The Experts below are selected from a list of 90 Experts worldwide ranked by ideXlab platform
Barry J Beaty - One of the best experts on this subject based on the ideXlab platform.
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dengue virus type 2 replication and tropisms in orally infected aedes aegypti mosquitoes
BMC Microbiology, 2007Co-Authors: Ma Isabel Salazar, Jason H Richardson, Irma Sanchezvargas, Ken E Olson, Barry J BeatyAbstract:Background To be transmitted by its mosquito vector, dengue virus (DENV) must infect midgut epithelial cells, replicate and disseminate into the hemocoel, and finally infect the salivary glands, which is essential for transmission. The extrinsic incubation period (EIP) is very relevant epidemiologically and is the time required from the ingestion of virus until it can be transmitted to the next vertebrate host. The EIP is conditioned by the kinetics and tropisms of virus replication in its vector. Here we document the Virogenesis of DENV-2 in newly-colonized Aedes aegypti mosquitoes from Chetumal, Mexico in order to understand better the effect of vector-virus interactions on dengue transmission.
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Dengue virus type 2: replication and tropisms in orally infected Aedes aegypti mosquitoes
BMC Microbiology, 2007Co-Authors: Ma Isabel Salazar, Jason H Richardson, Ken E Olson, Irma Sánchez-vargas, Barry J BeatyAbstract:Background To be transmitted by its mosquito vector, dengue virus (DENV) must infect midgut epithelial cells, replicate and disseminate into the hemocoel, and finally infect the salivary glands, which is essential for transmission. The extrinsic incubation period (EIP) is very relevant epidemiologically and is the time required from the ingestion of virus until it can be transmitted to the next vertebrate host. The EIP is conditioned by the kinetics and tropisms of virus replication in its vector. Here we document the Virogenesis of DENV-2 in newly-colonized Aedes aegypti mosquitoes from Chetumal, Mexico in order to understand better the effect of vector-virus interactions on dengue transmission. Results After ingestion of DENV-2, midgut infections in Chetumal mosquitoes were characterized by a peak in virus titers between 7 and 10 days post-infection (dpi). The amount of viral antigen and viral titers in the midgut then declined, but viral RNA levels remained stable. The presence of DENV-2 antigen in the trachea was positively correlated with virus dissemination from the midgut. DENV-2 antigen was found in salivary gland tissue in more than a third of mosquitoes at 4 dpi. Unlike in the midgut, the amount of viral antigen (as well as the percent of infected salivary glands) increased with time. DENV-2 antigen also accumulated and increased in neural tissue throughout the EIP. DENV-2 antigen was detected in multiple tissues of the vector, but unlike some other arboviruses, was not detected in muscle. Conclusion Our results suggest that the EIP of DENV-2 in its vector may be shorter that the previously reported and that the tracheal system may facilitate DENV-2 dissemination from the midgut. Mosquito organs (e.g. midgut, neural tissue, and salivary glands) differed in their response to DENV-2 infection.
Vorrapon Chaikeeratisak - One of the best experts on this subject based on the ideXlab platform.
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viral speciation through subcellular genetic isolation and Virogenesis incompatibility
Nature Communications, 2021Co-Authors: Vorrapon Chaikeeratisak, Erica A Birkholz, Amy Prichard, Mackennon E Egan, Avani Mylvara, Poochit Nonejuie, Katrina Nguyen, Joseph SugieAbstract:Understanding how biological species arise is critical for understanding the evolution of life on Earth. Bioinformatic analyses have recently revealed that viruses, like multicellular life, form reproductively isolated biological species. Viruses are known to share high rates of genetic exchange, so how do they evolve genetic isolation? Here, we evaluate two related bacteriophages and describe three factors that limit genetic exchange between them: 1) A nucleus-like compartment that physically separates replicating phage genomes, thereby limiting inter-phage recombination during co-infection; 2) A tubulin-based spindle that orchestrates phage replication and forms nonfunctional hybrid polymers; and 3) A nuclear incompatibility factor that reduces phage fitness. Together, these traits maintain species differences through Subcellular Genetic Isolation where viral genomes are physically separated during co-infection, and Virogenesis Incompatibility in which the interaction of cross-species components interferes with viral production.
