- Volume 91, Issue 7, 2010
Volume 91, Issue 7, 2010
- Review
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Porcine reproductive and respiratory syndrome virus entry into the porcine macrophage
Porcine reproductive and respiratory syndrome virus (PRRSV) emerged in the late 1980s and rapidly became one of the most significant viral pathogens in the swine industry. In vivo, the virus shows a very narrow cell tropism and targets specific subsets of porcine macrophages. The entry of PRRSV into its host cell is the first crucial step in infection and has been the focus of many fundamental studies. This review provides a comprehensive overview of the current knowledge on PRRSV entry into the porcine macrophage, covering virus binding, internalization and genome release, and integrates these findings into a general model of the entry process.
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- Animal
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- RNA viruses
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Practical evaluation of a mouse with chimeric human liver model for hepatitis C virus infection using an NS3-4A protease inhibitor
A small-animal model for hepatitis C virus (HCV) infection was developed using severe combined immunodeficiency (SCID) mice encoding homozygous urokinase-type plasminogen activator (uPA) transplanted with human hepatocytes. Currently, limited information is available concerning the HCV clearance rate in the SCID mouse model and the virion production rate in engrafted hepatocytes. In this study, several cohorts of uPA+/+/SCID+/+ mice with nearly half of their livers repopulated by human hepatocytes were infected with HCV genotype 1b and used to evaluate HCV dynamics by pharmacokinetic and pharmacodynamic analyses of a specific NS3-4A protease inhibitor (telaprevir). A dose-dependent reduction in serum HCV RNA was observed. At telaprevir exposure equivalent to that in clinical studies, rapid turnover of serum HCV was also observed in this mouse model and the estimated slopes of virus decline were 0.11–0.17 log10 h−1. During the initial phase of treatment, the log10 reduction level of HCV RNA was dependent on the drug concentration, which was about fourfold higher in the liver than in plasma. HCV RNA levels in the liver relative to human endogenous gene expression were correlated with serum HCV RNA levels at the end of treatment for up to 10 days. A mathematical model analysis of viral kinetics suggested that 1 g of the chimeric human liver could produce at least 108 virions per day, and this may be comparable to HCV production in the human liver.
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Hepatitis C virus core protein genotype 3a increases SOCS-7 expression through PPAR-γ in Huh-7 cells
More LessHepatitis C virus (HCV) core protein genotype 3a induces the expression of suppressor of cytokine signalling protein 7 (SOCS-7), which is partially involved in the development of insulin resistance. The aim of the present study was to investigate the mechanism through which the core protein regulates SOCS-7 expression. We have explored, in the in vitro model of Huh-7 cells expressing the HCV core protein of genotype 3a, whether the expression of SOCS-7 as well as of other members of the SOCS family (SOCS-1 and SOCS-3) was activated by the STAT3 pathway, using immunoblotting and real-time PCR upon alpha interferon (IFN-α) treatment. We found that, whilst IFN-α treatment induced STAT3 activation and consequently SOCS-1 and SOCS-3 upregulation in HCV genotype 3a core-expressing Huh-7 cells, SOCS-7 mRNA expression was independent of STAT3 and seemed to be modulated by peroxisome proliferator-activated receptor gamma (PPAR-γ) activity, as demonstrated by quantitative real-time PCR and immunoblot detection after treatment with the PPAR-γ agonist rosiglitazone or the PPAR-γ antagonist GW9262. In contrast to the other studied members of the SOCS family (1 and 3), which are regulated by STAT3 activation, SOCS-7 expression appears to be STAT3-independent and seems to be regulated instead by PPAR-γ. This is the first report proposing a molecular mechanism through which the HCV core protein (genotype 3a) modulates SOCS-7 expression.
