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Volume 79,
Issue 4,
1998
Volume 79, Issue 4, 1998
- Articles
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Human recombinant Puumala virus antibodies: cross-reaction with other hantaviruses and use in diagnostics.
A panel of seven human monoclonal Fabs against Puumala virus (PUU) nucleocapsid protein (N) was obtained by panning an antibody phage-display library prepared from the spleen of a PUU-immune individual. Three antibodies reacted in immuno-blotting and cross-reacted strongly with Tula and Sin Nombre virus recombinant N proteins. These antibodies mapped to the amino terminus of the N protein. One PUU glycoprotein 2 (G2)-specific Fab obtained against a novel epitope (G2c) cross-reacted with Khabarovsk virus but not with the other hantavirus serotypes. An N protein-specific Fab was successfully used as capture antibody to detect PUU-specific serum IgG and IgM antibodies in an enzyme immunoassay. The result demonstrates the usefulness of recombinant human Fabs as potential diagnostic tools.
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Pseudotype formation with La Crosse virus glycoproteins.
More LessPseudotype formation is a powerful tool for analysing mechanisms of virus neutralization and entry, since it allows for analysis of glycoprotein properties without the necessity for preparing recombinant genomes. Using recombinant vaccinia viruses, we prepared pseudotypes of La Crosse virus with recombinant glycoproteins cloned from the monoclonal antibody (MAb)-resistant variant V31. The resulting pseudotypes became partially resistant to MAb 807–31. Furthermore, when the V31 glycoproteins were incorporated into a second MAb-resistant variant (V33), the pseudotyped virus became sensitive to neutralization by the MAb (807–33) originally used in its selection. These results suggest a simple technique for the incorporation of glycoprotein mutations into bunya-viruses, allowing analysis of mechanisms of neutralization and other virus entry functions.
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Nucleotides in the panhandle structure of the influenza B virus virion RNA are involved in the specificity between influenza A and B viruses.
More LessInfluenza A and B viruses share common sequences and potentially similar panhandle structures in the terminal noncoding regions of virion RNA (vRNA). Interesting differences exist, however, in the number of conserved nucleotides at the 5′ and 3′ ends of the vRNAs, in base pairs constituting the panhandle duplex, and the length of uridine stretch (U stretch) juxtaposed to the RNA duplex. To analyse the contribution of these signals to the specificity between the two viruses, a transient ribonucleo-protein transfection method was used for the expression of the chloramphenicol acetyltransferase (CAT) reporter gene flanked by the noncoding nucleotides derived from influenza B vRNA. While the base pairing in the RNA duplex was primarily important for template activity, mismatch mutations G11 × G12′ and C12 × A13′ in the terminal RNA duplex region were utilized by influenza B virus, whereas these mutations were detrimental for influenza A virus. Different activity profiles were observed in the length preference of the RNA duplexes: maximum template activity was observed with 11 base pairs for influenza B virus, and 8 base pairs for influenza A virus. When the mutants with various lengths of U stretch were tested, highest CAT activities were observed with 5 to 7 uridine residues in influenza A virus, whereas in influenza B virus the activity was drastically decreased with 7 uridine residues. We suggest that the specific interaction of influenza virus RNA polymerase with these noncoding cis-acting signals in transcription of the RNA genome, along with unique coding strategies adopted by influenza B virus, has contributed to the divergence of these two closely related viruses.
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Sendai virus-like particles devoid of haemagglutinin-neuraminidase protein infect cells via the human asialoglycoprotein receptor.
More LessVirus-like particles with genetically defined envelope proteins were generated from cDNA in order to examine the requirement of Sendai virus haemagglutinin-neuraminidase (HN) protein for particle formation, and the role of fusion protein (F) in receptor binding and membrane fusion. Characterization of particles devoid of HN protein showed that particle formation was unimpaired by the absence of HN protein, indicating that HN protein is dispensable for virus assembly and budding. Infection studies further demonstrated that virus adsorption and penetration can be mediated solely by the F protein when the human asialoglycoprotein receptor is present at the surface of host cells.
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Immunological basis for protection in a murine model of tick-borne encephalitis by a recombinant adenovirus carrying the gene encoding the NS1 non-structural protein.
