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Volume 77,
Issue 4,
1996
Volume 77, Issue 4, 1996
- Animal
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- RNA viruses
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Vaccinia virus-expressed bovine ephemeral fever virus G but not GNS glycoprotein induces neutralizing antibodies and protects against experimental infection
Two related glycoproteins (G and GNS) encoded in the bovine ephemeral fever virus (BEFV) genome were expressed from recombinant vaccinia viruses (rVV). Both proteins were detected in lysates of rVV-infected cells by labelling with d-[6-3H]glucosamine or by immuno-blotting. The recombinant G protein (mol. mass 79 kDa) appeared slightly smaller than the native G protein but reacted with monoclonal antibodies directed against all defined neutralizing antigenic sites (G1, G2, G3a, G3b and G4). The recombinant GNS protein (mol. mass 90 kDa) was identical in size to the native GNS protein and failed to react by immunofluorescence with anti-G protein monoclonal or polyclonal antibodies. Antisera raised in rabbits against rVV-G or rVV-GNS both reacted strongly by immunofluorescence and immuno-electron microscopy with BEFV-infected cells. The G protein was localized intracellularly in the endoplasmic reticulum/Golgi complex and at the cell surface associated with budding and mature virus particles. The GNS protein also localized intracellularly in the endoplasmic reticulum/Golgi complex; however, at the cell surface it was associated with amorphous structures and not with budding or mature virions. Rabbits vaccinated with rVV-G developed high levels of antibodies which neutralized BEFV grown in either mammalian or insect cells. Cattle vaccinated with rVV-G also produced neutralizing antibodies and were protected against experimental BEFV infection. In contrast, rVV-GNS vaccinated rabbits and cattle failed to produce neutralizing antibodies and, after challenge, BEFV was isolated from two-thirds of the vaccinated cattle.
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Antigenic and immunogenic analysis of group A and group B respiratory syncytial virus G proteins expressed from recombinant baculoviruses
More LessThe attachment glycoprotein G plays a major role in the antigenic variability of respiratory syncytial (RS) virus. We have expressed from recombinant baculoviruses antigenic group A and group B RS virus G proteins (designated bacAG for the group A and bacBG for the group B virus G protein). The insect cell-produced G proteins migrated more rapidly in SDS-PAGE as compared to HEp-2 cell-derived G proteins owing to glycosylation differences. Antigenicity was tested by immunofluorescence; five of five group cross-reactive, five of six group A-specific, and six of six group B-specific MAbs reacted appropriately with bacAG and/or bacBG. In addition, bacAG and bacBG reacted with human polyclonal antibodies to RS virus. Cotton rats were immunized with bacAG, bacBG or a control lysate and challenged intranasally with a group A RS virus. The bacAG-immunized group had a statistically significant reduction in viral replication in the lungs (lung titres as mean log10 p.f.u./g ± sd, bacAG = 3.1 ± 1.2; control = 4.8 ± 0.6, P = 0.013). The bacBG-immunized group showed less reduction in viral titres (bacBG lung titres = 4.1 ± 0.6, P = 0.13 for bacBG compared to control). Thus, as expected, homologous protein (bacAG) immunization provided more protection against viral replication than immunization with the heterologous protein (bacBG). The G protein of RS virus expressed in insect cells had antigenic and immunogenic features which were similar to that of the G protein expressed in mammalian cells. The baculovirus-expressed G proteins should be useful for the study of immune responses to RS viruses.
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A point mutation in the F1 subunit of human respiratory syncytial virus fusion glycoprotein blocks its cell surface transport at an early stage of the exocytic pathway
More LessVaccinia virus recombinants expressing either wild-type or mutant forms of human respiratory syncytial (RS) virus (Long strain) fusion (F) glycoprotein were obtained. Proteolytic processing of the precursor, F0, and cell surface transport of the F glycoprotein were unaffected in the recombinants, except in those that contained the replacement Phe → Ser at position 237 of the F1 subunit. In recombinants containing this mutation, either alone or in combination with others, the traffic of the F molecule was arrested at some intermediate step of its transport to the cell surface and, consequently, the endoproteolytic cleavage of the F0 precursor was inhibited. Immunofluorescence staining of infected cells and endoglycosidase H (Endo-H) sensitivity assays indicated that the arrest occurred before the mid-Golgi compartment. Dimerization and folding of the F protein were also affected by the Phe237 → Ser substitution. Other amino acid replacements at positions 236 or 237 of the F1 subunit had various effects upon F0 maturation. These results are discussed in terms of the maturation requirements for the RS virus F molecule.
