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Volume 88,
Issue 9,
2007
Volume 88, Issue 9, 2007
- Review
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- Animal
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- RNA viruses
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Robust production of infectious viral particles in Huh-7 cells by introducing mutations in hepatitis C virus structural proteins
Recently, the characterization of a cell culture system allowing the amplification of an authentic virus, named hepatitis C virus cell culture (HCVcc), has been reported by several groups. To obtain higher HCV particle productions, we investigated the potential effect of some amino acid changes on the infectivity of the JFH-1 isolate. As a first approach, successive infections of naïve Huh-7 cells were performed until high viral titres were obtained, and mutations that appeared during this selection were identified by sequencing. Only one major modification, N534K, located in the E2 glycoprotein sequence was found. Interestingly, this mutation prevented core glycosylation of E2 site 6. In addition, JFH-1 generated with this modification facilitated the infection of Huh-7 cells. In a second approach to identify mutations favouring HCVcc infectivity, we exploited the observation that a chimeric virus containing the genotype 1a core protein in the context of JFH-1 background was more infectious than wild-type JFH-1 isolate. Sequence alignment between JFH-1 and our chimera, led us to identify two major positions, 172 and 173, which were not occupied by similar amino acids in these two viruses. Importantly, higher viral titres were obtained by introducing these residues in the context of wild-type JFH-1. Altogether, our data indicate that a more robust production of HCVcc particles can be obtained by introducing a few specific mutations in JFH-1 structural proteins.
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Efficient infection of tree shrew (Tupaia belangeri) with hepatitis C virus grown in cell culture or from patient plasma
More LessThe generation of a new, cost-effective, non-primate, small-animal model would greatly facilitate research into hepatitis C virus (HCV) pathogenesis and the development of novel therapeutic and preventative technologies to control the increasing HCV threat to public health. Native HCV from patient plasma and HCV grown in cell culture (HCVcc) were used to inoculate adult tree shrews. Each animal was inoculated with one HCV genotype. Alanine aminotransferase (ALT) levels, HCV RNA and viral load were determined in the animals before and after inoculation. For native HCV, 16/18 inoculated tree shrews (89 %) became infected; 12/16 (75 %) of these animals became chronically infected, whilst infection was resolved in the remaining four (25 %). For HCVcc, infection occurred in 10/12 inoculated tree shrews (83 %) and chronic infection was observed in two of these animals. HCVcc from Huh7 cells showed a higher infectivity than that from HeLa cells. The animals inoculated with inadequate amounts of HCV were not infected in either native HCV or HCVcc experiments. Peak viral loads reached 103–105 international units ml−1 in chronically infected animals. ALT level changes reflected the normal fluctuation range in most animals. Thus, tree shrews without immunosuppression can be infected efficiently by native HCV and HCVcc when the animal is inoculated with an adequate amount of single-genotype HCV.
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Increasing genetic diversity of hepatitis C virus in haemophiliacs with human immunodeficiency virus coinfection
Patients with inherited bleeding disorders who received clotting factor concentrates before 1987 have high rates of hepatitis C virus (HCV) or HCV/human immunodeficiency virus (HIV) infection. To determine whether the persistent nature of HIV affects the genetic diversity of HCV by less selective pressure through the immunosuppression of HIV/HCV-coinfected patients, both the change of genetic diversity and selective pressure were examined in the HCV envelope genes (E1 and E2) of 325 genotype 1a subclones from eight HIV-positive and five HIV-negative patients with two time points (more than 6 years apart). To infer the genetic diversity of HCV in each patient, we used two approaches. One method was to estimate the difference of total evolutionary distances in the phylogenetic tree between the two time points, and another was to estimate the changes of genetic diversity along the time based on the coalescence theory. The two results indicate that the HIV-positive group has significantly more diverse population structure than the HIV-negative group. A comparative analysis of the synonymous and non-synonymous substitutions found that the HIV-positive group was subject to less selective pressure than the HIV-negative group. In conclusion, HIV-positive patients would have a more diversified HCV population than HIV-negative patients due to less selective pressure from the immune system.
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Enterovirus surveillance reveals proposed new serotypes and provides new insight into enterovirus 5′-untranslated region evolution
Human enteroviruses are currently grouped into five species Human enterovirus A (HEV-A), HEV-B, HEV-C, HEV-D and Poliovirus. During surveillance for enteroviruses serologically non-typable enterovirus strains were found from acute flaccid paralysis patients and healthy individuals. In this study, we report isolates of recently described enterovirus types EV76 and EV90 of HEV-A species and characterize two new enterovirus type candidates, EV96 and EV97, to species HEV-C and HEV-B, respectively. Analysis of partial 3D regions of EV96 strains revealed sequence divergence consistent with several recombination events between EV96, other HEV-C viruses and polioviruses. Phylogenetic analysis of all available 5′-untranslated region sequences of human entero- and rhinovirus prototype strains and 10 simian enterovirus strains suggested interspecies recombination involving this region.