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viral speciation through subcellular genetic isolation and Virogenesis incompatibility
Nature Communications, 2021Co-Authors: Vorrapon Chaikeeratisak, Erica A Birkholz, Amy Prichard, Mackennon E Egan, Avani Mylvara, Poochit Nonejuie, Katrina Nguyen, Joseph SugieAbstract:Understanding how biological species arise is critical for understanding the evolution of life on Earth. Bioinformatic analyses have recently revealed that viruses, like multicellular life, form reproductively isolated biological species. Viruses are known to share high rates of genetic exchange, so how do they evolve genetic isolation? Here, we evaluate two related bacteriophages and describe three factors that limit genetic exchange between them: 1) A nucleus-like compartment that physically separates replicating phage genomes, thereby limiting inter-phage recombination during co-infection; 2) A tubulin-based spindle that orchestrates phage replication and forms nonfunctional hybrid polymers; and 3) A nuclear incompatibility factor that reduces phage fitness. Together, these traits maintain species differences through Subcellular Genetic Isolation where viral genomes are physically separated during co-infection, and Virogenesis Incompatibility in which the interaction of cross-species components interferes with viral production. Virus speciation cannot be fully explained by the evolution of different host specificities. Here, Chaikeeratisak et al. identify ways viruses can remain genetically isolated despite co-infecting the same cell, providing insight into how new virus species evolve.
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The Phage Nucleus and PhuZ Spindle: Defining Features of the Subcellular Organization and Speciation of Nucleus-Forming Jumbo Phages
'Frontiers Media SA', 2021Co-Authors: Vorrapon Chaikeeratisak, Erica A Birkholz, Joe PoglianoAbstract:Bacteriophages and their bacterial hosts are ancient organisms that have been co-evolving for billions of years. Some jumbo phages, those with a genome size larger than 200 kilobases, have recently been discovered to establish complex subcellular organization during replication. Here, we review our current understanding of jumbo phages that form a nucleus-like structure, or “Phage Nucleus,” during replication. The phage nucleus is made of a proteinaceous shell that surrounds replicating phage DNA and imparts a unique subcellular organization that is temporally and spatially controlled within bacterial host cells by a phage-encoded tubulin (PhuZ)-based spindle. This subcellular architecture serves as a replication factory for jumbo Pseudomonas phages and provides a selective advantage when these replicate in some host strains. Throughout the lytic cycle, the phage nucleus compartmentalizes proteins according to function and protects the phage genome from host defense mechanisms. Early during infection, the PhuZ spindle positions the newly formed phage nucleus at midcell and, later in the infection cycle, the spindle rotates the nucleus while delivering capsids and distributing them uniformly on the nuclear surface, where they dock for DNA packaging. During the co-infection of two different nucleus-forming jumbo phages in a bacterial cell, the phage nucleus establishes Subcellular Genetic Isolation that limits the potential for viral genetic exchange by physically separating co-infection genomes, and the PhuZ spindle causes Virogenesis Incompatibility, whereby interacting components from two diverging phages negatively affect phage reproduction. Thus, the phage nucleus and PhuZ spindle are defining cell biological structures that serve roles in both the life cycle of nucleus-forming jumbo phages and phage speciation
Ma Isabel Salazar - One of the best experts on this subject based on the ideXlab platform.
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dengue virus type 2 replication and tropisms in orally infected aedes aegypti mosquitoes
BMC Microbiology, 2007Co-Authors: Ma Isabel Salazar, Jason H Richardson, Irma Sanchezvargas, Ken E Olson, Barry J BeatyAbstract:Background To be transmitted by its mosquito vector, dengue virus (DENV) must infect midgut epithelial cells, replicate and disseminate into the hemocoel, and finally infect the salivary glands, which is essential for transmission. The extrinsic incubation period (EIP) is very relevant epidemiologically and is the time required from the ingestion of virus until it can be transmitted to the next vertebrate host. The EIP is conditioned by the kinetics and tropisms of virus replication in its vector. Here we document the Virogenesis of DENV-2 in newly-colonized Aedes aegypti mosquitoes from Chetumal, Mexico in order to understand better the effect of vector-virus interactions on dengue transmission.