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Antigenic and genetic evolution of equine H3N8 influenza A viruses
More LessEvolution of equine influenza A H3N8 viruses was examined by antigenic and genetic analysis of a collection of isolates from around the world. It was noted that antigenic and genetic variants of equine H3N8 viruses cocirculate, and in particular that variants currently circulating in Europe and the USA are distinguishable from one another both in terms of antigenic reactivity and genetic structure of the HA1 portion of the haemagglutinin (HA) molecule. Whilst the divergent evolution of American and European isolates may be due to geographical isolation of the two gene pools, some mixing is believed to occur as ‘American-like’ viruses have been isolated during outbreaks of equine influenza in the UK. The cocirculation of two antigenically and genetically distinct lineages of equine influenza H3N8 viruses has serious implications for vaccine strain selection.
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Evolution of the haemagglutinin-esterase gene of influenza C virus
More LessThe nucleotide sequences of the haemagglutininesterase (HE) genes of 18 influenza C virus strains isolated in Japan during the period from 1964 to 1988 (11 published and 7 new sequences) were analysed to examine their evolutionary relationships. The phylogenetic tree constructed by the maximum parsimony method revealed the existence of four discrete lineages (I to IV), one of which (lineage III) may have died out in the late 1970s. Sequential evolution was demonstrated within seven strains of lineage I, which allowed estimation of an evolutionary rate of 0.49 × 10−3 nucleotide substitutions per site per year, a value corresponding to about one-ninth of the rates of human influenza A virus haemagglutinin genes. In the previously proposed immunodominant region on HE protein (positions 178 to 217), there was little or no amino acid sequence divergence among viruses on the same lineage although considerable divergence was seen among those on different lineages, raising the possibility that immune selection may not have played a significant role in the evolution of the glycoprotein, at least not after separation into lineages occurred. It was also found that the HE genes of the seven isolates obtained outside Japan during 1966–1983 could be each assigned to one of lineages I, II and IV, which suggests that influenza C virus is capable of spreading worldwide.
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Influenza C virus RNA is uniquely stabilized in a steady state during primary and secondary persistent infections
More LessThe ability to establish persistent infections in vitro and in vivo has been illustrated for different human RNA viruses. However, little insight has been gained regarding the intracellular state of viral RNA species and the regulatory processes governing their long-term continuance. In this report, primary persistence of a variant of influenza C/Ann Arbor/1/50 virus in infected MDCK cells and secondary infections in human cell lines were investigated. Different PCR and staining techniques were applied for the description of low viral loads. The RNA pattern in primary persistence indicates that viral RNA synthesis is quantitatively linked to productive and non-productive phases, with negative-strand RNA being present continuously. In single cell cultures, derived from the primary line, all clones tested were positive by nested PCR and Southern blot screening. This suggests that a true steady-state persistence of influenza C virus is established in each individual cell of the infected population. Secondary infection experiments, in terms of transfer of the persistent virus variant to different cell types, showed that a re-establishment of persistence can be accomplished in vitro. The stable persistent status remained reserved for distinct host cell lines. Hereby, vRNA is stably maintained in a cell-type specific manner, whereas gene expression (e.g. HEF glycoprotein production) occurs in a variable fashion. These data point out novel characteristics in the understanding of influenza virus persistence.
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Khabarovsk virus: a phylogenetically and serologically distinct Hantavirus isolated from Microtus fortis trapped in far-east Russia
Two hantavirus strains, MF43 and MF113, isolated from Microtus fortis trapped in the Khabarovsk region of far-eastern Russia, were analysed by direct nucleotide sequencing of PCR generated fragments of the M and S segments, by immunofluorescence and by focus reduction neturalization tests (FRNT). The nucleotide sequences revealed that the two isolates were closely related to each other but distinct from all other hantaviruses. Phylogenetic analysis of the M and S segments showed that the MF strains form a separate branch in the Hantavirus tree, positioned between the branches of Prospect Hill and Puumala viruses. The strains were shown to be serologically distinct from the other hantavirus serotypes by FRNT using immune rabbit sera. Puumala virus was the closest relative, both genetically and serologically. We propose that this new hantavirus serotype should be named Khabarovsk (KBR).
