On the Nature of Poliovirus Genetic Recombinants

Cooper, Penny; Steiner-Pryor, Amy; Scotti, Paul D.; DeLong, Donald C.

doi:10.1099/0022-1317-23-1-41

Cited by 81 publications

(56 citation statements)

References 12 publications

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“…Such dual infection of the same patient by HEV from two distinct genotypes has been documented (43). Similar recombination events have been described for other plus-strand RNA viruses, such as poliovirus, alphaviruses, and more recently, dengue virus (8,14,34,46,51). Presumably the occurrence of recombination and the detection of multiple breakpoints are due to divergent HEV genomes coming into proximity during replication and strand switching occurring.…”

mentioning

confidence: 82%

Evidence of Recombination between Divergent Hepatitis E Viruses

Cuyck¹,

Fan

Robertson

et al. 2005

J Virol

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Phylogenetic and recombination analysis was performed on 32 complete hepatitis E virus (HEV) genomes from infected humans and pigs. For the first time, evidence for recombination between divergent HEV strains was obtained, with at least two strains being found to have discordant phylogenetic relationships consistent with the occurrence of intragenotype recombination. This finding confirms that humans can be dually infected with divergent HEV strains and has implications for the emergence and evolution of new HEV epidemics.Hepatitis E virus (HEV) is a causative agent of enterically transmitted hepatitis disease and, apart from infections of pregnant women, is generally associated with low mortality (11,17). Outbreaks of HEV have been described to occur in many regions of the world, including Asia, Africa, and Mexico (1, 33, 53), while sporadic cases have been documented in the United States, Africa (9), and Europe (27,37,38,60). HEV is presumed to be a zoonotic disease, as surveys of both wild and domestic animals have found evidence for human-related HEVs in rats (12, 22), pigs (2,7,21,29,32,56), deer (45), and wild boar (41). Direct animal-to-human transmission of HEV has been demonstrated, for example, from deer to human as a result of eating uncooked meat (45). Interestingly, HEV characterized from swine in countries where HEV is not endemic is usually closely related to cases of sporadic human HEVs from the same country, for example, in the United States and Japan (29,30,42,57), while in India, where HEV is endemic, human and swine HEV strains are not closely related (2). This suggests that in certain regions HEV is more established in the human population and that in other regions HEV is emerging as a result of direct contact with animal reservoirs for the virus. Divergent HEVs with no human counterparts have also been found in chickens (avian HEV). Avian HEV shares only 50 to 60% nucleotide sequence identity with HEV from humans and swine (15,16).HEV is a positive single-stranded RNA virus that is approximately 7,200 nucleotides (nt) in length. HEV's genome is capped and polyadenylated and has three open reading frames (ORF) (Fig. 1). As the organization of HEV's genome resembles that of Caliciviridae, at one time it was considered a mem-FIG. 1. Genomic organization of HEV. The scale at the bottom of the figure corresponds to nucleotides (in thousands). ORF1 encodes a nonstructural polyprotein which provides guanylyl-methyltransferase and RNA-dependent RNA polymerase activities and possibly other functions (23,25). The ORF2 and ORF3 proteins are believed to be encoded by individual subgenomic RNAs generated during replication (44, 58). ORF2 encodes the viral capsid protein; ORF3, which contains one potential phosphorylation site, encodes a very small protein of about 123 amino acids (59). ORF3 proteins partition with the cytoskeleton, and it has been suggested that an interaction between ORF2 and ORF3 is associated with the assembly of virions (47,50). ORF3 is also believed to interact with proteins involv...

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mentioning

confidence: 82%

Evidence of Recombination between Divergent Hepatitis E Viruses

Cuyck¹,

Fan

Robertson

et al. 2005

J Virol

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“…The exact mechanism of exchange of strand is not known, but could be promoted by the pause of the polymerase during chain elongation. Thus far, nearly all studies on the mechanisms of recombination in RNA viruses support a copy-choice model, originally proposed for poliovirus [114] . It is of note, that this template-switching mechanism greatly differs from the enzyme-driven breakage-rejoining mechanism of homologous recombination in DNA, mainly because it resorts to replication as an essential step of the process [112] .…”

Section: Recombinationmentioning

confidence: 99%

Hepatitis C virus genetic variability and evolution

Echeverría

Moratorio

Cristina

et al. 2015

WJH

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Hepatitis C virus (HCV) has infected over 170 million people worldwide and creates a huge disease burden due to chronic, progressive liver disease. HCV is a singlestranded, positive sense, RNA virus, member of the Flaviviridae family. The high error rate of RNA-dependent RNA polymerase and the pressure exerted by the host immune system, has driven the evolution of HCV into 7 different genotypes and more than 67 subtypes. HCV evolves by means of different mechanisms of genetic variation. On the one hand, its high mutation rates generate the production of a large number of different but closely related viral variants during infection, usually referred to as a quasispecies. The great quasispecies variability of HCV has also therapeutic implications since the continuous generation and selection of resistant or fitter variants within the quasispecies spectrum might allow viruses to escape control by antiviral drugs. On the other hand HCV exploits recombination to ensure its survival. This enormous viral diversity together with some host factors has made it difficult to control viral dispersal. Current treatment options involve pegylated interferon-α and ribavirin as dual therapy or in combination with a direct-acting antiviral drug, depending on the country. Despite all the efforts put into antiviral therapy studies, eradication of the virus or the development of a preventive vaccine has been unsuccessful so far. This review focuses on current available data reported to date on the genetic mechanisms driving the molecular evolution of HCV populations and its relation with the antiviral therapies designed to control HCV infection. Hepatitis C virus genetic variability and evolution no preventive vaccine, and though antiviral therapy has been improved in the past few years, not all patients eradicate the virus as a result of it. The main reason lies in the intrinsic genetic variability that characterises RNA viruses, such as HCV, whose RNA polymerase lacks proof-reading activity, leading to a high mutation rate and the generation of a wide range of genome variants better known as a quasispecies. Therefore this review summarises current data on HCV quasispecies dynamics, antiviral therapy and recombination events.Echeverría N, Moratorio G, Cristina J, Moreno P. Hepatitis C virus genetic variability and evolution. World J Hepatol 2015; 7(6): 831845 Available from:

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“…Recombination in a viral context generally occurs when a replicating RdRp stops copying one RNA strand and transfers to another (Copper et al, 1974). When the transfer sites share common sequences, the recombination event is said to be homologous; conversely, when the sites are unrelated, the recombination event is non-homologous.…”

Section: Recombination In Rna Virusesmentioning

confidence: 99%

“…RNA recombination is a property of positive-and negativestranded RNA viruses that infect plant (Bujarski & Kaesberg, 1986), animal (Copper et al, 1974) and bacterial (Munishkin et al, 1988) hosts. Recombination in a viral context generally occurs when a replicating RdRp stops copying one RNA strand and transfers to another (Copper et al, 1974).…”

Section: Recombination In Rna Virusesmentioning

confidence: 99%