The Experts below are selected from a list of 72 Experts worldwide ranked by ideXlab platform
Curtis A Suttle - One of the best experts on this subject based on the ideXlab platform.
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genome sequence and characterization of a virus harnav related to picorna like viruses that infects the marine Toxic bloom forming Alga heterosigma akashiwo
Virology, 2004Co-Authors: Andrew S Lang, Alexander I Culley, Curtis A SuttleAbstract:Heterosigma akashiwo (Rhaphidophyceae) is a unicellular, flagellated, bloom-forming, Toxic Alga of ecological and economic importance. Here, we report the results of sequencing and analyzing the genome of an 8.6-kb single-stranded RNA virus (HaRNAV-SOG263) that infects H. akashiwo. Our results show that HaRNAV is related to picorna-like viruses, but does not belong within any currently defined virus family. This is based on the genome organization and sequence comparisons of putative RNA-dependent RNA polymerase (RdRp), helicase, and capsid protein sequences. The genome sequence predicts a single open reading frame (orf) encoding a polyprotein that contains conserved picorna-like protein domains, with putative nonstructural protein domains present in the N-terminus and the structural proteins in the C-terminus of the polyprotein. We have analyzed and compared the virus structural proteins from infectious and noninfectious particles. In this way, we identified structural protein cleavage sites as well as protein processing events that are presumably important for maturation of virus particles. The combination of genome structure and sequence relationships to other viruses suggests that HaRNAV is the first member of a proposed new virus family (Marnaviridae), related to picorna-like viruses.
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viruses causing lysis of the Toxic bloom forming Alga heterosigma akashiwo raphidophyceae are widespread in coastal sediments of british columbia canada
Limnology and Oceanography, 2002Co-Authors: Janice E Lawrence, Amy M Chan, Curtis A SuttleAbstract:Viruses that infect and cause lysis of the Toxic Alga Heterosigma akashiwo are abundant and widespread in the Strait of Georgia, Canada, and adjacent inlets during the summer months when blooms of this Alga occur. Because viruses are subjected to many mechanisms of removal and their host is intermittently dormant, the persistence of viruses may be dependent on environmental reservoirs. We extracted pore water from sediments collected in the Strait of Georgia and screened for the presence of infectious agents that cause lysis of H. akashiwo. Lytic agents were widespread throughout the study region, being detected in 17 of 20 sites surveyed. Lytic agents were present in sediments ranging from highly organic to clay-rich and were retrieved from cores taken at water depths of 25−285 m. The highest concentration of lytic agents was found at the sediment-water interface; however, lytic agents were found as deep as 40 cm below the sediment-water interface. Examination of agents isolated from various sites revealed virus-like particles ~50 nm in diameter. These are similar to other virus-like particles that have been isolated that infect this Alga. This suggests that the most abundant lytic agents in the sediments are viruses and that these viruses may be long-lived once buried in the sediments. The widespread presence of viral-size lytic agents that infect H. akashiwo is consistent with viral infection being a mortality agent of this Alga in the overlying waters and suggests that they may play in important role in regulating their population dynamics.
Janet Y M Tang - One of the best experts on this subject based on the ideXlab platform.
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Hydrogen peroxide is not the cause of fish kills associated with Chattonella marina: cytological and physiological evidence.
Aquatic Toxicology, 2005Co-Authors: Janet Y M Tang, Donald M. Anderson, Doris W.t. AuAbstract:Abstract Chattonella marina, a harmful Algal bloom (HAB) causative species, was used to study the mortality, physiology, and pathology of a marine stenohaline fish, goldlined seabream exposed to the Toxic Alga. The median lethal time (LT50) was 3 h upon exposure to 8000 cells/ml of C. marina. Significant induction of filamental chloride cells (CCs) [i.e. increases in CC fractional area and in the volume density of CCs], concomitant with significant reduction of blood osmolality, were found in C. marina treated fish. To verify whether the Toxicity of C. marina was mediated through oxidative stress, a hydrogen peroxide exposure experiment was carried out and the Toxicity as well as cytological and physiological changes were compared with the C. marina treatment. Hydrogen peroxide at a concentration of 500 μM H2O2, (i.e. 25 times higher than that produced by 8000 cells/ml of C. marina (20 μM H2O2)) was unable to induce similar CC alterations and osmoregulatory impairment in fish as observed in the C. marina treatment. Non-specific membrane damage such as severe loss of microvilli projections on the CC apical opening and rupture of epithelial membranes in the lamellae were observed. The LT50 was 6 h, two times longer than that with 8000 cells/ml of C. marina. Based on the cytological and physiological evidence and Toxicity data, the mechanism by which C. marina kills fish appears to be very different from that caused by H2O2/ROS. Osmoregulatory distress is the major cause of fish death upon exposure to C. marina.