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Attachment and internalization of feline infectious peritonitis virus in feline blood monocytes and Crandell feline kidney cells
More LessIn this study, kinetics of attachment and internalization of feline infectious peritonitis virus (FIPV) serotype I strain Black and serotype II strain 79-1146 were determined in feline monocytes from two cats and in Crandell feline kidney (CrFK) cells. Attached FIPV I (Black) particles were observed on almost all monocytes. Within 1 h, 17 particles were bound per cell and, within 1 min, 89 % of the bound particles were internalized. For FIPV II (79-1146), attachment was observed on 66 and 95 % of all monocytes from the two cats. After 1 h, respectively five and 20 particles were bound per cell (all cells considered). Within 1 min, 60 % of the bound particles were internalized. Internalization in monocytes was efficient and proceeded via endocytosis. In CrFK cells, attachment and internalization were less efficient, especially for FIPV I (Black), so this cell line is not suitable for studying FIPV entry.
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Functional consequences of attenuating mutations in the haemagglutinin–neuraminidase, fusion and polymerase proteins of a wild-type mumps virus strain
Wild-type mumps viruses (MuVs) are highly neurotropic and, prior to widespread vaccination programmes, were a major cause of viral meningitis and encephalitis in most developed countries. At present, there are no markers for virus attenuation, apart from the failure of a passaged isolate to produce clinical symptoms in vaccinees. Indeed, some MuV vaccines have retained residual neurovirulence properties and have caused aseptic meningitis in vaccinees. Three amino acid changes associated with the neuroattenuation of a wild-type MuV strain were identified previously. This study evaluated the impact of these changes on the function of the respective proteins. The data demonstrated that the Ser→Asp amino acid substitution at position 466 in the haemagglutinin–neuraminidase protein resulted in decreased receptor binding and neuraminidase activity, the Ala/Thr→Thr selection in the fusion protein resulted in decreased fusion activity, and the Ile→Val substitution in the polymerase resulted in increased replicative/transcriptional activity. These data suggest a polygenic component (i.e. specific and inter-related roles of these amino acid changes) to MuV neuroattenuation.
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Cis-acting elements in the antigenomic promoter of Nipah virus
More LessGenome synthesis in paramyxoviruses, including Nipah virus (NiV), is controlled by sequence elements that reside in the non-coding nucleotides at the 5′-trailer (3′-antigenomic) end that make up the antigenomic promoter (AGP). Using a chloramphenicol acetyl transferase-based plasmid-driven minigenome system, the terminal 96 nt of NiV AGP were first mutagenized in blocks of three hexamers to enable broad mapping of the minigenome functional regions. This was followed by further dissection of these functional regions to define the cis-acting elements contained therein. Results based on RNA analysis and reporter gene activity identified a bipartite promoter structure similar to that seen in related viruses, but with some distinct differences: in NiV, each of the two discrete replication control elements was bimodal, characterized by a critical conserved region (nt 1–12 and 79–91) and a contiguous non-conserved region (nt 13–36 and 73–78), which appeared less important. The regulatory role of these less critical regions was underscored by the use of a two-step mutation strategy, which revealed the additive detrimental effect of substitutions in this part of the terminal element. The structure and sequence characteristics of the internal control element was also different: it involved four contiguous hexamers, and the region encompassing three of these (nt 79–96, corresponding to hexamers 14, 15 and 16), although analogous in position to the equivalent element in the Sendai virus AGP, was characterized by the distinct 5′-(GNNNUG)14–15(GNNNNN)16 motif.
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Local immune response to respiratory syncytial virus infection is diminished in senescence-accelerated mice
More LessThe effect of ageing on the local defence system against respiratory syncytial virus (RSV) infection was investigated using an aged mouse model of the senescence-accelerated mouse (SAM) strain P1. Following intranasal infection with RSV, SAM-P1 mice showed a marked loss in weight, with elevated virus growth in the lungs and prolonged virus shedding. The increased susceptibility to RSV infection was associated mainly with diminished cellular immunity by local virus-specific cytotoxic T lymphocytes and natural killer cells. The deficiency in cellular immune responses was due to a lack of clonal expansion of CD4+ and CD8+ T lymphocytes, together with an imbalance of T-helper type 1 (Th1)/Th2 cytokine production in the respiratory tract, including the lungs. Furthermore, the production of virus-specific local IgA antibody was restrained. Prolonged virus loading in the lungs of SAM-P1 mice caused a massive infiltration of CD16+/32+ inflammatory cells, which was one factor responsible for severe pneumonia. The adoptive transfer of immune-competent spleen cells achieved an appreciable protection for SAM-P1 mice against RSV challenge infection. These results suggested that age-related immune dysfunction, especially defects in cellular immune responses, accounts for the increased morbidity and mortality in RSV infection of the elderly.