The humoral immune response to flaviviruses is mainly directed to the major envelope protein, E, and a glycosylated non-structural protein, NS1. Cell-mediated immune responses, however, appear to be directed mainly against non-structural proteins. Experiments described here show that a defective recombinant adenovirus (Rad51) containing the gene encoding the NS1 protein of tick-borne encephalitis virus can induce a strong protective immune response against several pathogenic tick-borne flaviviruses in an experimental animal model, and can enhance the efficacy of conventional vaccine preparations. A protective immune response against a lethal virus challenge can also be induced by the passive transfer of antibodies, B cells or T cells from animals vaccinated with Rad51. Raised levels of non-neutralizing antibodies and cytokines associated with a T helper cell-type 1 immune response are also observed. These data demonstrate the importance of non-structural viral proteins in the protective immune response against flaviviruses and support the use of non-structural viral proteins as vaccine components.
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Definition of the region on NS3 which contains multiple epitopes recognized by dengue virus serotype-cross-reactive and flavivirus-cross-reactive, HLA-DPw2-restricted CD4+ T cell clones.
More LessThe epitopes recognized by sixCD4 CD8 cytotoxic T lymphocyte (CTL) clones established from a dengue-3 virus-immune donor were defined. (i) Three CTL clones, JK10, JK34 and JK39, were crossreactive for dengue virus types 1–4. (ii) One clone, JK28, was cross-reactive for dengue virus types 1–4 and West Nile virus. (iii) Two clones, JK26 and JK49, were cross-reactive for dengue virus types 1–4, West Nile virus and yellow fever virus. The clones, except for JK49, recognized the same epitope on NS3 in an HLA-DPw2-restricted fashion. The smallest synthetic peptide recognized by the five CTL clones was a 10 aa peptide which comprises aa 255–264 on dengue virus NS3. JK49 recognized the overlapping epitope which comprises aa 257–266 in an HLA-DPw2-restricted fashion. Analysis of T cell receptor (TCR) usage by these T cell clones revealed that (i) JK10 and JK34 use Vα11,and JK34 and JK28 use Vβ23, and (ii) the amino acid sequences of the V(D)J junctional region of the TCR were different among these five CTL clones. There were, however, single amino acid conservations among TCRs of some of these T cell clones. These results indicate that the region on NS3 which comprises aa 255–266 contains multiple epitopes recognized by dengue serotype-cross-reactive and flavivirus-cross-reactive CD4 CTL in an HLA-DPw2-restricted fashion and that a single epitope can be recognized by T cells which have heterogeneous virus specificities.
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Low level or absent in vivo replication of hepatitis C virus and hepatitis G virus/GB virus C in peripheral blood mononuclear cells.
More LessTo investigate which subsets of peripheral blood mononuclear cells (PBMCs) are susceptible to infection with hepatitis C virus (HCV) and hepatitis G virus (HGV) or GB virus C (GBV-C), a PCR-based assay using tagged primers in the core region (HCV) and NS3 region (HGV/GBV-C) for the specific detection of negative strand (replicating) viral RNA sequences was developed. In liver biopsy samples both positive and negative strands of HCV RNA were detected, at levels ranging from 3 to 11 × 106 RNA copies per 106 cells and 3·7–4·2 × 103 copies per 106 cells respectively, while lower frequencies of positive strands of GBV-C/HGV RNA were detected (from 13 biopsies, the highest frequency was 7·3 × 103 per 106 cells). In no samples were negative RNA strands detected. To investigate extra-hepatic replication of HCV and GBV-C/HGV, CD4 , CD8 and B lymphocytes, monocytes and putative dendritic cell populations were separated from PBMCs from ten study subjects. Detection of positive strand HCV RNA was largely confined to B lymphocytes (at levels of up to 5 × 103 copies per 106 cells), while detection of negative strands was confined to a single subset (dendritic cells) of one of the study individuals. Similarly, GBV-C/HGV was detected at low levels in only twelve of twenty PBMC samples, while negative strands were uniformly absent. The low levels of HCV and GBV-C/HGV RNA in PBMCs suggest that these cells are at most a minor reservoir for virus replication. The absence of detectable replication of GBV-C/HGV suggests that the actual site of GBV-C/HGV replication remains to be discovered.
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A common RNA motif in the 3′ end of the genomes of astroviruses, avian infectious bronchitis virus and an equine rhinovirus.
More LessIn the 3′ non-coding region of the genomes of infectious bronchitis virus, an avian coronavirus and the picornavirus equine rhinovirus serotype 2, there is a motif with remarkable similarity, both in sequence and folding, to the second RNA stem-loop from the 3′ end of the genomes of human astro-viruses. This motif was also found in astroviruses of sheep, pig and turkey, suggesting that it is a common feature of all astroviruses. The conserved nature of the motif indicates that there has been strong selection for its preservation. There is significant homology between the regions flanking this motif in infectious bronchitis virus and a continuous RNA sequence at the same distance from the 3′ poly(A) tail in some related mammalian coronaviruses. These observations suggest that the presence of the motif in these three viral families is the result of at least two separate RNA recombination events.