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GB virus C quasispecies detected in plasma and lymphocyte subsets in a natural human infection
Genomic heterogeneity and quasispecies composition of GB virus C (GBV-C) within plasma and lymphocyte subsets in a naturally infected blood donor were investigated. For this purpose, fragments from the 5′ untranslated region (5′ UTR) and the E2 gene recovered from plasma, B and T lymphocytes, were cloned and sequenced. A total of 63 clones was analysed: 95.2 % of them (n=60) – obtained from plasma and cells – were assigned to genotype 2b, while only three derived from plasma corresponded to genotyope 3. The G215A transition within this region was present in 90.9 % of the clones from B lymphocytes, but absent in the remaining cell compartments (P<0.01). Apparently, most of the circulating GBV-C quasispecies in this blood donor were related to the viral population infecting CD8+ T cells, and B cells to a lesser extent. This is the first report showing the quasispecies nature of GBV-C in lymphocyte subsets within peripheral blood mononuclear cells.
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Replication of not-known-vector flaviviruses in mosquito cells is restricted by intracellular host factors rather than by the viral envelope proteins
Chimeric yellow fever virus 17D (YFV-17D) and dengue virus type 2 (DENV2) carrying the surface proteins of Modoc virus (MODV), a not-known-vector (NKV) flavivirus, replicated efficiently in mammalian (Vero-B) and mosquito (C6/36) cells, whereas MODV failed to replicate in mosquito cells. Transfection of C6/36 cells with MODV RNA did not result in virus replication; however, transfection of these mosquito cells with YFV-17D or DENV2 RNA did. The inability of NKV viruses (such as MODV) to infect and replicate in arthropod cells is thus not determined by the viral envelope, but by a post-entry event.
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Sites of feline coronavirus persistence in healthy cats
More LessFeline coronavirus (FCoV) is transmitted via the faecal–oral route and primarily infects enterocytes, but subsequently spreads by monocyte-associated viraemia. In some infected cats, virulent virus mutants induce feline infectious peritonitis (FIP), a fatal systemic disease that can develop in association with viraemia. Persistently infected, healthy carriers are believed to be important in the epidemiology of FIP, as they represent a constant source of FCoV, shed either persistently or intermittently in faeces. So far, the sites of virus persistence have not been determined definitely. The purpose of this study was to examine virus distribution and viral load in organs and gut compartments of specified-pathogen-free cats, orally infected with non-virulent type I FCoV, over different time periods and with or without detectable viraemia. The colon was identified as the major site of FCoV persistence and probable source for recurrent shedding, but the virus was shown also to persist in several other organs, mainly in tissue macrophages. These might represent additional sources for recurrent viraemia.
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Identification of key amino acid residues required for horseshoe bat angiotensin-I converting enzyme 2 to function as a receptor for severe acute respiratory syndrome coronavirus
More LessAngiotensin-I converting enzyme 2 (ACE2) is the receptor for severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV). A previous study indicated that ACE2 from a horseshoe bat, the host of a highly related SARS-like coronavirus, could not function as a receptor for SARS-CoV. Here, we demonstrate that a 3 aa change from SHE (aa 40–42) to FYQ was sufficient to convert the bat ACE2 into a fully functional receptor for SARS-CoV. We further demonstrate that an ACE2 molecule from a fruit bat, which contains the FYQ motif, was able to support SARS-CoV infection, indicating a potentially much wider host range for SARS-CoV-related viruses among different bat populations.
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Murine norovirus-1 3Dpol exhibits RNA-dependent RNA polymerase activity and nucleotidylylates on Tyr of the VPg
We investigated the roles and biochemical properties of recombinant murine norovirus-1 (MNV-1) 3Dpol in RNA synthesis and virus genome-linked protein (VPg) nucleotidylylation. We therefore expressed VPg and 3Dpol of MNV-1 in Escherichia coli. MNV-1 3Dpol exhibited RNA-dependent RNA polymerase (RdRp) activity in vitro with poly(A) RNA as a template and MnCl2 as a cofactor. MNV-1 3Dpol demonstrated optimum RNA-synthesis activity at pH 7.4 and 37 °C in the absence of a primer. Further, VPg was guanylylated by MNV-1 3Dpol in the presence of MnCl2 in a template-independent manner. The guanylylation reaction conducted with VPg substitution mutants (Y26F, Y40F, Y45F and Y117F) and a deletion mutant (Δ117–124) indicated that Tyr117 was the probable target site of guanylylation. Homopolymeric RNAs did not enhance VPg guanylylation, whereas in vitro-transcribed (−) subgenomic (SG) and (+)SG RNA enhanced VPg guanylylation by 9.2 and 3.2 times, respectively. Within (−)SG RNA, the (−)ORF3 region played a critical role in enhancing VPg guanylylation, suggesting that the MNV-1 ORF3 region of negative-strand RNA contains a cis-acting element that stimulates 3Dpol-mediated VPg guanylylation.
