- Volume 80, Issue 10, 1999
Volume 80, Issue 10, 1999
- Review Article
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- Animal: RNA Viruses
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Ecology and evolution of rabies virus in Europe
The evolution of rabies viruses of predominantly European origin was studied by comparing nucleotide sequences of the nucleoprotein and glycoprotein genes, and by typing isolates using RFLP. Phylogenetic analysis of the gene sequence data revealed a number of distinct groups, each associated with a particular geographical area. Such a pattern suggests that rabies virus has spread westwards and southwards across Europe during this century, but that physical barriers such as the Vistula river in Poland have enabled localized evolution. During this dispersal process, two species jumps took place – one into red foxes and another into raccoon dogs, although it is unclear whether virus strains are preferentially adapted to particular animal species or whether ecological forces explain the occurrence of the phylogenetic groups.
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Protection and antibody responses in different strains of mouse immunized with plasmid DNAs encoding influenza virus haemagglutinin, neuraminidase and nucleoprotein
Protection against influenza virus infection and antibody responses in mice vaccinated with plasmid DNAs encoding haemagglutinin (HA), neuraminidase (NA) and nucleoprotein (NP) were compared among BALB/c (H-2d), B10 (H-2b) and C3H (H-2k ) mice. Mice were inoculated with each DNA construct twice, 3 weeks apart, at a dose of 1 μg per mouse by particle-mediated DNA transfer (gene gun) to the epidermis. They were challenged with a lethal dose of the homologous virus 7 days after the second vaccination. NA-DNA provided significant protection in all strains of mouse, whereas HA-DNA afforded significant protection only in BALB/c mice. The serum antibody titres against NA or HA molecules in BALB/c, C3H and B10 mice were high, intermediate and low, respectively. NP-DNA failed to provide protection in any strain of mouse, and elicited low titres of anti-NP antibodies. These results suggest that NA-DNA can be used as a vaccine component to provide effective protection against influenza virus infection in various strains of mouse.
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Interaction of influenza virus polymerase with viral RNA in the ‘corkscrew’ conformation
More LessThe influenza virus RNA (vRNA) promoter structure is known to consist of the 5′- and 3′-terminal sequences of the RNA, within very narrow boundaries of 16 and 15 nucleotides, respectively. A complete set of single nucleotide substitutions led to the previously proposed model of a binary hooked or ‘corkscrew’ conformation for the vRNA promoter when it interacts with the viral polymerase. This functional structure is confirmed here with a complete set of complementary double substitutions, of both the regular A:U and G:C type and also the G:U type of base-pair exchanges. The proposed structure consists of a six base-pair RNA rod in the distal element in conjunction with two stem–loop structures of two short-range base- pairs (positions 2–9; 3–8). These support an exposed tetranucleotide loop within each branch of the proximal element, in an overall oblique organization due to a central unpaired A residue at position 10 in the 5′ sequence. Long-range base-pairing between the entire 5′ and 3′ branches, as required for an unmodified ‘panhandle’ model, has been excluded for the proximal element, while it is known to represent the mode of interaction within the distal element. A large number of short-range base-pair exchanges in the proximal element constitute promoter-up mutations, which show activities several times above that of the wild- type in reporter gene assays. The unique overall conformation and rather few invariant nucleotides appear to be the core elements in vRNA recognition by polymerase and also in viral ribonucleoprotein packaging, to allow discrimination against the background of other RNA molecules in the cell.
