Con A) in vitro. Rather, FV-TC acts as a mitogen to nonspecifically stimulate the proliferation of BALB/c thymocytes. The mitogenicity of in vitro-derived FV complex is directly associated with the presence of type-C virus particles, is a heat-labile and UV-sensitive property of the virus, and may be primarily due to LLV since equivalent amounts of LLV with or without SFFV present are equally mitogenic. One in vivo passage of FV-TC resulted in the total loss of this mitogenic property with the reappearance of full immunosuppressive properties. This result demonstrates a clear association between in vivo growth of FV and its ability to suppress mouse thymocytes, and suggests that FV complex (SFFV-LLV) is not inherently immunosuppressive for these cells. While the mechanism of this interconversion between immunostimulatory and fully suppressive virus is unknown, both virus markers appear to be dependent upon the presence of infectious FV.

Animals↗
PubMed1984

Variation in homotypic and heterotypic interference by defective interfering viruses derived from different strains of Semliki Forest virus and from Sindbis virus.

There was strong interference between various virulent and avirulent strains of Semliki Forest virus (SFV) and their respective defective interfering (DI) viruses but in other combinations interference was variable: it could be equally strong, weak or could not be demonstrated. On passage, this spectrum of interfering activity changed, some combinations showing greater interference than before and others less. Heterotypic interference between DI SFV, DI Sindbis virus and standard viruses was clearly demonstrated although this was strongest between DI SFV preparations and Sindbis standard virus than in the reciprocal combinations. Variation in interference between DI SFVs and different SFV strains was similar in magnitude to that between DI SFVs and Sindbis virus, suggesting that a similar DI RNA sequence is recognized by both viruses.

Animals↗
PubMed1990

The malignant histiocytosis sarcoma virus, a recombinant of Harvey murine sarcoma virus and Friend mink cell focus-forming virus, has acquired myeloid transformation specificity by alterations in the long terminal repeat.

The malignant histiocytosis sarcoma virus (MHSV), in contrast to other viruses with the ras oncogene, induces acute histiocytosis in newborn and adult mice. Molecular structure and function studies were initiated to determine the basis of its unique macrophage-transforming potential. Characterization of the genomic structure showed that the virus evolved by recombination of the Harvey murine sarcoma virus (Ha-MuSV) and a virus of the Friend-mink cell focus-forming virus family. Structural analysis of MHSV showed two regions of the genome that are basically different from the Ha-MuSV: (i) the ras gene, which is altered by a point mutation in codon 181 leading to a Cys----Ser substitution of the p21 protein, and (ii) the U3 region of the long terminal repeat, which is largely derived from F-MCFV and contains a deletion of one direct repeat as well as a duplication of an altered enhancer-like region. Biological studies of Ha-MuSV, MHSV, and recombinants between the two viruses show that the U3 region of the MHSV long terminal repeat is essential for the malignancy and specificity of the disease. A contributing role of the ras point mutation in determining macrophage specificity, however, cannot be excluded.

Amino Acid Sequence↗
PubMed1988

Suramin inhibits in vitro infection by duck hepatitis B virus, Rous sarcoma virus, and hepatitis delta virus.

Suramin blocked in vitro infection by duck hepatitis B virus, a hepadnavirus, and Rous sarcoma virus, a retrovirus. Although suramin was able to inhibit the virus-encoded reverse transcriptase activities of these two viruses, this inhibition did not appear to account for the anti-viral effect of the drug. In particular, suramin was unable to block synthesis within cells of full-length viral DNAs when added subsequent to infection. The results are consistent with the hypothesis that suramin acted by blocking virus uptake or uncoating. As further support of this hypothesis, we found that suramin also blocked infection by hepatitis delta virus, an RNA virus that is not known to employ reverse transcriptase during the initiation of infection.

Animals↗
PubMed1995

GP mRNA of Ebola virus is edited by the Ebola virus polymerase and by T7 and vaccinia virus polymerases.

The glycoprotein gene of Ebola virus contains a translational stop codon in the middle, thus preventing synthesis of full-length glycoprotein. Twenty percent of the mRNA isolated from Ebola virus-infected cells was shown to be edited, containing one additional nontemplate A in a stretch of seven consecutive A residues. Only the edited mRNA species encoded full-length glycoprotein, whereas the exact copies of the viral template coded for a smaller secreted glycoprotein. Expression of the glycoprotein by an in vitro transcription/translation system, by the vaccinia virus/T7 polymerase system, and by recombinant vaccinia virus revealed that full-length glycoprotein was synthesized not only when the edited glycoprotein gene (8A's) was used as a template for T7 and vaccinia virus polymerases, but also when the nonedited (genomic) glycoprotein gene was used. Analysis of mRNA produced by T7 and vaccinia virus polymerase from the 7A's construct revealed that 1-5% contained alterations at the same site that was also edited by the Ebola virus polymerase. Our data indicate that the editing site in the Ebola virus glycoprotein gene is recognized not only by Ebola virus polymerase but also by DNA-dependent RNA polymerases of different origin.

Amino Acid Sequence↗
PubMed1995

Search for optimal parent for recombinant vaccinia virus vaccines. Study of three vaccinia virus vaccinal strains and several virus lines derived from them.