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Development and characterization of promoterless helper RNAs for the production of alphavirus replicon particle
More LessAlphavirus-based replicon systems are frequently used as preclinical vectors and as antigen discovery tools, and they have recently been assessed in clinical vaccine trials. Typically, alphavirus replicon RNAs are delivered within virus-like replicon particles (VRP) that are produced following transfection of replicon RNA and two helper RNAs into permissive cells in vitro. The non-structural proteins expressed from the replicon RNA amplify the replicon RNA in cis and the helper RNAs in trans, the latter providing the viral structural proteins necessary to package the replicon RNA into VRP. Current helper RNA designs incorporate the alphavirus 26S promoter to direct the transcription of high levels of structural gene mRNAs. We demonstrate here that the 26S promoter is not required on helper RNAs to produce VRP and propose that such promoterless helper RNAs, by design, reduce the probability of generating replication-competent virus that may otherwise result from RNA recombination.
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Role of heat-shock protein 90 in hepatitis E virus capsid trafficking
p239 is a virus-like particle constituted from hepatitis E virus (HEV) recombinant proteins. It can be used as a surrogate for HEV and as an investigative tool to study cellular interactions because of its ability to adsorb to and penetrate HepG2 cellular membranes. Our objective was to use p239 to define the role of HEV capsid proteins during the early stages of infection. Pull-down and MALDI-TOF MS experiments identified three host-cell proteins, Grp 78/Bip, α-tubulin and heat-shock protein 90 (HSP90), and the latter was investigated further. Antibodies to p239 alone or HSP90 alone could detect p239 or HSP90, suggesting the formation of a complex between p239 and HSP90. In the HepG2 cell, geldanamycin (GA), an HSP90-specific inhibitor, blocked intracellular transportation of p239, but had no effect on the binding and cellular entry of p239, suggesting that HSP90 was important for HEV capsid intracellular transportation. RT-PCR results showed that the efficiency of wild-type HEV infection was inhibited significantly by GA treatment, suggesting the importance of HSP90 in virus infectivity. It was concluded that HSP90 plays a crucial role in the intracellular transportation of viral capsids in the early stage of HEV infection.
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Mutations in the NS1 C-terminal tail do not enhance replication or virulence of the 2009 pandemic H1N1 influenza A virus
The ‘classical’ swine H1N1 influenza A virus lineage was established after the devastating 1918 human pandemic virus entered domestic pig herds. A descendent of this lineage recently re-emerged in humans as the 2009 pandemic H1N1 virus. Adaptation in pigs has led to several changes in the multifunctional viral NS1 protein as compared with the parental 1918 virus, most notably a K217E substitution that abolishes binding to host Crk/CrkL signalling adapters, and an 11 aa C-terminal truncation. Using reverse genetics, we reintroduced both these features into a prototype 2009 H1N1 strain, A/California/04/09. Restoration of Crk/CrkL binding or extension of NS1 to 230 aa had no impact on virus replication in human or swine cells. In addition, minimal effects on replication, pathogenicity and transmission were observed in mouse and ferret models. Our data suggest that the currently circulating 2009 H1N1 virus is optimized to replicate efficiently without requiring certain NS1 functions.