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The BM2 protein of influenza B virus is synthesized in the late phase of infection and incorporated into virions as a subviral component
More LessThe influenza B virus genome RNA segment 7 encodes the M1 and BM2 proteins. The BM2 protein is synthesized by a coupled translational termination–reinitiation mechanism at the overlapping stop–start pentanucleotide in a bicistronic mRNA transcribed from RNA segment 7. However, features and functions of this protein remain unclear. In this study the BM2 protein was characterized by using an antiserum raised to the BM2 protein of influenza virus strain B/Yamagata/1/73. In cells infected with B/Yamagata virus the αBM2 antibody specifically detected the BM2 protein with a molecular mass of 12 kDa and also a polypeptide with a molecular mass of 17 kDa. When infected cells were labelled with 32Pi and immunoprecipitated with the αBM2 antibody, the 32 P-labelled 17 kDa polypeptide was specifically precipitated. In the presence of casein kinase inhibitor CKI-7 the synthesis of the 17 kDa and BM2 proteins was completely suppressed, although other viral proteins, except for the polymerase protein, were synthesized normally. These results suggest that the 17 kDa species is a phosphorylated form of the BM2 protein. These species were substantially synthesized in the late phase of infection and localized in the cytoplasm throughout infection. Moreover, they were transported to the plasma membrane and thereafter were incorporated into virions. These results therefore suggest that the BM2 and the 17 kDa proteins are necessary for the life-cycle of influenza B virus.
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The RNA-dependent RNA polymerases of different members of the family Flaviviridae exhibit similar properties in vitro
More LessThe virus-encoded RNA-dependent RNA polymerase (RdRp), which is required for replication of the positive-strand RNA genome, is a key enzyme of members of the virus family Flaviviridae. By using heterologously expressed proteins, we demonstrate that the 77 kDa NS5B protein of two pestiviruses, bovine viral diarrhoea virus and classical swine fever virus, and the 100 kDa NS5 protein of the West Nile flavivirus possess RdRp activity in vitro. As originally shown for the RdRp of hepatitis C virus, RNA synthesis catalysed by the pestivirus and flavivirus enzymes is strictly primer- dependent in vitro. Accordingly, initiation of RNA polymerization on homopolymeric RNAs and heteropolymeric templates, the latter with a blocked 3′-hydroxyl group, was found to be dependent on the presence of complementary oligonucleotide primer molecules. On unblocked heteropolymeric templates, including authentic viral RNAs, the RdRps were shown to initiate RNA synthesis via intramolecular priming at the 3′-hydroxyl group of the template and ‘copy-back’ transcription, thus yielding RNase- resistant hairpin molecules. Taken together, the RdRps of different members of the Flaviviridae were demonstrated to exhibit a common reactivity profile in vitro, typical of nucleic acid- polymerizing enzymes.
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Involvement of β2-microglobulin and integrin αvβ3 molecules in the coxsackievirus A9 infectious cycle
It is becoming apparent that many viruses employ more than one cell surface molecule for their attachment and cell entry. In this study, we have tested the role of integrin αvβ3 and MHC class I molecules in the coxsackievirus A9 (CAV-9) infectious cycle. Binding experiments utilizing CHO cells transfected and expressing human integrin αvβ3, revealed that CAV- 9 particles were able to bind to cells, but did not initiate a productive cell infection. Antibodies specific for integrin αvβ3 molecules significantly reduced CAV-9 infection in susceptible cell lines. Moreover, MAbs specific for β2- microglobulin (β2-m) and MHC class I molecules completely inhibited CAV-9 infection. To assess the effect of these antibodies on virus binding, we analysed CAV-9 binding by flow cytometry in the presence of β2-m- or integrin α vβ3-specific antibodies. The results showed a reduction in CAV-9 binding in the presence of integrin αvβ3- specific antibodies while there was no reduction in the presence of β2-m-specific MAb. Taken together, these data suggest that integrin αvβ3 is required for CAV-9 attachment but is not sufficient for cell entry, while β2 -m, although not directly involved in CAV-9 binding, plays a post- attachment role in the CAV-9 infectious process, possibly being involved in virus entry.
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Two determinants in the capsid of a persistent type 3 poliovirus exert different effects on mutant virus uncoating
More LessMutant polioviruses (PV) have been previously found to be capable of establishing persistent infections in HEp-2c cells. Together, two amino acid substitutions in the viral capsid of a type 3 poliovirus (PV-3), at positions VP213 and VP1290, are sufficient to confer the persistent phenotype to a normally lytic virus. When susceptible cells are infected, the double mutant T7L+2L 131N290 undergoes unique conformational changes in the capsid, modifying its sedimentation coefficient from 160S to 147S. In the present study, we have further investigated mutant PV decapsidation and, in particular, the effect of each determinant independently. Our results indicate that the novel 147S form was also generated by a mutant carrying only the determinant 1N290. This form was not produced as a result of inherent capsid instability and it was generated only upon specific PV–host cell interactions. The second viral determinant, 2L13, also modified receptor-induced conformational changes, although differently from 1N290.