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osmotic distress a probable cause of fish kills on exposure to a subbloom concentration of the Toxic Alga chattonella marina
Environmental Toxicology and Chemistry, 2004Co-Authors: Janet Y M TangAbstract:Mortality, changes in blood osmolality, and pO2 in the goldlined seabream (Rhabdosargus sarba) on exposure to a subbloom concentration (2,000 cells/ml) of a Toxic red tide Alga, Chattonella marina, were investigated and related to quantitative ultrastructural alterations of the gill. The median lethal time (LT50) was 6 h. Significant induction of filamental chloride cells (CCs) (increases in CC density, apical opening area, fractional area, volume densities of CCs, and mitochondria within CCs), concomitant with a significant reduction in blood osmolality, was found within 3 h of exposure to C. marina. Further reduction in blood osmolality (67%) and a drastic decline of pO2 (70%) were detected in moribund fish after 6 h. Fish were also subjected to severe salinity stress (abrupt transfer to 0 and 60‰ salinities), and the same parameters were measured. Our quantitative ultrastructural and physiological data suggest that fish exposed for 6 h to C. marina (2,000 cells/ml) suffered similar but more severe osmotic distress as compared to that induced by abrupt transfer to 60‰ persaline water. Results of the salinity stress experiment also showed that suffocation was not a secondary response induced by osmotic impairment in the moribund fish. Osmoregulatory failure in conjunction with suffocation may be the cause of death following exposure to C. marina. The findings of this study provide evidence that C. marina, even in concentrations below visible blooms, can pose a significant threat to marine fish.
Andrew S Lang - One of the best experts on this subject based on the ideXlab platform.
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genome sequence and characterization of a virus harnav related to picorna like viruses that infects the marine Toxic bloom forming Alga heterosigma akashiwo
Virology, 2004Co-Authors: Andrew S Lang, Alexander I Culley, Curtis A SuttleAbstract:Heterosigma akashiwo (Rhaphidophyceae) is a unicellular, flagellated, bloom-forming, Toxic Alga of ecological and economic importance. Here, we report the results of sequencing and analyzing the genome of an 8.6-kb single-stranded RNA virus (HaRNAV-SOG263) that infects H. akashiwo. Our results show that HaRNAV is related to picorna-like viruses, but does not belong within any currently defined virus family. This is based on the genome organization and sequence comparisons of putative RNA-dependent RNA polymerase (RdRp), helicase, and capsid protein sequences. The genome sequence predicts a single open reading frame (orf) encoding a polyprotein that contains conserved picorna-like protein domains, with putative nonstructural protein domains present in the N-terminus and the structural proteins in the C-terminus of the polyprotein. We have analyzed and compared the virus structural proteins from infectious and noninfectious particles. In this way, we identified structural protein cleavage sites as well as protein processing events that are presumably important for maturation of virus particles. The combination of genome structure and sequence relationships to other viruses suggests that HaRNAV is the first member of a proposed new virus family (Marnaviridae), related to picorna-like viruses.
Janice E Lawrence - One of the best experts on this subject based on the ideXlab platform.
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viruses causing lysis of the Toxic bloom forming Alga heterosigma akashiwo raphidophyceae are widespread in coastal sediments of british columbia canada
Limnology and Oceanography, 2002Co-Authors: Janice E Lawrence, Amy M Chan, Curtis A SuttleAbstract:Viruses that infect and cause lysis of the Toxic Alga Heterosigma akashiwo are abundant and widespread in the Strait of Georgia, Canada, and adjacent inlets during the summer months when blooms of this Alga occur. Because viruses are subjected to many mechanisms of removal and their host is intermittently dormant, the persistence of viruses may be dependent on environmental reservoirs. We extracted pore water from sediments collected in the Strait of Georgia and screened for the presence of infectious agents that cause lysis of H. akashiwo. Lytic agents were widespread throughout the study region, being detected in 17 of 20 sites surveyed. Lytic agents were present in sediments ranging from highly organic to clay-rich and were retrieved from cores taken at water depths of 25−285 m. The highest concentration of lytic agents was found at the sediment-water interface; however, lytic agents were found as deep as 40 cm below the sediment-water interface. Examination of agents isolated from various sites revealed virus-like particles ~50 nm in diameter. These are similar to other virus-like particles that have been isolated that infect this Alga. This suggests that the most abundant lytic agents in the sediments are viruses and that these viruses may be long-lived once buried in the sediments. The widespread presence of viral-size lytic agents that infect H. akashiwo is consistent with viral infection being a mortality agent of this Alga in the overlying waters and suggests that they may play in important role in regulating their population dynamics.
Doris W.t. Au - One of the best experts on this subject based on the ideXlab platform.
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Hydrogen peroxide is not the cause of fish kills associated with Chattonella marina: cytological and physiological evidence.
Aquatic Toxicology, 2005Co-Authors: Janet Y M Tang, Donald M. Anderson, Doris W.t. AuAbstract:Abstract Chattonella marina, a harmful Algal bloom (HAB) causative species, was used to study the mortality, physiology, and pathology of a marine stenohaline fish, goldlined seabream exposed to the Toxic Alga. The median lethal time (LT50) was 3 h upon exposure to 8000 cells/ml of C. marina. Significant induction of filamental chloride cells (CCs) [i.e. increases in CC fractional area and in the volume density of CCs], concomitant with significant reduction of blood osmolality, were found in C. marina treated fish. To verify whether the Toxicity of C. marina was mediated through oxidative stress, a hydrogen peroxide exposure experiment was carried out and the Toxicity as well as cytological and physiological changes were compared with the C. marina treatment. Hydrogen peroxide at a concentration of 500 μM H2O2, (i.e. 25 times higher than that produced by 8000 cells/ml of C. marina (20 μM H2O2)) was unable to induce similar CC alterations and osmoregulatory impairment in fish as observed in the C. marina treatment. Non-specific membrane damage such as severe loss of microvilli projections on the CC apical opening and rupture of epithelial membranes in the lamellae were observed. The LT50 was 6 h, two times longer than that with 8000 cells/ml of C. marina. Based on the cytological and physiological evidence and Toxicity data, the mechanism by which C. marina kills fish appears to be very different from that caused by H2O2/ROS. Osmoregulatory distress is the major cause of fish death upon exposure to C. marina.