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Induction of protective immunity in chickens vaccinated with infectious bronchitis virus S1 glycoprotein expressed by a recombinant baculovirus.
A recombinant baculovirus containing the S1 glycoprotein gene of the virulent nephropathogenic KM91 strain of infectious bronchitis virus (IBV) was constructed in order to investigate protective immunity in vaccinated chickens. Results from the protection test were evaluated by re-isolation of virus from the kidneys and tracheas of vaccinated chickens after challenge with strain KM91. After three immunizations, the recombinant S1 (rS1) glycoprotein induced 50% protection of the kidney, whilst inactivated KM91 induced 88% and 50% protection of the kidney and trachea, respectively. In chickens primed with the attenuated H120 vaccine strain, which is heterologous to KM91, the rS1 glycoprotein induced 83% protection of the kidney after two immunizations. Haemagglutination-inhi-bition titres were also increased in chickens immunized with the rS1 glycoprotein after three immunizations, and significantly higher titres were detected after challenge. These data indicate that the expressed rS1 glycoprotein alone can induce a protective immune response as well as an antibody response.
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Identification of mutations in the rotavirus protein VP4 that alter sialic-acid-dependent infection.
To explore further the role of VP4 as the rotavirus cell attachment protein, VP7 monoreassortants derived from the sialic-acid-dependent simian strain RRV and from the sialic-acid-independent human strains D, DS-1 and ST-3 were tested for susceptibility of infectivity of neuraminidase-treated MA-104 cells. Infectivity of RRV × D VP7 and RRV × ST-3 VP7 monoreassortants decreased when sialic acid was removed from the cell surface. However, of three separate RRV × DS-1 VP7 monoreassortants tested, only one was sialic-acid-dependent. Sequence analysis showed that both sialic-acid-independent strains contained a single amino acid change, Lys to Arg, at position 187. In addition, sialic-acid-independent infectivity was seen in one of 14 RRV VP4 neutralization escape mutants tested, and this strain was found to have a Gly to Glu change at amino acid position 150. These results indicate that positions 150 and 187 of VP4 play an important role in early rotavirus-cell interactions.
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Antimicrobial peptides melittin and cecropin inhibit replication of human immunodeficiency virus 1 by suppressing viral gene expression
Antimicrobial peptides are effectors of innate immunity, providing their hosts with rapid non-specific defence against parasitic invaders. In this report, the effects are assessed of two well-characterized antimicrobial amphipathic peptides (melittin and cecropin) on human immunodeficiency virus 1 (HIV-1) replication and gene expression in acutely infected cells at subtoxic concentrations. Production of infectious, cell-free virus was inhibited in a dose-dependent manner, with ID50 values in the range 0·9–1·5 μM for melittin and 2–3 μM for cecropin. Analysis of the effect of melittin on cell-associated virus production revealed decreased levels of Gag antigen and HIV-1 mRNAs. Transient transfection assays with HIV long terminal repeat (LTR)-driven reporter gene plasmids indicated that melittin has a direct suppressive effect on activity of the HIV LTR. HIV LTR activity was also reduced in human cells stably transfected with retroviral expression plasmids for the melittin or cecropin gene. It is concluded that antimicrobial peptides such as melittin and cecropin are capable of inhibiting cell-associated production of HIV-1 by suppressing HIV-1 gene expression.
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Replication of human immunodeficiency virus type 1 (HIV-1), simian immunodeficiency virus strain mac (SIVmac) and chimeric HIV-1/SIVmac viruses having env genes derived from macrophage-tropic viruses: an indication of different mechanisms of macrophage-tropism in human and monkey cells.
To investigate the transferability of macrophage (Mϕ)-tropism among primate lentiviruses, we constructed recombinants of human immunodeficiency virus type 1 (HIV-1), simian immunodeficiency virus strain mac (SIVmac) and chimeric HIV-1/SIVmac (SHIV) having env region Mϕ-tropic determinants. A recombinant HIV-1 having env partially derived from a Mϕ-tropic HIV-1 strain (JR-FL) replicated in human macrophages but not in monkey macrophages. Conversely, a recombinant SIVmac having env from a Mϕ-tropic strain (SIVmac316) replicated in monkey macrophages but not in human macrophages. A new SHIV (designated NM-3rN/JRFL) carrying the LTR and gag, pol, vif, vpx and nef of SIVmac and vpr, tat, rev, vpu and env of HIV-1 with env partially replaced by that of JR-FL was replication-competent in human macrophages but not in monkey macrophages. These results suggest that the Mϕ-tropic determinant is specific to each host species and that the mechanism of Mϕ-tropism is different between HIV and SIV.