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Processing and intracellular location of human astrovirusnon-structural proteins
More LessHuman astrovirus (HAst) non-structural polyproteins are encoded in two open reading frames linked in expression by a ribosomal frameshifting event. The first of these (ORF 1a) specifies the serine protease, whilst the second (ORF 1b) encodes the virus RNA-dependent RNA polymerase. The ORF 1a product contains an unusual motif for small RNA viruses which could potentially direct proteins to the cell nucleus. We have expressed part of ORF 1a containing this motif and the whole of ORF 1b separately in recombinant baculovirus and raised specific antisera to each. We now report that expressed proteins from ORF 1a accumulate in the nucleus of both baculovirus-infected insect cells and HAst-infected CaCo-2 cells. In contrast the products of ORF 1b remain predominantly cytoplasmic.
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Isolation and phylogeny of endogenous retrovirus sequences belonging to the HERV-W family in primates
More LessAn investigation was undertaken of primate pol gene sequences from a novel endogenous retrovirus family, ERV-W, related to a new human endogenous retrovirus family (HERV-W) that includes multiple sclerosis-associated retrovirus (MSRV) sequences identified in particles recovered from monocyte cultures from patients with multiple sclerosis. The pol gene sequences of the ERV-W family were detected in hominoids and Old World monkeys, but not in New World monkeys, whereas ERV-W long terminal repeat-like elements were detected in all primates (hominoids, Old World monkeys and New World monkeys). Thirty-two pol gene sequences from hominoids and Old World monkeys showed a high degree of sequence identity to MSRV and other HERV-W sequences. Phylogenetic analysis indicated close relationships of pol gene sequences across primate species. The analysis suggests that the ERV-W family has evolved independently but in constrained patterns (‘parallel evolution’) in different primate species, including man. The ratio of synonymous to non- synonymous substitutions indicated that negative selective pressure is acting on CHW1-1 from chimpanzee, HBW6-6 from baboon and HWX5 from man, sequences that have no disruption by point mutation or insertions/deletions. Therefore, these pol gene sequences could be associated with an active provirus in primates. The findings indicate that the ERV-W family has continued to evolve in the course of the primate radiation and may include members with a capacity to influence gene function and possibly cause disease.
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Replication-deficient recombinant adenoviruses expressing the human immunodeficiency virus Env antigen can induce both humoral and CTL immune responses in mice
An effective vaccine against infection with human immunodeficiency virus type 1 (HIV-1) is thought likely to require both a humoral and a CTL immune response. A non-replicating adenovirus vector system has been developed that can induce both a humoral and CTL response to HIV-1 envelope in mice. It is demonstrated that the stimulatory tat/rev 5′ splice-donor site sequence is required for efficient expression of HIV-1 env by this adenovirus vector system. rev can be provided bicistronically or in trans to result in good expression of env in vitro. A humoral immune response was detected after two immunizations with a bicistronic recombinant adenovirus (RAd142). The response was dose dependent, 5×107 p.f.u. inducing a response in some, but not all, animals and 1×108 p.f.u. giving a consistent antibody response. However, CTLs were induced by the lower dose of virus and after only one immunization with the higher dose. A positive CTL response was also seen consistently when the two monocistronic adenoviruses (RAd501 expressing env and RAd46 expressing rev) were given together, although two immunizations were required to give approximately the same level of response as seen with the bicistronic virus. RAd501 on its own also gave a low CTL response when two immunizations were given. It is suggested that a lower level of env expression is required to produce a CTL response than a humoral response and that this non- replicating adenovirus vector is a good system for inducing CTL.