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Vaccination with whole inactivated virus vaccine affects the induction of heterosubtypic immunity against influenza virus A/H5N1 and immunodominance of virus-specific CD8+ T-cell responses in mice
It was recently shown that the use of an experimental subunit vaccine protected mice against infection with a human A/H3N2 influenza virus, but consequently affected the induction of heterosubtypic immunity to a highly pathogenic A/H5N1 influenza virus, which was otherwise induced by the A/H3N2 infection. As whole inactivated virus (WIV) vaccines are widely used to protect against seasonal influenza and also contain inner viral proteins such as the nucleoprotein (NP), the potential of a WIV vaccine to induce protective immunity against infection was tested with a homologous A/H3N2 (A/Hong Kong/2/68) and a heterosubtypic A/H5N1 influenza virus (A/Indonesia/5/05). As expected, the vaccine afforded protection against infection with the A/H3N2 virus only. In addition, it was demonstrated that the use of WIV vaccine for protection against A/H3N2 infection affected the induction of heterosubtypic immunity that was otherwise afforded by A/H3N2 influenza virus infection. The reduction in protective immunity correlated with changes in the immunodominance patterns of the CD8+ T-cell responses directed to the epitopes located in the acid polymerase subunit of the viral RNA polymerase (PA224–233) and the NP (NP366–374). In unvaccinated mice that experienced infection with the A/H3N2 influenza virus, the magnitude of the CD8+ T-cell response to both peptides was similar on secondary infection with A/H5N1 influenza virus. In contrast, prior vaccination with WIV affected the immunodominance pattern and skewed the response after infection with influenza virus A/Indonesia/5/05 towards a dominant NP366–374-specific response. These findings may have implications for vaccination strategies aimed at the induction of protective immunity to seasonal and/or pandemic influenza.
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High yields of influenza A virus in Madin–Darby canine kidney cells are promoted by an insufficient interferon-induced antiviral state
More LessBecause of their high susceptibility to infection with various influenza virus strains, Madin–Darby canine kidney (MDCK) cells have been widely used as a substrate for influenza virus isolation and vaccine production. However, MDCK cells are also interferon (IFN) competent, and the type I IFN response is commonly thought to be a factor strongly inhibiting virus replication. Therefore, the inhibition of influenza virus replication by IFN signalling was analysed for an adherent MDCK cell line used in vaccine manufacturing. Depending on the respective virus strain, different levels of IFN induction and a corresponding upregulation of the IFN-induced myxovirus resistance protein 1 (Mx1) were observed. Suppression of IFN induction by transient expression of the viral non-structural protein 1 protein enhanced replication of an influenza virus lacking NS1, but not wild-type strains. In agreement with this, stimulation of cells with MDCK cell-derived IFN prior to infection resulted only in a decrease in replication rate, and not in a change of final yields for wild-type influenza viruses. This lack of IFN-induced antiviral activity correlated with missing anti-influenza activity of MDCK Mx proteins. No inhibitory effect on viral polymerase activity was found for canine Mx1 (cMx1) and cMx2 in minireplicon assays. In conclusion, in MDCK cells, IFN expression is not a limiting factor for influenza virus replication and this might partially be caused by a lack of anti-influenza activity of canine Mx proteins.
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Generation of E3-deleted canine adenovirus type 2 expressing the Gc glycoprotein of Seoul virus by gene insertion or deletion of related terminal region sequences
Seoul virus (SEOV) is one of the four hantaviruses known to cause haemorrhagic fever with renal syndrome. The medium genome segment encodes the Gn/Gc glycoproteins of SEOV, which form the major structural part of the virus envelope. Gc and/or Gn are the candidate antigens of hantavirus for induction of a highly immunogenic response for hantavirus vaccine. In this study, the immune response induced by a replication-competent recombinant canine adenovirus type 2 expressing the Gc protein of SEOV was evaluated in BALB/c mice. Sera from immunized mice contained neutralizing antibodies that could specifically recognize SEOV and neutralize its infectivity in vitro. Moreover, the recombinant virus induced complete protection against an intensive infectious challenge with ∼1000 50 % infective doses for SEOV strain CC-2. Protective-level neutralizing antibodies were maintained for at least 20 weeks. This recombinant virus is therefore a potential alternative to the inactivated vaccine.