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Modifications of the PSAP region of the matrix protein lead to attenuation of vesicular stomatitis virus in vitro and in vivo
More LessThe matrix (M) protein of vesicular stomatitis virus (VSV) is a multi-functional protein involved in virus assembly, budding and pathogenesis. The 24PPPY27 late (L) domain of the M protein plays a key role in virus budding, whereas amino acids downstream of the PPPY motif contribute to host protein shut-off and pathogenesis. Using a panel of 37PSAP40 recombinant viruses, it has been demonstrated previously that the PSAP region of M does not possess L-domain activity similar to that of PPPY in BHK-21 cells. This study reports the unanticipated finding that these PSAP recombinants were attenuated in cell culture and in mice compared with control viruses. Indeed, PSAP recombinant viruses exhibited a small-plaque phenotype, reduced CPE, reduced levels of activated caspase-3, enhanced production of IFN-β and reduced titres in the lungs and brains of infected mice. In particular, recombinant virus M6PY>A4-R34E was the most severely attenuated, exhibiting little or no CPE in cell culture and undetectable titres in the lungs and brains of infected mice. These findings indicate an important role for the PSAP region (aa 33–44) of the M protein in the pathology of VSV infection and may have implications for the development of VSV as a vaccine and/or oncolytic vector.
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Virus-associated host CD62L increases attachment of human immunodeficiency virus type 1 to endothelial cells and enhances trans infection of CD4+ T lymphocytes
More LessPrevious studies have identified several host-derived cell-surface proteins incorporated within emerging human immunodeficiency virus type 1 (HIV-1) particles. Some of these molecules play a role in different steps of the virus life cycle and are often advantageous for the virus. We report here that the leukocyte L-selectin (also called CD62L) remains functional when inserted within the envelope of HIV-1. Indeed, we demonstrate that adsorption of virions to endothelial cells is enhanced upon acquisition of host-derived CD62L. The more important binding of CD62L-bearing HIV-1 particles resulted in a more efficient virus transmission to CD4+ T lymphocytes. Capture and eventual transfer of such CD62L-bearing virions by the endothelium could play a role in the pathogenesis of HIV-1 infection.
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Effects of feline immunodeficiency virus on feline monocyte-derived dendritic cells infected by spinoculation
More LessDuring type 1 human immunodeficiency virus infection, not only can dendritic cells (DCs) prime T cells against the virus, but they can also infect them in trans. Feline AIDS is caused by feline immunodeficiency virus (FIV) and is considered a model for the human illness because the two diseases have many features in common. Little is known about the interaction of feline DCs with FIV; therefore, this study attempts to tackle such an issue. Infection of feline monocyte-derived DCs (MDDCs) was attempted by spinoculation with FIV strains Petaluma (FIV-Pet) and M2. FIV-Pet was released rapidly in the supernatants of both infected MDDCs and activated T cells after spinoculation. It is shown that FIV-Pet was produced by MDDCs by monitoring viral content in the supernatants of infected MDDCs, by intracellular staining for p25 and by showing its cytopathic effect. Although activated T cells were better substrates for FIV replication, leading to prolonged viral shedding, both immature MDDCs and MDDCs matured with lipopolysaccharide supported virus production, mostly during the first 2 days after infection. At later times, FIV induced syncytium formation by MDDCs. Concerning the FIV receptors, MDDCs were shown to be CD134-negative and CXCR4-positive, a phenotype compatible with permissiveness to FIV-Pet. These results also suggest that maturation is not hampered by FIV infection and that virus exposure itself does not induce MDDC maturation. It is also shown that infected MDDCs can infect activated PBMCs efficiently in trans. It is concluded that MDDCs can be infected by FIV, although infection does not appear to influence their functionality.