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Interaction of YB-1 with human immunodeficiency virus type 1 Tat and TAR RNA modulates viral promoter activity
More LessTranscriptional regulation of the human immunodeficiency virus type 1 (HIV-1) genome is mediated by viral and cellular factors. TAR, an unusual RNA regulatory element with a stem–bulge–loop structure at the 5′ ends of all nascent viral transcripts is critical for HIV-1 transcription. TAR is the target for Tat, a viral transcription factor encoded early in the HIV-1 life-cycle and essential for gene expression. Evidence demonstrating the interaction of a cellular ssDNA/RNA binding protein, YB-1, with TAR through a region which is important for Tat interaction is presented. Interestingly, results from protein–protein interaction studies revealed that YB-1 can also form a complex with Tat. Results from mapping experiments suggest that while the region spanning aa 125–203 within YB-1 is essential for its association with TAR, a truncated YB-1 spanning aa 1–125 can weakly bind to Tat. Functionally, overexpression of full-length YB-1 enhanced Tat-induced activation of the HIV-1 minimal promoter containing TAR sequences, whereas mutant YB-1 with no ability to bind to Tat and TAR failed to affect Tat-mediated activation. Expression of mutant YB-1(1–125), which binds to Tat but not RNA, decreased Tat- mediated enhancement of virus transcription. These observations suggest that while full-length YB-1 may function as a facilitator and, by interaction with both Tat and TAR, increase the level of Tat:TAR association, mutant YB-1 with no TAR binding activity, by complexing with Tat, may prevent Tat interaction with TAR. The importance of these findings in light of the proposed mechanism of Tat function is discussed.
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Envelope gene sequences encoding variable regions 3 and 4 are involved in macrophage tropism of feline immunodeficiency virus
The envelope is of cardinal importance for the entry of feline immunodeficiency virus (FIV) into its host cells, which consist of cells of the immune system including macrophages. To characterize the envelope glycoprotein determinants involved in macrophage tropism, chimeric infectious molecular clones were constructed containing envelope gene sequences from isolates that had been propagated in peripheral blood mononuclear cells (PBMC). The progeny virus was examined for growth in PBMC and bone marrow-derived macrophages and viruses with different replication kinetics in macrophages were selected. Envelope-chimeric viruses revealed that nucleotide sequences encoding variable regions 3 and 4 of the surface glycoprotein, SU, are involved in macrophage tropism of FIV. To assess the biological importance of this finding, the phenotypes of envelope proteins of viruses derived from bone marrow, brain, lymph node and PBMC of an experimentally FIV-infected, healthy cat were examined. Since selection during propagation had to be avoided, provirus envelope gene sequences were amplified directly and cloned into an infectious molecular clone of FIV strain Petaluma. The viruses obtained were examined for their replication properties. Of 15 clones tested, 13 clones replicated both in PBMC and macrophages, two (brain-derived clones) replicated in PBMC only and none replicated in Crandell feline kidney cells or astrocytes. These results indicate that dual tropism for PBMC and macrophages is a common feature of FIV variants present in vivo.
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- Animal: DNA Viruses
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Hepatitis B viral core proteins with an N-terminal extension can assemble into core-like particles but cannot be enveloped
More LessThe structure of hepatitis B virus (HBV) nucleocapsids has been revealed in great detail by cryoelectron microscopy. How nucleocapsids interact with surface antigens to form enveloped virions remains unknown. In this study, core mutants with N-terminal additions were created to address two questions: (1) can these mutant core proteins still form nucleocapsids and (2) if so, can the mutant nucleocapsids interact with surface antigens to form virion-like particles. One plasmid encoding an extra stretch of 23 aa, including six histidine residues, fused to the N terminus of the core protein (designated HisC183) was expressed in Escherichia coli and detected by Western blot. CsCl gradient and electron microscopy analyses indicated that HisC183 could self-assemble into nucleocapsids. When HisC183 or another similar N-terminal fusion core protein (designated FlagC183) was co-expressed with a core-negative plasmid in human hepatoma cells, both mutant core proteins self-assembled into nucleocapsids. These particles also retained kinase activity. Using an endogenous polymerase assay, a fill-in HBV DNA labelled with isotope was obtained from intracellular nucleocapsids formed by mutant cores. In contrast, no such signal was detected from the transfection medium, which was consistent with PCR and Southern blot analyses. Results indicate that core mutants with N-terminal extensions can form nucleocapsids, but are blocked during the envelopment process and cannot form secreted virions. The mutant nucleocapsids generated from this work should facilitate further study on how nucleocapsids interact with surface antigens.