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Characterization of the nucleocapsid protein of Hantaan virus strain 76-118 using monoclonal antibodies
We characterized the antigenic sites on the nucleocapsid protein (NP) of Hantaan virus (HTN) using 10 monoclonal antibodies (MAbs). At least seven antigenic sites were revealed by a competitive binding assay and divided into three partially overlapping antigenic regions (I, II and III). Regions I [amino acids (aa) 1–103], II (aa 104–204) and III (aa 205–402) were mapped on NP by examining the reactivity of truncated gene products. Those that corresponded to region I reacted with immune mouse serum, indicating that the region contained major linear epitopes as reported with Four corners virus (FCV) and Puumala virus (PUU) NP. At least one MAb to each region inhibited viral growth when they were introduced into cells by scrape-loading. In addition, they conferred protection from a lethal HTN challenge to newborn mice. A PEPSCAN assay localized the epitope of MAb E5/G6 between aa 166–175. Since E5/G6, which had the highest inhibitory effect both in cells and in mice, showed no virus neutralization activity by ordinary neutralization test, this region is suggested to be important for the virus growth after entry into the cells.
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Protection of adult but not newborn mice against lethal intracerebral challenge with Japanese encephalitis virus by adoptively transferred virus-specific cytotoxic T lymphocytes: requirement for L3T4+ T cells
More LessThe protective ability of cytotoxic T cells (CTL) raised in vitro against Japanese encephalitis virus (JEV) was examined by adoptive transfer experiments. Adoptive transfer of anti-JEV effectors by intracerebral (i.c.) but not by intraperitoneal (i.p.) or intravenous (i.v.) routes protected adult BALB/c mice against lethal i.c. JEV challenge. In contrast to adult mice, adoptive transfer of anti-JEV effectors into newborn (4-day-old) and suckling (8–14-day-old) mice did not confer protection. However, virus-induced death was delayed in suckling mice compared to newborn mice upon adoptive transfer. The specific reasons for lack of protection in newborn mice are not clear but virus load was found to be higher in newborn mice brains compared to those of adults and virus clearance was observed only in adult mice brains but not in newborn mice brains upon adoptive transfer. Specific depletion of Lyt 2.2+, L3T4+ or Thy-1+ T cell populations before adoptive transfer abrogated the protective ability of transferred effectors. However, when Lyt 2.2+ cell-depleted and L3T4+ cell-depleted effectors were mixed and transferred into adult mice the protective activity was retained, demonstrating that both Lyt 2.2+ and L3T4+ T cells are necessary to confer protection. Although the presence of L3T4+ T cells in adoptively transferred effector populations enhanced virus-specific serum neutralizing antibodies, the presence of neutralizing antibodies alone without Lyt 2.2+ cells was not sufficient to confer protection.
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The major echovirus group is genetically coherent and related to coxsackie B viruses
More LessIn order to determine the overall molecular heterogeneity of echoviruses (EVs) we performed a genetic analysis of the prototype strains. Nucleotide and derived amino acid sequences from different genomic regions (5′UTR, capsid protein-coding and 3D polymerase genes) were used for molecular comparisons. On the basis of a comparison of partial amino acid sequences from the capsid protein VP2, all the sequenced EVs excluding EV22 and EV23 form a single cluster which is genetically homogeneous. All previously sequenced coxsackie B viruses (CBVs) and coxsackievirus A9 also belong to this same genetic cluster. Similar results were obtained when the 5′UTR or 3D polymerase gene sequences were used in comparisons. When amino acid sequences of the major capsid proteins of EV1 and EV16 were compared to those of previously sequenced enteroviruses, the length of the loops connecting the β-sheets appeared to be relatively constant in the EV/CBV cluster. It can be concluded that EVs and CBVs have diverged relatively late in evolution.