Three vaccinia virus strains (Praha, DD--a DRYVAX Wyeth vaccine-derived virus-and LIVP) were examined for growth in various cell cultures and for virulence and immunogenicity in mice. The viruses did not differ by their growth rates in monkey kidney cells (CV-1), human diploid cells (LEP), rat TK cells (RAT 2) or primary dog kidney cells. The immunogenicity of Praha and DD viruses was similar, the virus LIVP was somewhat more immunogenic. In terms of virulence in 3-day-old mice, the DD virus was the most attenuated. Single-plaque progenies were derived from the original smallpox vaccines VARIE Sevac (strain Praha) and DRYVAX Wyeth and tested for the above markers and DNA restriction patterns. The results obtained demonstrated biological and molecular heterogeneity of the original virus populations. Close linkage was observed between immunogenic activity and virulence in 3-day but not in 3-week mice. The results indicate that smallpox vaccine preparations may serve as an abundant source of virus mutants.

3T3 Cells↗
PubMed2001

A rapid assay for evaluation of antiviral activity against coxsackie virus B3, influenza virus A, and herpes simplex virus type 1.

In order to identify new potential antiviral drugs, small amounts of extracts or compounds have to be examined for cytotoxicity and antiviral activity in primary screening using a rapid, easy, inexpensive, and highly standardised test system. In this study, high-throughput cytopathic effect (CPE) inhibitory assays were established for coxsackie virus B3 on HeLa Ohio cells, influenza virus A on Madin-Darby canine kidney cells, and herpes simplex virus type 1 (HSV-1) on green monkey kidney cells that meet these requirements. The cytotoxic and the antiviral effects were quantified using a crystal violet uptake assay allowing automated handling of large numbers of candidate agents. To ensure comparable results with plaque reduction assays, the 50 and 90% plaque inhibitory concentrations of guanidine, amantadine, and phosphonoformic acid were used to standardise the anti-coxsackie virus B3, anti-influenza virus A, and anti-HSV-1 tests, respectively. The strong correlation between the antiviral activity determined by CPE-inhibitory assays and plaque reduction assay was further proved for other antivirals. In summary, low amounts of large numbers of compounds may be tested inexpensively and standardised within 24 h (coxsackie virus B3 and influenza virus A) or 48 h (herpes simplex virus type 1) post-infection using CPE inhibitory assays.

Amantadine↗
PubMedDate not supplied

Immunological relationships between rabies virus and rabies-related viruses studied with monoclonal antibodies to Mokola virus.

Specific monoclonal antibodies (mAb) were prepared against a rabies-related lyssavirus, Mokola virus. A strain isolated in the Central African Republic, Mok-3, was used as immunogen. After 3 fusions more than 90 hybridoma cultures secreting mAb were identified. According to their different patterns of reactivity against rabies and rabies-related viruses, 61 ascites fluids were obtained. The antibody class was IgM for 2 of them and IgG for 59. They were specific for one of the 4 major viral proteins, as determined by immunofluorescence, neutralization and immunoblotting tests. Their patterns of reactivity were determined against 6 different strains of rabies-related viruses: Lagos-bat virus from Nigeria (Lag-1) and the Central African Republic (Lag-2), Duvenhage virus from the Republic of South Africa (Duv-1) and Federal Republic of Germany (Duv-3), Mokola virus from Nigeria (Mok-1) and Cameroon (Mok-2) and a fixed strain of rabies virus, the challenge virus strain (CVS). According to their reactivities with these strains and the pattern of fluorescence, the mAb were classified into 11 different groups with intracytoplasmic fluorescence and 7 groups with cell surface fluorescence. A differential diagnosis of these lyssaviruses is possible in tissue culture using some of these mAb.

Animals↗
PubMed2000

Virus-induced immune dysregulation as a triggering factor for the development of drug rashes and autoimmune diseases: with emphasis on EB virus, human herpesvirus 6 and hepatitis C virus.

There are a considerable amount of empirical and theoretic medical literature regarding the possible role of viruses in the development of drug rashes and autoimmune diseases: under these conditions, interactions of viruses with the immune system would serve as an accelerating factor of disease pathogenesis. Recent reports have provided evidence to indicate that immune responses against infections with Epstein Barr (EB) virus and human herpesvirus 6 (HHV-6), which are lymphotropic members of the herpes virus group, not only aid the direct elimination of the virus but also contribute to a favorable milieu for the initiation or acceleration of drug rashes. Viruses that can persist for the lifetime of the host despite strong immune responses against them, such as EB virus and hepatitis C virus (HCV), would be also relevant to the pathogenesis of autoimmune diseases. HCV has been reportedly associated with a wide variety of dermatoses that, in common, show histologically the lichenoid tissue reaction. Although porokeratosis that manifests lichenoid histopathological features had long been regarded as being associated with immunosuppression, we found that HCV could act as trigger for the development of porokeratosis during states of immunosuppression. Thus, the main purpose of this review is to describe recent work on the etiology of drug rashes and autoimmune disease with special reference to viral infections.

Autoimmune Diseases↗