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- Shedding of Viral Hemorrhagic Septicemia Virus (Genotype IVb) by Experimentally Infected Muskellunge (Esox masquinongy)
- Robert K. Kim , Mohamed Faisal
- J. Microbiol. 2012;50(2):278-284. Published online April 27, 2012
- DOI: https://doi.org/10.1007/s12275-012-1145-2
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- 26 Scopus
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Abstract
- Previous experimental infection demonstrated that juvenile muskellunge (Esox masquinongy) can survive experimental infection of viral hemorrhagic septicemia virus, Genotype IVb (VHSV IVb) at a low concentration of exposure. Herein we report that survivors of experimental infection with VHSV IVb shed the virus into the surrounding environment for an extended period of time. When muskellunge were exposed to VHSV IVb by immersion at a concentration of 1,400 plaque forming units (PFU)/ml, VHSV IVb was detected in the water of surviving fish for up to 15 weeks postexposure (p.e.) with the highest levels of shedding occurring between weeks 1 and 5 p.e. We estimated that each juvenile muskellunge can shed upwards of 1.36×105 PFU/fish/h after initial exposure signifying the uptake and amplification of VHSV to several orders of magnitude above the original exposure concentration. Muskellunge surviving low concentration exposure were re-infected with VHSV IVb by immersion at week 22 p.e. at concentrations ranging from 0 to 106 PFU/ml. Viral shedding was detected in all re-exposed fish, including mock rechallenged controls up to 15 consecutive weeks. Rates of viral shedding were substantially higher following rechallenge in the first 5 weeks. The highest rate of viral shedding was approximately 4.6×106 PFU/fish/h and shedding did not necessarily correspond to the re-exposure VHSV concentration. The results of this study shed new light into the dynamics of VHSV IVb shedding in a highly susceptible host and provide useful insights to fishery managers to design effective control strategies to this deadly virus.
- Genetic Manipulation of Rhabdoviruses : New Insights to Virus Replication, Transcription and Assembly
- Michael A. Whitt
- J. Microbiol. 1998;36(1):1-8.
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Abstract
- Rhabdoviruses, together with the other members of the Rhabdoviridae family, are one of the most widely distributed groups of viruses in nature. Rhabdoviruses have been isolated from virtually all vertebrates, several different species of insects, as well as many plant (65). It is thought that insects were the original hosts for this group of viruses and that rhabdoviruses have since adapted to grow in both vertebrates and invertebrates. This adaptation undoubtedly contributed to one of the disdinguishing features of the prototypic rhabdovirus, vesicular stomatitis virus (VSV), namely the ability to replicate in most primary cell cultures and essentially all established mammalian cell lines, as well as a number of insect and amphibian cell lines. Because VSV has a broad host range, is relatively easy to grow and replicates to high titers in cell culture it has been used extensively as a model system to study many aspects of rhabdovirus entry (32, 69, 70), replication (3, 4) and assembly(36, 55, 58).
- Overexpression of Fish DRG2 Induces Cell Rounding
- Jeong Jae Park , Seung Ju Cha , Myoung Seok Ko , Wha Ja Cho , Won Joon Yoon , Chang Hoon Moon , Jeong Wan Do , Sung Bum Kim , Hebok Song , Dae Kyun Chung , In Seob Han , KyuBum Kwack , Jeong Woo Park
- J. Microbiol. 2002;40(4):295-300.
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Abstract
- Previously, we reported induced expression of developmentally regulated GTP-binding protein 2 (DRG2) in fish cells at the late stage of rhabdovirus infection. To investigate the biological role of fish DRG2 (fDRG2), we transfected CHSE-214 cells with an expression vector containing complete fDRG2 fused to the N-terminal end of an enhanced green fluorescent protein (EGFP). Low level expression of fDRG2-EGFP did not induce morphological change or cell death. However, a high level expression of fDRG2-EGFP induced cell rounding and caused depletion of the cell population in FACS analysis. Several truncated fragments were fused to EGFP. FACS analysis was conducted to determine the presence of cells expressing high levels of the resulting chimera. While cells expressing a high level of N-terminus were detected, those expressing high levels of the C-terminal fragment 243-290 containing the G4 motif were absent in FACS analysis. Based on these observations, we propose that overexpression of fDRG2 may induce cell rounding, a representative cytopathic effect of virus-infected cells in the late stage of infection and the C-terminus of the fDRG2 is essential for this function.
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