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Recognition of foot-and-mouth disease virus and its capsid protein VP1 by bovine peripheral T lymphocytes
More LessThe role of T cells in immunity to foot-and-mouth disease virus is still poorly defined compared to that of the humoral response. In this paper we describe a systematic, longitudinal study on the cellular recognition of FMDV and its subunit protein VP1 by bovine peripheral blood T lymphocytes. Multiple vaccination with a single virus serotype induced a serotype cross-reactive proliferative T cell repertoire that varied in magnitude between individual animals and with the serotype of the vaccine used. Primary proliferative T cell responses of vaccinated and acutely infected cattle were weak relative to the magnitude of responses determined for the same animals after boosting. In contrast, the level of circulating antibody produced after both primary and secondary exposure to virus was good. Phenotypic analysis of lymphocytes from vaccinated or infected cattle showed a small increase in CD8+ T cells after infection compared to vaccination. However, in general the profiles of circulating lymphocytes elicited were similar. Thus, we were not able to use proliferative or phenotypic analyses to distinguish between vaccinated and convalescent cattle. T cell recognition of VP1 by multiply-vaccinated cattle was serotype-specific implying that the cross-reactive responses observed with whole virus may be attributed to proteins other than VP1. In contrast to other studies, immunization with recombinant VP1 induced only low levels of neutralizing antibody and failed to elicit profound proliferative responses or protection even after two immunizations.
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Depletion of Mac1-positive macrophages protects DBA/2 mice from encephalomyocarditis virus-induced myocarditis and diabetes
More LessDBA/2 mice treated with anti-Mac1 monoclonal antibody (MAb) failed to develop encephalomyocarditis virus (EMCV)-induced diabetes and myocarditis. Virus concentrations and the number of viral RNA-positive cells in the pancreas and heart were significantly reduced in mice treated with anti-Mac1 MAb. Mac1-positive macrophages seem to be involved in EMCV-induced disease and to affect the replication of EMCV in target organs.
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Gag-Gag interactions in the C-terminal domain of human immunodeficiency virus type 1 p24 capsid antigen are essential for Gag particle assembly
More LessSeven internal deletions within the p24 domain of the human immunodeficiency virus type 1 Gag precursor have been assessed for their effect on Gag particle formation following their expression using recombinant baculoviruses. In addition, each deleted molecule was assessed for its ability to bind soluble p24 antigen in vitro. The mutants fell into three different phenotypic groups: (i) three mutants that had no effect on either p24 binding or Gag particle assembly, (ii) three mutants that abolished both features and (iii) one mutant that bound p24 in vitro but failed to assemble particles. Mutations that abolished both in vitro p24 binding and particle assembly mapped to the C terminus of p24 confirming this region as critical for virion assembly. We suggest the division of virion assembly into at least two distinct phases and suggest a model in which the critical sequences mapped to date are combined with available structural information.
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Rapid selection for an N-linked oligosaccharide by monoclonal antibodies directed against the V3 loop of human immunodeficiency virus type 1
More LessThe V3 loop of the human immunodeficiency virus (HIV) surface protein, gp120, constitutes a principal neutralizing determinant. HIV strains lacking a naturally conserved N-linked oligosaccharide (at position 306) within the V3 loop are highly sensitive to neutralization. We subjected molecular clones of HIVLAI lacking this 306 N-glycan to in vitro immune selection with MAbs directed against the V3 loop. In all, ten clones were characterized, and all proved resistant to V3-directed neutralization. Sequencing of the V3 loop revealed that six of the clones had become resistant at least partly by reacquisition of the 306 N-glycan. Only two of the clones possessed mutations within the binding site of the antibody itself, while the two remaining clones did not display changes within the V3 loop itself. Thus, HIV strains lacking the 306 N-glycan primarily develop resistance to V3-directed neutralization through acquisition of the specific oligosaccharide. This demonstrates that protein glycosylation can be a primary modifier of virus antigenicity of possible importance for the interaction of HIV with the host immune response.