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Dengue virus type 2: replication and tropisms in orally infected Aedes aegypti mosquitoes
BMC Microbiology, 2007Co-Authors: Ma Isabel Salazar, Jason H Richardson, Ken E Olson, Irma Sánchez-vargas, Barry J BeatyAbstract:Background To be transmitted by its mosquito vector, dengue virus (DENV) must infect midgut epithelial cells, replicate and disseminate into the hemocoel, and finally infect the salivary glands, which is essential for transmission. The extrinsic incubation period (EIP) is very relevant epidemiologically and is the time required from the ingestion of virus until it can be transmitted to the next vertebrate host. The EIP is conditioned by the kinetics and tropisms of virus replication in its vector. Here we document the Virogenesis of DENV-2 in newly-colonized Aedes aegypti mosquitoes from Chetumal, Mexico in order to understand better the effect of vector-virus interactions on dengue transmission. Results After ingestion of DENV-2, midgut infections in Chetumal mosquitoes were characterized by a peak in virus titers between 7 and 10 days post-infection (dpi). The amount of viral antigen and viral titers in the midgut then declined, but viral RNA levels remained stable. The presence of DENV-2 antigen in the trachea was positively correlated with virus dissemination from the midgut. DENV-2 antigen was found in salivary gland tissue in more than a third of mosquitoes at 4 dpi. Unlike in the midgut, the amount of viral antigen (as well as the percent of infected salivary glands) increased with time. DENV-2 antigen also accumulated and increased in neural tissue throughout the EIP. DENV-2 antigen was detected in multiple tissues of the vector, but unlike some other arboviruses, was not detected in muscle. Conclusion Our results suggest that the EIP of DENV-2 in its vector may be shorter that the previously reported and that the tracheal system may facilitate DENV-2 dissemination from the midgut. Mosquito organs (e.g. midgut, neural tissue, and salivary glands) differed in their response to DENV-2 infection.
Joseph Sugie - One of the best experts on this subject based on the ideXlab platform.
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viral speciation through subcellular genetic isolation and Virogenesis incompatibility
Nature Communications, 2021Co-Authors: Vorrapon Chaikeeratisak, Erica A Birkholz, Amy Prichard, Mackennon E Egan, Avani Mylvara, Poochit Nonejuie, Katrina Nguyen, Joseph SugieAbstract:Understanding how biological species arise is critical for understanding the evolution of life on Earth. Bioinformatic analyses have recently revealed that viruses, like multicellular life, form reproductively isolated biological species. Viruses are known to share high rates of genetic exchange, so how do they evolve genetic isolation? Here, we evaluate two related bacteriophages and describe three factors that limit genetic exchange between them: 1) A nucleus-like compartment that physically separates replicating phage genomes, thereby limiting inter-phage recombination during co-infection; 2) A tubulin-based spindle that orchestrates phage replication and forms nonfunctional hybrid polymers; and 3) A nuclear incompatibility factor that reduces phage fitness. Together, these traits maintain species differences through Subcellular Genetic Isolation where viral genomes are physically separated during co-infection, and Virogenesis Incompatibility in which the interaction of cross-species components interferes with viral production.
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viral speciation through subcellular genetic isolation and Virogenesis incompatibility
Nature Communications, 2021Co-Authors: Vorrapon Chaikeeratisak, Erica A Birkholz, Amy Prichard, Mackennon E Egan, Avani Mylvara, Poochit Nonejuie, Katrina Nguyen, Joseph SugieAbstract:Understanding how biological species arise is critical for understanding the evolution of life on Earth. Bioinformatic analyses have recently revealed that viruses, like multicellular life, form reproductively isolated biological species. Viruses are known to share high rates of genetic exchange, so how do they evolve genetic isolation? Here, we evaluate two related bacteriophages and describe three factors that limit genetic exchange between them: 1) A nucleus-like compartment that physically separates replicating phage genomes, thereby limiting inter-phage recombination during co-infection; 2) A tubulin-based spindle that orchestrates phage replication and forms nonfunctional hybrid polymers; and 3) A nuclear incompatibility factor that reduces phage fitness. Together, these traits maintain species differences through Subcellular Genetic Isolation where viral genomes are physically separated during co-infection, and Virogenesis Incompatibility in which the interaction of cross-species components interferes with viral production. Virus speciation cannot be fully explained by the evolution of different host specificities. Here, Chaikeeratisak et al. identify ways viruses can remain genetically isolated despite co-infecting the same cell, providing insight into how new virus species evolve.