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Establishment of productively infected walleye dermal sarcoma explant cells
More LessWalleye dermal sarcoma virus (WDSV) is a complex retrovirus associated with dermal sarcomas in walleye fish. Virus expression is tightly regulated and limited to accessory gene transcripts throughout tumour development. During tumour regression, this regulation is lost and the replication of virus is greatly enhanced. Cultured walleye fibroblasts infected in vitro do not produce significant quantities of infectious virus. Tissue culture cells established by explantation of tumour cells were found to harbour WDSV provirus and to express accessory and structural proteins. The sequence of the provirus showed little variation from a previous WDSV isolate. Retroviral particles were isolated from supernatants from these cells and were able to transfer infection to uninfected walleye fibroblasts. In addition to the virus present in supernatants, much of the virus was cell associated and liberated only by sonication. This virus was found at internal cellular membranes, including mitochondria, and was infectious.
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A novel virus isolated from the aphid Brevicoryne brassicae with similarity to Hymenoptera picorna-like viruses
More LessA novel virus, Brevicoryne brassicae virus (BrBV), has been identified in the cabbage aphid using a method based on the random amplification of encapsidated RNA. The complete sequence of the RNA genome of BrBV has been determined. The positive-strand genomic RNA is 10 161 nt, excluding the 3′ poly(A) tail, and contains a single open reading frame (positions 793–9744) encoding a putative polyprotein of 2983 aa. The N-terminal part of the polyprotein shows similarity with the structural proteins of iflaviruses. The C-terminal part possesses consensus sequences of the helicase, cysteine protease and RNA-dependent RNA polymerase similar to those of iflaviruses and other picorna-like viruses. The highest sequence similarity observed was with iflaviruses from honeybee and an endoparasitic wasp. Replication and transmission of BrBV was not dependent on endoparasitic wasp infestation of the aphids.
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- DNA viruses
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Structure of the C-terminal head domain of the fowl adenovirus type 1 long fiber
More LessAvian adenovirus CELO (chicken embryo lethal orphan virus, fowl adenovirus type 1) incorporates two different homotrimeric fiber proteins extending from the same penton base: a long fiber (designated fiber 1) and a short fiber (designated fiber 2). The short fibers extend straight outwards from the viral vertices, whilst the long fibers emerge at an angle. In contrast to the short fiber, which binds an unknown avian receptor and has been shown to be essential to the invasiveness of this virus, the long fiber appears to be unnecessary for infection in birds. Both fibers contain a short N-terminal virus-binding peptide, a slender shaft domain and a globular C-terminal head domain; the head domain, by analogy with human adenoviruses, is likely to be involved mainly in receptor binding. This study reports the high-resolution crystal structure of the head domain of the long fiber, solved using single isomorphous replacement (using anomalous signal) and refined against data at 1.6 Å (0.16 nm) resolution. The C-terminal globular head domain had an anti-parallel β-sandwich fold formed by two four-stranded β-sheets with the same overall topology as human adenovirus fiber heads. The presence in the sequence of characteristic repeats N-terminal to the head domain suggests that the shaft domain contains a triple β-spiral structure. Implications of the structure for the function and stability of the avian adenovirus long fiber protein are discussed; notably, the structure suggests a different mode of binding to the coxsackievirus and adenovirus receptor from that proposed for the human adenovirus fiber heads.
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The CD4+ T-cell response to adenovirus is focused against conserved residues within the hexon protein
Adenovirus is a significant pathogen in immunocompromised patients and is widely utilized as a gene delivery vector, so a detailed understanding of the human immune response to adenovirus infection is critical. This study characterized the adenovirus-specific CD4+ T-cell response of healthy donors by incubation with whole virus or with individual hexon and fiber proteins. Adenovirus-specific CD4+ T cells averaged 0.26 % of the CD4+ T-cell pool and were detectable in all donors. T cells recognizing the highly conserved hexon protein accounted for 0.09 %, whereas no response was observed against the fiber protein. A panel of hexon-specific CD4+ T-cell clones was generated and shown to lyse targets infected with adenovirus from different serotypes and species. Three CD4 T-cell epitopes are described, which map to highly conserved regions of the hexon protein.