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Neutralization sensitivity and accessibility of continuous B cell epitopes of the feline immunodeficiency virus envelope
More LessAntibodies elicited during natural infection of domestic cats by the feline immunodeficiency virus (FIV) recognize continuous epitopes in nine domains of the virus envelope glycoproteins. Whereas antibodies directed against the V3 envelope region can neutralize laboratory-adapted virus, neutralization of FIV has been shown to depend upon cellular substrate, and virus adaptation to laboratory cell lines may alter sensitivity to neutralizing antibodies. We therefore undertook a systematic analysis of the continuous B cell epitopes of the envelope of a primary FIV isolate, Wo. The capacity of feline antisera elicited against nine envelope domains to neutralize primary and laboratory-adapted virus was evaluated in feline peripheral blood mononuclear cells (PBMC). The laboratory-adapted strain Petaluma was used to compare neutralization in PBMC and Crandell feline kidney cells (CrFK). Antibodies specific for the V3 region neutralized both primary and laboratory-adapted virus whether residual infectivity was measured in CrFK or in feline PBMC. However, a large discrepancy in the efficiency of neutralization was observed in these ex vivo models of infection, perhaps reflecting diversity in the interaction between virus and different cellular targets. We also examined the accessibility of epitopes on the functional oligomeric envelope complex of FIV. Most of the epitopes were poorly exposed on native envelope glycoproteins at the surface of live infected cells. The most accessible domain was the only domain sensitive to neutralizing antibodies. These results suggest that inaccessibility on oligomeric envelope glycoproteins may frequently underlie the insensitivity of diverse lentivirus B cell epitopes to neutralization.
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Simian immunodeficiency virus infection in a patas monkey (Erythrocebus patas): evidence for cross-species transmission from African green monkeys (Cercopithecus aethiops sabaeus) in the wild
Socio-ethological studies on troops of African green monkeys (AGMs) (Cercopithecus aethiops sabaeus) and patas monkeys (Erythrocebus patas) in Senegal have documented physical contacts between these two species. Elevated simian immunodeficiency virus (SIV) seroprevalence rates have been reported for the different AGM subspecies. We report here the extent to which patas monkeys are infected and compare the relatedness of the viruses isolated from these two different species. Among the 85 AGMs and 54 patas monkeys studied, 47% and 7.5%, respectively, had antibodies that cross-reacted with HIV-2 envelope proteins. From two AGMs a virus was isolated. From the patas monkeys, virus isolation was generally not possible, but from one animal that was ill a virus designated pamG31 was amplified by PCR. In addition, for the two SIVagm isolates, an 830 bp region spanning the env and nef genes was amplified and sequenced. Comparisons of sequences from the env/nef region revealed 80% identity between pamG31 and SIVagm isolates from AGMs of the sabaeus subspecies, and 94% identity between the two SIVagm isolates. Phylogenetic analysis showed that pamG31 belongs to the SIVagm sabaeus subgroup. This is the first report of a lentiviral infection in a patas monkey. The close genetic relatedness between pamG31 and SIVagm sabaeus viruses is a strong argument in favour of cross-species transmission of SIV between AGMs and patas monkeys in the wild. For these reasons, we propose to refer to this patas virus as SIVagm-pamG31.
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Consistent risk group-associated differences in human immunodeficiency virus type 1 vpr, vpu and V3 sequences despite independent evolution
Human immunodeficiency virus type 1 vpr, vpu and V3 sequences from 15 homosexual men and 19 intravenous drug users in the Amsterdam Cohort studies were analysed. Previously, we reported that V3 domains of viruses from drug users are distinguishable from those of homosexual men on the basis of two silent mutations. Phylogenetic analysis of vpr, vpu and V3 shows that differences in all three regions correlate with risk group. Two positions in both vpr and vpu were found to differ significantly between the risk groups. The distinguishing positions were confirmed for sequences from 11 Scottish and four German samples. The three regions show relatively independent evolution patterns; they resulted in different phylogenies, the only stable clustering being that based on the risk group distinction. Pairwise differences between sequences of the genes were moderately correlated (around 0.30). Surprisingly, when only silent changes were counted, the correlations dropped almost to zero, indicating that the evolution towards independence was more advanced in the silent than in the non-silent positions. This suggests that selection at the amino acid level is not the primary driving force for the independent evolutionary behaviour of the genes. Recombination, combined with restrictions on certain amino acids because of epistatic interactions between the genes, could be an alternative explanation of this phenomenon.