P S Mellor - One of the best experts on this subject based on the ideXlab platform.
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effect of temperature on african horse sickness virus infection in culicoides
Archives of virology. Supplementum, 1998Co-Authors: P S Mellor, Peter Rawlings, Matthew Baylis, Martin P WellbyAbstract:This paper shows that both the infection rate and the rate of Virogenesis of African horse sickness virus (AHSV) within vector Culicoides are temperature dependent. As temperature is reduced from permissive levels the lifespan of the vector itself is extended but the rate of Virogenesis decreases and infection rate falls dramatically so that at 10°C virtually all midges are free from virus by 13 days post infection (dpi). When vectors that had been kept at this temperature for 35 days were moved to a permissive temperature for 3 days; however, the apparent zero infection rate increased to 15.5%. It therefore appears that at low temperature (≤ 15°C) AHSV does not replicate but virus may persist in some vectors at a level below that detectable by traditional assay systems and when the temperature later rises to permissive levels virus replication is able to commence. On the basis of this information an overwintering mechanism for AHSV is suggested. The temperature at which the immature stages of Culicoides are reared may also influence infection with AHSV. A 5-10°C rise in larval developmental temperature resulted in an increase in oral infection rate of a normally non-vector species of Culicoides, from 10%. A mechanism is suggested.
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effect of temperature on survival and rate of Virogenesis of african horse sickness virus in culicoides variipennis sonorensis diptera ceratopogonidae and its significance in relation to the epidemiology of the disease
Bulletin of Entomological Research, 1996Co-Authors: Martin P Wellby, Matthew Baylis, Peter Rawlings, P S MellorAbstract:Culicoides variipennis sonorensis Wirth & Jones and C. nubeculosus (Meigen) were orally infected with African horse sickness virus (AHSV) type 9 and subsequently incubated at 10, 15, 20 and 25°C (R.H. 80%±10%). A time course of infection rates and virus titres was recorded by assaying flies individually or in pools, and survival rates of flies were also estimated. Survival rates at 10, 15 and 20°C were very similar and 80–90% of flies remained alive after 14 days; at 25°C after the same period survival was reduced to 40%. None of the C. nubeculosus became persistently infected with AHSV, but the virus took longer to clear as the incubation temperature dropped. At temperatures of 10, 15, 20 and 25°C virus was undetectable on days 12, 8, 5, and 4 days post infection (dpi), respectively. In C. v. sonorensis both the infection rate and rate of Virogenesis were related to temperature. At 25°C a maximum mean titre of 10 4.3 TCID 50 /fly was reached by 9 dpi and the infection rate remained between 60 and 80%. At 20°C Virogenesis was slower and a maximum mean titre of 10 4.3 TCID 50 /fly was reached only after 23 days; the infection rate was also reduced to 50–70%. At 15°C there was an overall decline in virus titre with time, although between 12 and 15 dpi some pools of flies contained 10 3.0 –10 4.0 TCID 50 /fly, demonstrating that Virogenesis can occur. The infection rate at this temperature decreased dramatically to 0–15% after 9 dpi. At 10°C there was no detectable Virogenesis and all pools tested at 13 dpi were negative. The apparent infection rate dropped to 0–5% between 13 and 35 days post infection. However, when surviving flies were then returned to 25 °C for 3 days the infection rate increased to 15.5%. It therefore appears that at low temperatures the virus does not replicate but infectious virus may persist at a level below that detectable by the usual assay systems. The implications of these findings for the epidemiology of AHS are discussed.