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Endotoxin treatment of equine infectious anaemia virus-infected horse macrophage cultures decreases production of infectious virus.
More LessLentiviruses replicate in cells of the immune system, and activation of immune cells has been shown to modulate virus replication. To determine the effects of macrophage activation on replication of equine infectious anaemia virus (EIAV), primary horse macrophage cultures (HMCs) were established from 20 different horses, infected with an avirulent strain of EIAV, and stimulated with 5 μg/ml of bacterial endotoxin. Supernatants collected from HMCs were assayed for the presence of tumour necrosis factor (TNF-α) and for production of infectious virus. Results indicated that EIAV replication in vitro varied significantly (P ⩽ 0·0001) from horse to horse, regardless of the treatment of HMCs. Also, EIAV replication was significantly (P ⩽ 0·0001) decreased in HMCs stimulated with bacterial endotoxin as compared to untreated HMCs. No significant correlation was found between virus replication and production of TNF-α following treatment of virus-infected cells with bacterial endotoxin. However, when HMCs were treated with endotoxin prior to virus infection, inhibition of EIAV replication was proportional to increasing levels of endotoxin. PCR and RT-PCR were used to amplify EIAV proviral DNA and mRNA sequences, respectively, at various time-points following infection. The results indicated that the early events of EIAV replication, up to and including transcription of multiple-spliced mRNAs, were not inhibited by treatment of EIAV-infected macrophages with bacterial endotoxin. This suggests that endotoxin treatment inhibits a posttranscriptional step in the virus replication cycle.
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Antigenic variants of J subgroup avian leukosis virus: sequence analysis reveals multiple changes in the env gene.
K Venugopal, L M Smith, K Howes and L N PayneHPRS-103, the prototype of avian leukosis virus (ALV) subgroup J, was isolated in 1989 from meat-type chickens from commercial flocks where it induces myelocytic myeloid leukosis (ML). The HPRS-103 env gene differs considerably from other ALV subgroups but shows high identity (75–97%) to env-like sequences of the different members of the EAV family of endogenous avian retroviruses. Recently, we have isolated several viruses related to HPRS-103 from cases of ML. Although these isolates showed properties of ALV subgroup J, the majority of them resisted neutralization by HPRS-103-specific serum, suggesting antigenic variation. The nucleotide sequence of the env gene of the variant viruses showed several substitutions resulting in amino acid changes especially clustered in the variable regions hr1, hr2 and vr3. Analysis of the data suggests that selection pressure, probably from the immune response, is driving the antigenic variation among the isolates. Phylogenetic analysis of the sequences showed the evolutionary relationships of the isolates with HPRS-103 and the EAV family of endogenous avian retroviruses. The epidemiological significance of the antigenic variation and the emergence of variant viruses are discussed.
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Properties of tumour suppressor p53 in murine hepatocyte lines transformed by hepatitis B virus X protein.
Persistent infection by hepatitis B virus (HBV) correlates with the prevalence of hepatocellular carcinoma. It has recently been demonstrated that the complete viral genome very efficiently transforms the immortalized murine hepatocyte line FMH202 in vitro. Here it is shown that the viral transactivating protein X (HBx) is sufficient to transform FMH202 cells, albeit with lower efficiency. Clonal cell lines expressing HBx mRNA in moderate or high amounts grew in soft agar and formed tumours in nude mice. Growth efficiency in soft agar of HBx transformed cell lines was much lower than that of cell lines transformed with the complete genome, and latency of tumour induction in nude mice was significantly longer after inoculation of HBx than of HBV transformed FMH202 cell lines. A marker of complete transformation, p53, was found to be phosphorylated more strongly in HBx transfected cell lines than in controls, and a cellular kinase was found to be associated with p53 complexes from HBx transformed cell lines. p53 was of wild-type conformation and was located in the nucleus of transformed cells.
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Detection of new human papillomavirus sequences in skin lesions of a renal transplant recipient and characterization of one complete genome related to epidermodysplasia verruciformis-associated types.
