Maturation of Poliovirus Rna With Capsid Protein Coded by Heterologous Enteroviruses

Holland, John J.; Cords, Carl E.

doi:10.1073/pnas.51.6.1082

Cited by 31 publications

(14 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Injured RNA genomes, even if they are dead, as such, may survive for at least some generations due to complementation, i.e., help provided in trans by proteins (or RNA cis-elements) encoded by their coinfecting viruses. This mechanism of cooperative interaction was described long ago for the case of drug-sensitive and drug-resistant (or -dependent) picornaviruses (293)(294)(295)(296)(297), but its wider biological relevance became especially appreciated after the realization that viral populations are represented by quasispecies, i.e., swarms of closely related but distinct individuals (10,14,32,73,(298)(299)(300)(301). The prolonged survival of impaired genomes owing to intrapopulation complementation may provide time for their adaptive remodeling, resulting in the restoration of their capacity for independent existence.…”

Section: Natural Tools For Curing Damaged Rna Genomesmentioning

confidence: 89%

Emergency Services of Viral RNAs: Repair and Remodeling

Agol

Gmyl

2018

Microbiol Mol Biol Rev

View full text Add to dashboard Cite

Reproduction of RNA viruses is typically error-prone due to the infidelity of their replicative machinery and the usual lack of proofreading mechanisms. The error rates may be close to those that kill the virus. Consequently, populations of RNA viruses are represented by heterogeneous sets of genomes with various levels of fitness. This is especially consequential when viruses encounter various bottlenecks and new infections are initiated by a single or few deviating genomes. Nevertheless, RNA viruses are able to maintain their identity by conservation of major functional elements. This conservatism stems from genetic robustness or mutational tolerance, which is largely due to the functional degeneracy of many protein and RNA elements as well as to negative selection. Another relevant mechanism is the capacity to restore fitness after genetic damages, also based on replicative infidelity. Conversely, error-prone replication is a major tool that ensures viral evolvability. The potential for changes in debilitated genomes is much higher in small populations, because in the absence of stronger competitors low-fit genomes have a choice of various trajectories to wander along fitness landscapes. Thus, low-fit populations are inherently unstable, and it may be said that to run ahead it is useful to stumble. In this report, focusing on picornaviruses and also considering data from other RNA viruses, we review the biological relevance and mechanisms of various alterations of viral RNA genomes as well as pathways and mechanisms of rehabilitation after loss of fitness. The relationships among mutational robustness, resilience, and evolvability of viral RNA genomes are discussed.

show abstract

Section: Natural Tools For Curing Damaged Rna Genomesmentioning

confidence: 89%

Emergency Services of Viral RNAs: Repair and Remodeling

Agol

Gmyl

2018

Microbiol Mol Biol Rev

View full text Add to dashboard Cite

show abstract

“…It is important to note that capsid proteins can be provided in trans during the production of infectious FMDV particles [51], and phenotypic hiding has been known for many years in a variety of picornaviruses [56-58]. Other factors may enhance or reduce the effects of complementation.…”

Section: Discussionmentioning

confidence: 99%

Phenotypic mixing and hiding may contribute to memory in viral quasispecies

Wilke

Novella

2003

BMC Microbiol

View full text Add to dashboard Cite

Background: In a number of recent experiments with food-and-mouth disease virus, a deleterious mutant, RED, was found to avoid extinction and remain in the population for long periods of time. Since RED characterizes the past evolutionary history of the population, this observation was called quasispecies memory. While the quasispecies theory predicts the existence of these memory genomes, there is a disagreement between the expected and observed mutant frequency values. Therefore, the origin of quasispecies memory is not fully understood.

show abstract

“…In positive-stranded viruses, translation and replication are coupled (25); therefore, many functions need to be provided in cis and cannot be rescued by complementation (33,37). Other proteins can freely interact with heterologous genomes or replicons, even from different viral species (18,21). In the absence of compartmentalization or other limitations to the diffusion of viral products, soluble proteins can interact with any genome inside the cell, potentially changing the phenotype of the virions and masking targets for natural selection to operate.…”

mentioning

confidence: 99%

Density-Dependent Selection in Vesicular Stomatitis Virus

Novella

Reissig

Wilke

2004

J Virol

View full text Add to dashboard Cite

We used vesicular stomatitis virus to test the effect of complementation on the relative fitness of a deleterious mutant, monoclonal antibody-resistant mutant (MARM) N, in competition with its wild-type ancestor. We carried out competitions of MARM N and wild-type populations at different multiplicities of infection (MOIs) and initial ratios of the wild type to the mutant and found that the fitness of MARM N relative to that of the wild type is very sensitive to changes in the MOI (i.e., the degree of complementation) but depends little, if at all, on the initial frequencies of MARM N and the wild type. Further, we developed a mathematical model under the assumption that during coinfection both viruses contribute to a common pool of protein products in the infected cell and that they both exploit this common pool equally. Under such conditions, the fitness of all virions that coinfect a cell is the average fitness in the absence of coinfection of that group of virions. In the absence of coinfection, complementation cannot take place and the relative fitness of each competitor is only determined by the selective value of its own products. We found good agreement between our experimental results and the model predictions, which suggests that the wild type and MARM N freely share all of their gene products under coinfection.RNA viruses form highly polymorphic populations called quasispecies (8,9,13). The origin of much of their genetic diversity is high mutational pressure. Most RNA viruses have mutation rates on the order of one miscopied base per genome and generation (10, 11). However, high mutational pressure is not necessarily the only factor promoting genetic diversity. Niche differentiation can allow stable polymorphisms in an infected host. For instance, during a polyclonal immune response, different subpopulations may have different sensitivities to individual antibodies; variation within a host can also be related to differences in the tropism of different viral subpopulations. Virus-virus interactions may also promote stable polymorphisms in an infected host. In cell culture, such interactions readily occur during replication inside a cell and are likely to be an important contributor to the maintenance of variation. When two or more virions coinfect the same cell, complementation can take place. Not every function can be complemented in trans. In positive-stranded viruses, translation and replication are coupled (25); therefore, many functions need to be provided in cis and cannot be rescued by complementation (33, 37). Other proteins can freely interact with heterologous genomes or replicons, even from different viral species (18,21). In the absence of compartmentalization or other limitations to the diffusion of viral products, soluble proteins can interact with any genome inside the cell, potentially changing the phenotype of the virions and masking targets for natural selection to operate. A remarkable example of this phenomenon is phenotypic mixing and hiding, particularly for monoclonal antibody (...

show abstract

Maturation of Poliovirus Rna With Capsid Protein Coded by Heterologous Enteroviruses

Cited by 31 publications

References 6 publications

Emergency Services of Viral RNAs: Repair and Remodeling

Emergency Services of Viral RNAs: Repair and Remodeling

Phenotypic mixing and hiding may contribute to memory in viral quasispecies

Density-Dependent Selection in Vesicular Stomatitis Virus

Contact Info

Product

Resources

About