- Volume 94, Issue 4, 2013
Volume 94, Issue 4, 2013
- Animal
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- RNA viruses
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Inter-species transmission of viral hemorrhagic septicemia virus (VHSV) from turbot (Scophthalmus maximus) to rainbow trout (Onchorhynchus mykiss)
More LessSuccessful viral infection is a complex mechanism, involving many host–pathogen interactions that developed during coevolution of host and pathogen, and often result in host-species specificity. Nevertheless, many viruses are able to infect several host species and sporadically cross species barriers. The viral hemorrhagic septicemia virus (VHSV), a rhabdovirus with high economic impact on the aquaculture industry, has developed an exceptionally wide host range across marine and freshwater environments. Transmission of VHSV between host species therefore represents a potential risk for aquaculture, which currently is not addressed in biosecurity managements. The objective of this study was to investigate the inter-species transmission potential of VHSV and evaluate whether infected marine wild fish pose a potential risk on marine cultured rainbow trout. A cohabitation infection trial with turbot as donor and rainbow trout as recipient host species was conducted. Turbot were intraperitoneally injected with either a marine-adapted (MA) or a trout-adapted (TA) VHSV isolate and subsequently grouped with naïve rainbow trout. Both VHSV isolates were able to replicate and cause mortality in turbot, while only the TA isolate was able to cross the species barrier and infect rainbow trout with fatal outcome. The results demonstrate that a marine fish species can function as reservoir and transmitter of TA VHSV isolates.
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Novel mutations in Marburg virus glycoprotein associated with viral evasion from antibody mediated immune pressure
More LessMarburg virus (MARV) and Ebola virus, members of the family Filoviridae, cause lethal haemorrhagic fever in humans and non-human primates. Although the outbreaks are concentrated mainly in Central Africa, these viruses are potential agents of imported infectious diseases and bioterrorism in non-African countries. Recent studies demonstrated that non-human primates passively immunized with virus-specific antibodies were successfully protected against fatal filovirus infection, highlighting the important role of antibodies in protective immunity for this disease. However, the mechanisms underlying potential evasion from antibody mediated immune pressure are not well understood. To analyse possible mutations involved in immune evasion in the MARV envelope glycoprotein (GP) which is the major target of protective antibodies, we selected escape mutants of recombinant vesicular stomatitis virus (rVSV) expressing MARV GP (rVSVΔG/MARVGP) by using two GP-specific mAbs, AGP127-8 and MGP72-17, which have been previously shown to inhibit MARV budding. Interestingly, several rVSVΔG/MARVGP variants escaping from the mAb pressure-acquired amino acid substitutions in the furin-cleavage site rather than in the mAb-specific epitopes, suggesting that these epitopes are recessed, not exposed on the uncleaved GP molecule, and therefore inaccessible to the mAbs. More surprisingly, some variants escaping mAb MGP72-17 lacked a large proportion of the mucin-like region of GP, indicating that these mutants efficiently escaped the selective pressure by deleting the mucin-like region including the mAb-specific epitope. Our data demonstrate that MARV GP possesses the potential to evade antibody mediated immune pressure due to extraordinary structural flexibility and variability.
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In vitro and in vivo replication of influenza A H1N1 WSN33 viruses with different M1 proteins
The M1 protein is a major structural protein that has multiple functions in various steps within the life cycle of the influenza A virus (IAV). However, little is currently known about the role of M1 in IAV replication in vivo and the associated pathogenesis. In this study, six isogenic H1N1 WSN33 viruses, constructed to express unique M1 proteins derived from various strains, subtypes or WSN33 itself, were tested to determine in vitro and in vivo functional exchangeability of M1 proteins in the replication and pathogenesis of the WSN33 virus. Despite five chimeric M1 viruses replicating to levels similar to those of the parental WSN33 virus in cell cultures, all M1 chimeras exhibited improved replication and enhanced virulence in mice when compared with the WSN33 virus. Interestingly, M1 proteins derived from swine viruses caused more severe clinical diseases than those from human or quail. These data indicate that the M1 protein is an important determinant of viral replication and pathogenic properties in mice, although the functions of M1 observed in vivo are not adequately reflected in simple infections of cultured cells. Chimeric M1 viruses that are variable in their clinical manifestations described here will aid future understanding of the role of M1 in IAV pathogenesis.
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- Phage
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Proteomic profiles and kinetics of development of bacteriophage T4 and its rI and rIII mutants in slowly growing Escherichia coli
Bacteriophage T4 survival in its natural environment requires adjustment of phage development to the slow bacterial growth rate or the initiation of mechanisms of pseudolysogeny or lysis inhibition (LIN). While phage-encoded RI and probably RIII proteins seem to be crucial players in pseudolysogeny and LIN phenomena, the identity of proteins involved in the regulation of T4 development in slowly growing bacteria has remained unknown. In this work, using a chemostat system, we studied the development of wild-type T4 (T4wt) and its rI (T4rI) and rIII (T4rIII) mutants in slowly growing bacteria, where T4 did not initiate LIN or pseudolysogeny. We determined eclipse periods, phage propagation times, latent periods and burst sizes of T4wt, T4rI and T4rIII. We also compared intracellular proteomes of slowly growing Escherichia coli infected with either T4wt or the mutants. Using two-dimensional PAGE analyses we found 18 differentially expressed proteins from lysates of infected cells. Proteins whose amounts were different in cells harbouring T4wt and the mutants are involved in processes of replication, phage–host interactions or they constitute virion components. Our data indicate that functional RI and RIII proteins – apart from their already known roles in LIN and pseudolysogeny – are also necessary for the regulation of phage T4 development in slowly growing bacteria. This regulation may be more complicated than previously anticipated, with many factors influencing T4 development in its natural habitat.
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Genomic characterization of lytic Staphylococcus aureus phage GH15: providing new clues to intron shift in phages
Phage GH15 is a polyvalent phage that shows activity against a wide range of Staphylcoccus aureus strains. This study analysed the genome of GH15. The genome size of GH15 (139 806 bp) was found to be larger than that of the known staphylococcal phages, and the G+C content (30.23 mol%) of GH15 was lower than that of any other staphylococcal myovirus phages. By mass spectrometry, ten structural proteins were identified. Analysis revealed that GH15 was closely related to phages G1, ISP, A5W, Sb-1 and K, and was moderately related to Twort. In light of the variability in identity, coverage, G+C content and genome size, coupled with the large number of mosaicisms, there certainly were close evolutionary relationships from K to Sb-1, A5W, ISP, G1 and finally GH15. Interestingly, all the introns and inteins present in the above phages were absent in GH15 and there appeared to be intron loss in GH15 compared with the intron gain seen in other phages. A comparison of the intron- and intein-related genes demonstrated a clear distinction in the location of the insertion site between intron-containing and intron-free alleles, and this might lead to the establishment of a consensus sequence associated with the presence of an intron or intein. The comparative analysis of the GH15 genome sequence with other phages not only provides compelling evidence for the diversity of staphylococcal myovirus phages but also offers new clues to intron shift in phages.
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Volumes and issues
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Volume 105 (2024)
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Volume 99 (2018)
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Volume 37 (1977)
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Volume 36 (1977)
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Volume 35 (1977)
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Volume 34 (1977)
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Volume 33 (1976)
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Volume 11 (1971)
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Volume 10 (1971)
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Volume 9 (1970)
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Volume 8 (1970)
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Volume 7 (1970)
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Volume 6 (1970)
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Volume 5 (1969)
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Volume 4 (1969)
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Volume 3 (1968)
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Volume 2 (1968)
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Volume 1 (1967)