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Hepatitis B virus maturation is affected by the incorporation of core proteins having a C-terminal substitution of arginine or lysine stretches
More LessAssembly of replication-competent hepadnavirus nucleocapsids requires interaction of core protein, polymerase and encapsidation signal (ϵ) with viral pregenomic RNA. The N-terminal portion (aa 1–149) of the core protein is able to self-assemble into nucleocapsids, whereas the C-terminal portion (aa 150–183) is known to interact with pregenomic RNA. In this study, two hepatitis B virus (HBV) core mutants (C144Arg and C144Lys) in which the C-terminal SPRRR (Ser-Pro-Arg-Arg-Arg) motif was replaced by a stretch of arginine or lysine residues were generated to test their role in pregenome encapsidation and virus maturation. Mutant or wild-type core-expression plasmids were co-transfected with a core-negative plasmid into human hepatoma HuH-7 cells to compare trans-complementation efficiency for virus replication. Both low- and high-density capsids were present in the cytoplasm and culture medium of HuH-7 cells in all transfections. Nucleocapsids formed by C144Arg and C144Lys, however, lost the endogenous polymerase activity to repair HBV DNA. Furthermore, in co-transfection of pHBVC144Arg or pHBVC144Lys with a plasmid which produces replication-competent nucleocapsids, the HBV DNA repairing signal was reduced 40- to 80-fold. This is probably due to formation of mosaic particles of wild-type and mutant cores. Results indicated that the SPRRR motif at the core protein C terminus is important for HBV DNA replication and maturation. Additionally, triple-plasmid transfection experiments showed that nucleocapsids containing various amounts of C144Arg and wild-type core proteins exhibited a bias in selecting a shorter pregenome for encapsidation and DNA replication. It is therefore suggested that unknown factors are also involved in HBV pregenome packaging.
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A novel negative cis-regulatory element on the hepatitis B virus S-(+)-strand
More LessHepatitis B virus (HBV) has a double-stranded DNA genome. The minus-strand contains coding regions for all known HBV proteins and most of the cis-regulatory elements. Little is known about transcription from the S-(+)-strand and its regulation. Thus, the presence of regulatory elements located on the S-(+)-strand was investigated by inserting nt 1038–1783 of HBV in both orientations between the human cytomegalovirus (HCMV) promoter and a luciferase gene. Transfection experiments revealed that the plasmid containing this HBV DNA fragment in an orientation allowing expression from the S-(+)-strand (antisense) led to inhibition of luciferase gene expression compared to the plasmid containing this sequence in an orientation that allows gene expression from the L-(−)-strand (sense). Deletion analyses delimit the sequence essential for the inhibitory effect to a 150 bp region that also carries part of the enhancerII/core promoter complex. However, the possible influence of this regulatory element has been excluded in various experiments. The repressing HBV sequence acts in an orientation- and position-dependent manner; no inhibition was observed when this DNA element was inserted upstream of the HCMV promoter or downstream of the luciferase gene. Northern blot analyses revealed reduced luciferase mRNA steady-state levels in cells transfected with constructs containing the essential HBV sequence in antisense orientation compared to plasmids containing this sequence in sense orientation. Since nuclear run-on experiments showed similar transcription initiation rates with these plasmids, the diminished luciferase mRNA steady-state levels must be due to altered stabilities, suggesting that nt 1783–1638 of HBV encode an RNA-destabilizing element.
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Hepatitis B virus genomes from long-term immunosuppressed virus carriers are modified by specific mutations in several regions
More LessThere is increasing evidence that hepatitis B virus (HBV) infection of an immunosuppressed host is associated with the appearance of virus mutants. To characterize the virus circulating in patients in detail, eleven full-length HBV genomes, isolated from the serum of five highly viraemic renal transplant recipients with liver disease, were cloned and sequenced. The genomes contained deletions in the C gene, deletions in the pre-S1/2 region frequently removing the pre-S2 initiation codon, premature termination codons in the pre-S1 or S region, and/or deletions/insertions in the X gene/core promoter. The mutations occurred at different positions and in various combinations; even mutant genomes circulating within a patient differed strikingly. It is concluded that long-term immunosuppression is associated with the occurrence of heterogeneous populations of partially defective HBV characterized by a specific mutation pattern. Efficient intracellular trans-complementation probably enables high virus replication in vivo.