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Requirements for mouse mammary tumour virus internalization in mouse mammary epithelial cells
More LessMethylamine, a lysosomotropic alkalinizing agent, blocked mouse mammary tumour virus (MMTV) infection in normal mouse mammary epithelium, suggesting that internalization and acidification are necessary for cell penetration. This mechanism was further supported by the fact that intact MMTV induced the translocation of its cellular binding protein from the plasmalemma to the microsomes; however, isolated gp52, the MMTV envelope protein that binds this receptor, did not redistribute the binding protein. These data suggest that either another viral component, in addition to gp52, is needed for cell entry or that internalization requires receptor aggregation, which only the multivalent viral envelope can induce.
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- DNA viruses
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Proliferative T cell responses to human papillomavirus type 16 L1 peptides in patients with cervical dysplasia
Human papillomavirus type 16 (HPV-16) can cause genital warts, cervical dysplasias and carcinoma of the cervix. Cell-mediated immunity is thought to be important in protection against the virus and in its elimination, but little is known about the mechanisms involved. In a cross-sectional study we have demonstrated proliferative T cell responses to peptides representing the HPV-16 L1 capsid protein (aa 199–409) in the peripheral blood of 63% of patients (n = 41) with histological evidence of cervical dysplasia and in 45% of healthy age-matched controls (n = 11). This was achieved by generating short-term T cell lines (STLs) from each individual in vitro against a β-galactosidase-HPV-16 L1 (aa 199–409) fusion protein for 2 weeks, and then identifying the HPV epitopes they recognized with overlapping synthetic peptides (15-mers) spanning this region in 3 day specificity assays. Histological grading and HPV typing by PCR were performed on patients’ cervical biopsies taken at the same clinical visit as the peripheral blood samples. An immunogenic region was identified between aa 311–345 in 73% of patients (18% in controls) who responded to HPV-16 L1 (aa 199–409). The number of responders to this region was significantly higher in patients with HPV-16-positive biopsies when compared to those with HPV-16-negative biopsies (P = 0.006), as was the number of responders to individual peptides 311–325 (NLASSNYFPTPSGSM; P = 0.04) and 321–335 (PSGSMVTSDAQIFNK; P = 0.004) representing this region. The mean level of response to each individual peptide was also higher in the patient group than the controls (P < 0.05). The most significant finding was that all patients with evidence of a current HPV-16 infection responded to one or more L1 peptides (P = 0.0004) and 92% had high grade cervical intraepithelial neoplasia (CIN III). We also found that the CIN III group was more likely to respond to any L1 peptide than either the atypical group (P = 0.04) or the controls (P = 0.05). Data from four individuals showed that the majority of peptide-specific STLs were CD4+ but some CD8+ STLs were also detected.
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Partial transcriptional mapping of the fowlpox virus genome and analysis of the EcoRI L fragment
More LessSeveral fowlpox virus (FPV) DNA fragments were selected by differential hybridization using cDNA of transcripts that were strongly transcribed early and/or late after infection of QT-35 cells. The EcoRI L fragment contained three strongly transcribed FPV genes: L1L, a late 1452 bp partial (amino end) ORF; L2R, an early/late 522 bp ORF; and L3R, a late 948 bp ORF. The protein products of L1L, L2R and L3R shared homology with the products of vaccinia virus (VV) genes H4L (RAP94), H5R (Ag35) and H6R (topoisomerase), respectively, suggesting a conservation of gene structure and order between VV and FPV. The 5′ upstream non-coding sequences of L1L and L3R were A + T rich and the sequence 5′ TAAATG 3′ overlapped the predicted translation start codon. Primer extension analysis of the L2R transcript mapped the transcriptional start sites of early and late mRNAs 14 nt downstream of a VV early promoter-like critical region sequence, AAAATTGAAAAAAAAA. A VV-like TAAAT late transcriptional element was present 20 nt upstream of the L2R ATG translational start codon. A plasmid with the putative early L2R promoter cloned upstream of the Newcastle disease virus haemagglutinin-neuraminidase (HN) cDNA as a reporter gene was at least 6-fold more effective in generating HN mRNA than plasmids containing the P7.5 or P11 VV promoters in transient expression assays in FPV-infected CEF cells treated with cytosine arabinoside. The L2R promoter was also able to express an amount of HN mRNA equal to that expressed by the VV promoters late in infection.
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