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Analysis of genetic diversity and molecular evolution of human group B rotaviruses based on whole genome segments
Group B rotavirus (GBR) is a rare enteric pathogen that causes severe diarrhoea, primarily in adults. Nearly full-length sequences of all 11 RNA segments were determined for human GBRs detected recently in India (IDH-084 in 2007, IC-008 in 2008), Bangladesh (Bang117 in 2003) and Myanmar (MMR-B1 in 2007), and analysed phylogenetically with the sequence data of GBRs reported previously. All RNA segments of GBR strains from India, Bangladesh and Myanmar showed >95 % nucleotide sequence identities. Among the 11 RNA segments, the VP6 and NSP2 genes showed the highest identities (>98 %), whilst the lowest identities were observed in the NSP4 gene (96.1 %), NSP5 gene (95.6 %) and VP8*-encoding region of the VP4 gene (95.9 %). Divergent or conserved regions in the deduced amino acid sequences of GBR VP1–VP4 and NSP1–NSP5 were similar to those in group A rotaviruses (GARs), and the functionally important motifs and structural characteristics in viral proteins known for GAR were conserved in all of the human GBRs. These findings suggest that, whilst the degree of genetic evolution may be dependent on each RNA segment, human GBR may have been evolving in a similar manner to GAR, associated with the similar functional roles of individual viral proteins.
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Rotavirus NSP5 orchestrates recruitment of viroplasmic proteins
More LessRotavirus genome replication and the first steps of virus morphogenesis take place in cytoplasmic viral factories, called viroplasms, containing four structural (VP1, VP2, VP3 and VP6) and two non-structural (NSP2 and NSP5) proteins. NSP2 and NSP5 have been shown to be essential for viroplasm formation and, when co-expressed in uninfected cells, to form viroplasm-like structures (VLS). In the present work, VLS formation was shown upon co-expression of NSP5 with the core protein VP2 despite the absence of NSP2, indicating a central role for NSP5 in VLS assembly. Since VP2 and NSP2 also induce NSP5 hyperphosphorylation, the possible correlation between VLS formation and the NSP5 phosphorylation status was investigated without evidence of a direct link. In VLS induced by NSP2, the polymerase VP1 was recruited, while the middle layer protein VP6 was not, forming instead tubular structures. On the other hand, VLS induced by VP2 were able to recruit both VP1 and VP6. More importantly, in VLS formed when NSP5 was expressed with both inducers, all viroplasmic proteins were found co-localized, resembling their distribution in viroplasms. Our results suggest a key role for NSP5 in architectural assembly of viroplasms and in recruitment of viroplasmic proteins. A new role for VP2 as an inducer of viroplasms and of NSP5 hyperphosphorylation is also described. These data may contribute to the understanding of rotavirus morphogenesis.
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Convalescent phase sera from children infected with G12 rotavirus cross-neutralize rotavirus strains belonging to the Wa genogroup
More LessThe emergence of G12 rotaviruses raises questions about the ability of candidate vaccines in providing protection against such emerging genotypes. Therefore, we assessed cross-neutralization against four reference rotavirus strains namely Wa (G1P[8]), DS-1 (G2P[4]), 116E (G9P[11]) and RV024 (G12P[6]) using paired sera from 28 children infected with G1P[8], G2P[4], G9P[6/8] or G12P[6] genotypes. Convalescent sera of G12P[6]-infected children demonstrated heterotypic response against 116E and Wa strains (50 and 33.3 %). In contrast, none of the four G2P[4]-infected children seroconverted against Wa or RV024 rotaviruses. The geometric mean neutralizing antibody titre in convalescent sera of G12P[6]-infected children was eightfold higher against strains belonging to the Wa genogroup (i.e. G1, G9 and G12 rotavirus) than against strains belonging to the DS-1 genogroup (G2 rotavirus). In conclusion, this study demonstrates that neutralization in part may be genogroup specific, and thus a monovalent vaccine based on the Wa genogroup is likely to protect against the G12 rotaviruses.