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An African swine fever virus ORF with similarity to C-type lectins is non-essential for growth in swine macrophages in vitro and for virus virulence in domestic swine
An African swine fever virus (ASFV) ORF, 8CR, with similarity to the C-type lectin family of adhesion proteins has been described in the pathogenic isolate Malawi Lil-20/1. The similarity of 8CR to cellular and poxvirus genes associated with cell adhesion, cell recognition and virus infectivity suggested that 8CR may be of significance to ASFV–host cell interactions. Sequence analysis of the 8CR ORF from additional pathogenic ASFV isolates demonstrated conservation among isolates from both pig and tick sources. Northern blot analysis demonstrated 8CR mRNA transcription late in the virus replication cycle. A Malawi Lil-20/1 8CR deletion mutant (Δ8CR) was constructed to analyse 8CR function further. The growth characteristics in vitro of Δ8CR in porcine macrophage cell cultures were identical to those observed for parental virus. In domestic swine, Δ8CR exhibited an unaltered parental Malawi Lil- 20/1 disease and virulence phenotype. Thus, although well conserved among pathogenic ASFV field isolates, 8CR is non-essential for growth in porcine macrophages in vitro and for virus virulence in domestic swine.
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Mapping T and B lymphocyte epitopes of bovine herpesvirus-1 glycoprotein B
More LessGlycoprotein B (gB) is a major envelope protein of bovine herpesvirus-1 (BHV-1). As a subunit vaccine, the extracellular domain of recombinant gB induces neutralizing antibody and T cell responses that engender protection against virus challenge. Here, lymphocytes from animals of different parentage were analysed for T cell proliferation to the gB extracellular domain for immune recognition. Four truncated overlapping gB gene segments encoding 742 amino acids were expressed from a baculovirus vector to identify antigenic regions. One immunodominant region (amino acids 254–532) was recognized by T cells from immune individuals of different parentage. Serial synthetic peptides spanning this region localized the T cell (amino acids 319–340 and 415–436) and B cell (amino acids 331–352, 475–496 and 487–508) epitopes. Elucidation of gB epitopes indicates the diverse and distinctive recognition by T cells and antibodies of this envelope glycoprotein by cattle, the natural host of BHV-1.
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Temporal mapping of transcripts in human herpesvirus-7
Transcription of human herpesvirus-7 (HHV-7) in cultures of productively infected T-cells was studied. Transcription of HHV-7 was regulated by the typical herpesvirus cascade in which α, β and γ genes are sequentially transcribed. Transcripts of U10, U14, U18, U31, U39, U41, U42, U53, U73 and U89/90 were detected 3 h after infection and were not inhibited by the absence of protein synthesis and therefore were α functions. U19 and U18/20 were β genes; their transcription was inhibited by cycloheximide but not by phosphonoacetate, an inhibitor of DNA synthesis. U60/66 and U98/100 were γ genes since their spliced transcripts were not detected in cells treated with phosphonoacetate. HHV-7 transcription was regulated by complex mechanisms, which involve the temporal coordinated activation of specific viral promoters and post-transcriptional processing. Splice mechanisms were also temporally regulated. Transcription of U89/90 pre-mRNA and splice took place simultaneously in the immediate-early phase. On the other hand, U16/17 pre-mRNA was synthesized with typical α kinetics, but the spliced product was regulated as a β function. Likewise, the primary transcripts of U60/66 and U98/100 were α and β, respectively, but both spliced products were synthesized in the late phase of virus replication. Finally, HHV-7 supported a bona fide latent infection in the adult population, since viral transcripts were not detected in peripheral blood mononuclear cells of healthy donors infected with HHV-7.
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Volumes and issues
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