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Systematic analysis of longitudinal serological responses of pigs infected experimentally with African swine fever virus
More LessThe protective immune response to African swine fever virus (ASFV) includes both cellular and serological components. In this study, the role of antibodies in the pathogenicity and diagnosis of African swine fever (ASF) was explored. Accordingly, total and Ig isotype antibody responses against the 12 viral proteins previously demonstrated to be the main targets of serological immunity were evaluated in longitudinally collected sera from pigs infected experimentally with the non-pathogenic ASFV/NH/P68 isolate. Strong total IgG antibody responses were observed against viral proteins E183L/p54, K205R/‘unassigned’, A104R/histone-like and B602L/‘unassigned’; therefore, IgM, IgG1 and IgG2 responses to these proteins were also determined. One protein stimulating IgM (K205R) may have practical potential for the detection of recently infected animals. There was a clear trend towards an IgG1 response to all of the proteins. This may reflect a dominant Th2-controlled immune response. In order to identify possible correlations between these serological responses and the pathogenesis of ASF, total IgG responses to the 12 recombinant proteins were compared in asymptomatic and chronically infected animals. For the proteins NP419L/DNA ligase, CP312R, B646L/p73, K196R/thymidine kinase and K205R, the antibody titres were significantly higher in animals developing lesions. One exception was the antibody response to the A104R/histone-like protein, which was higher in asymptomatic than in chronically infected pigs, suggesting that antibodies against this protein might be an indicator of an effective immune response or that this response is somehow involved in protection.
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An activation-defective mutant of the human cytomegalovirus IE2p86 protein inhibits NF-κB-mediated stimulation of the human interleukin-6 promoter
More LessThe IE2p86 protein of human cytomegalovirus is an essential activator of early- and late-phase viral gene expression. Whilst IE2p86 activates expression of a number of cellular genes, it also represses certain cellular genes, particularly those activated by nuclear factor κB (NF-κB). As the interleukin-6 (IL-6) promoter can be activated by both NF-κB and IE2p86, it was examined whether there is competition between these two factors. Here, it is reported that both wild-type and mutant IE2p86 can block activation of the IL-6 promoter in response to interleukin-1β. By using an artificial activator in which the activation domain of NF-κB is directed to the promoter by the GAL4 DNA-binding domain, it is shown that the mutant form of IE2p86 can inhibit NF-κB-mediated activation at a step subsequent to promoter recruitment. These data therefore suggest a novel mechanism for inhibition of NF-κB by IE2p86.
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Anti-IE1 CD4+ T-cell clones kill peptide-pulsed, but not human cytomegalovirus-infected, target cells
More LessCellular immunity plays a major role in the control of human cytomegalovirus (HCMV) infection. CD4+ T lymphocytes have been shown to contribute to this function but their precise role is a matter of debate. Although CD4+ T cells have been shown to kill target cells through the perforin/granzyme pathway, whether HCMV-specific CD4+ T cells are capable of killing HCMV-infected targets has not yet been documented. In the present paper, we have taken advantage of well established cellular reagents to address this issue. Human CD4+ T-cell clones specific for the major immediate-early protein IE1 were shown to perform perforin-based cytotoxicity against peptide-pulsed targets. However, when tested on infected anitgen presenting cell targets, cytotoxicity was not detectable, although gamma interferon (IFN-γ) production was significant. Furthermore, cytotoxicity against peptide-pulsed targets was inhibited by HCMV infection, whereas IFN-γ production was not modified, suggesting that antigen processing was not altered. Remarkably, degranulation of CD4+ T cells in the presence of infected targets was significant. Together, our data suggest that impaired cytotoxicity is not due to failure to recognize infected targets but rather to a mechanism specifically related to cytotoxicity.
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Sequence analysis of the equid herpesvirus 2 chemokine receptor homologues E1, ORF74 and E6 demonstrates high sequence divergence between field isolates
More LessEquid herpesvirus 2 (EHV-2), in common with other members of the subfamily Gammaherpesvirinae, encodes homologues of cellular seven-transmembrane receptors (7TMR), namely open reading frames (ORFs) E1, 74 and E6, which each show some similarity to cellular chemokine receptors. Whereas ORF74 and E6 are members of gammaherpesvirus-conserved 7TMR gene families, E1 is currently unique to EHV-2. To investigate their genetic variability, EHV-2 7TMRs from a panel of equine gammaherpesvirus isolates were sequenced. A region of gB was sequenced to provide comparative sequence data. Phylogenetic analysis revealed six ‘genogroups’ for E1 and four for ORF74, which exhibited approximately 10–38 and 11–27 % amino acid difference between groups, respectively. In contrast, E6 was highly conserved, with two genogroups identified. The greatest variation was observed within the N-terminal domains and other extracellular regions. Nevertheless, analysis of the number of non-synonymous (d N) and synonymous (d S) substitutions per site generally supported the hypothesis that the 7TMRs are under negative selective pressure to retain functionally important residues, although some site-specific positive selection (d N>d S) was also observed. Collectively, these data are consistent with transmembrane and cytoplasmic domains being less tolerant of mutations with adverse effects upon function. Finally, there was no evidence for genetic linkage between the different gB, E1, ORF74 and E6 genotypes, suggesting frequent intergenic recombination between different EHV-2 strains.
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