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Implications of the release of high-mobility group box 1 protein from dying cells during human immunodeficiency virus type 1 infection in vitro
More LessPlasma levels of high-mobility group box 1 protein (HMGB1) are elevated during the course of human immunodeficiency virus type 1 (HIV-1) infection and the molecule has an impact on virus replication. This study investigated the mode of cell death and release of HMGB1 during HIV-1 infection in vitro. MT4 cells and primary CD4+ T cells were infected with HIV-1 isolates, and HMGB1 release was monitored in relation to cytopathic effects (CPE) and apoptosis. HMGB1 release from cells was analysed by Western blotting. For MT4 cells, an enzyme-linked immunosorbent spot (ELISPOT) assay was adapted to measure the release during necrosis. Lactate dehydrogenase (LDH) activity was quantified using a commercial assay. Flow cytometry was used to determine the level of infection and apoptosis. MT4 cells were ≥90 % infected at 48 h post-infection (p.i.). CPE was first observed at 60 h and correlated with release of HMGB1, LDH activity and caspase-3 (C3) activation. HMGB1 spots were clearly detected by ELISPOT assay at 72 h p.i. Annexin V and C3 staining showed that apoptosis was substantially involved in HIV-1-related cell death. Addition of Z-VAD (a caspase inhibitor) in a single dose at 24 or 40 h p.i. decreased both the number of caspase-positive cells and the release of HMGB1. Infection of primary CD4+ T cells showed a 22 % (median) infection rate at 96 h. Related CPE corresponded to LDH and HMGB1 release. Both necrosis and apoptosis contributed to HMGB1 liberation during HIV-1-induced cell death and the protein could induce tumour necrosis factor-α release from peripheral mononuclear blood cells. These data imply that passive HMGB1 release contributes to the excessive immune activation characteristic of HIV-1 pathogenesis.
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Genetic diversity of simian lentivirus in wild De Brazza’s monkeys (Cercopithecus neglectus) in Equatorial Africa
De Brazza’s monkeys (Cercopithecus neglectus) are non-human primates (NHP) living in Equatorial Africa from South Cameroon through the Congo-Basin to Uganda. As most of the NHP living in sub-Saharan Africa, they are naturally infected with their own simian lentivirus, SIVdeb. Previous studies confirmed this infection for De Brazza’s from East Cameroon and Uganda. In this report, we studied the genetic diversity of SIVdeb in De Brazza’s monkeys from different geographical areas in South Cameroon and from the Democratic Republic of Congo (DRC). SIVdeb strains from east, central and western equatorial Africa form a species-specific monophyletic lineage. Phylogeographic clustering was observed among SIVdeb strains from Cameroon, the DRC and Uganda, but also among primates from distinct areas in Cameroon. These observations suggest a longstanding virus–host co-evolution. SIVdeb prevalence is high in wild De Brazza’s populations and thus represents a current risk for humans exposed to these primates in central Africa.
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- DNA viruses
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Residue 752 in DNA polymerase of equine herpesvirus type 1 is non-essential for virus growth in vitro
More LessA single amino acid variation in the equine herpesvirus type 1 (EHV-1) DNA polymerase (Pol) (D752/N752) determines its neuropathogenic potential. Here, an EHV-1 strain RacL11 mutant with a deletion of Pol residue 752 was constructed. The deletion virus was then repaired to encode D752 or N752, respectively. The Δ752 mutant virus replicated with kinetics indistinguishable from those of D752 and N752 viruses. In addition, we could demonstrate that the deletion mutant was significantly more resistant to aphidicolin, a drug targeting Pol, compared with the N752 but not the D752 variant. In equine peripheral blood mononuclear cells, no significant difference was detected between the mutants with respect to cellular tropism or virus replication. The results demonstrated that amino acid residue 752 in EHV-1 Pol is not required for virus growth, and that only the N752 mutation confers a drug-sensitive phenotype to the virus.
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Volumes and issues
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Volume 105 (2024)
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Volume 104 (2023)
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Volume 103 (2022)
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Volume 99 (2018)
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Volume 97 (2016)
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Volume 3 (1968)
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Volume 2 (1968)
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Volume 1 (1967)