More LessHuman papillomavirus (HPV) DNA, originally isolated from patients suffering from the skin disease epidermodysplasia verruciformis (EV), and a growing number of related sequences have recently been detected in a high percentage of benign and malignant skin lesions of both immunosuppressed and immunocompetent people. HPV L1 DNA fragments (374– 389 bp long) from a solar keratosis and a squamous cell carcinoma (SCC) of a renal transplant recipient were amplified, cloned and sequenced. In 54 clones, six different HPV sequences were identified. One of these six corresponded to the known type HPV-8 and two (RTRX3 and RTRX7) have been described previously in cutaneous lesions of immunosuppressed patients. The remaining three sequences were different from all known HPV types: an HPV-9-related sequence (77·4% identity), an RTRX2-related sequence (82·6% identity), and an HPV-22-related sequence (83·7% identity). These three sequences, representing putatively new HPV types, were named RTRX8, RTRX9 and RTRX10, respectively. RTRX7 was found in the majority of clones from both lesions. The complete genome of RTRX7 (7731 bp) was cloned as six overlapping subgenomic fragments, generated by nested PCR with DNA extracts from the SCC. RTRX7 showed a genome organization typical of HPVs associated with EV. The L1 DNA sequence differed by 15% from the corresponding region of its closest known relative, HPV- 12; thus, RTRX7 can be regarded as a new HPV type. RTRX7 DNA could not be detected by Southern blot hybridization with the homologous probe, indicating that the DNA concentration was below one copy per 10 cells in the investigated SCC.
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Human polyomavirus JC control region variants in persistently infected CNS and kidney tissue.
More LessThe question of a possible role for JC virus (JCV) genomic rearrangements in the pathogenesis of progressive multifocal leukoencephalopathy (PML) was addressed by analysis of the genomic complexity and the transcriptional control region (TCR) of the JCV DNA population in persistently infected CNS and kidney tissue. After cloning of full-length viral DNA, no extensive changes were detected in the coding regions of the JCV genome by restriction analysis suggesting an intact JCV DNA population. For further analysis of the distribution of JCV subtypes, the non-coding region was amplified by PCR. Molecular analysis revealed homogeneous JCV TCR populations in almost 50% of the individuals. Heterogeneity was found in two CNS samples with three and five different JCV subtypes, respectively, and in four kidney specimens with two TCR subtypes. Altogether, seven TCR subtypes were identified. One in each group represented single promoter element TCRs without duplication of sequences. The TCR of the major variant JCV-W1 was comparable in sequence and structure to that of the PML prototype JCV Mad-1 DNA. The identification of dominant PML-derived JCV TCR subtypes in most persistently infected individuals suggests that rearrangements of the JCV TCR can be associated with the persistent state of infection. However, it appears unlikely that PML-associated JCV subtypes are generated anew in each individual host in the course of persistence. The findings rather suggest that a limited number of stable JCV subtypes circulate in different geographical regions of the world.
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JC virus Type 1 has multiple subtypes: three new complete genomes.
More LessThe complete genomes of three new Type 1 strains of JC virus (JCV) from urine have been analysed. These were subtype 1A, subtype 1B and Type 4 as assigned from a short typing fragment in the VP1 gene. They differ from Mad1 (subtype 1A) by less than 10% of the DNA sequence. Based on its complete genome, the JCV Type 4 strain falls into a Type 1 subgroup. Type 4, with several Type 3-like sites in the short typing fragment, is a possible recombinant strain. The consensus of Type 1 DNA sequences is distinguished within the coding region from both Type 2 (strain GS/B) and five Type 3 (African and African American) strains at 64 sites. Most mutations are silent, but at 21 positions amino acid changes occur. Our findings define the subtypes of JCV Type 1 and support the validity of genotyping within the short VP1 fragment.
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Glycoprotein C-deficient mutants of two strains of herpes simplex virus type 1 exhibit unaltered adsorption characteristics on polarized or non-polarized cells.
More LessMutants of herpes simplex virus type 1 (HSV-1) strain SC16, lacking each of the dispensable glycoproteins C, G, E, I or J, were examined for their ability to infect the apical or basolateral surfaces of polarized human epithelial cells. None of the mutants was significantly different from the wild- type parent when assayed on either surface. Since a previous report had demonstrated that glycoprotein C (gC) was necessary for the infection of apical surfaces of polarized epithelium, a second gC-negative mutant was constructed on a background of HSV-1 strain HFEM. This mutant dis- played no phenotype when assayed on the apical surface. Furthermore, neither gC-negative mutant differed from its wild-type parent in its adsorption kinetics or specific infectivity on non-polarized Vero cells, a result which is inconsistent with the view that interactions between gC and cell surface proteoglycans constitute the initial adsorption process. Our findings thus conflict with previous reports and suggest that proposed functions of HSV-1 gC in the infection of polarized and non-polarized cells may be strain-dependent.
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