Which viruses have segmented genomes

In this process, the RNA molecules of different virus strains are mixed or reshuffled in doubly infected cells during replication and morphogenesis. In this way, progeny viruses can obtain new combinations of RNA segments and thus gain novel properties. This mechanism, which is referred to as antigenic shift, is particularly common and well studied in influenza A viruses, the causative agents of viral influenza or genuine flu Sect.

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Plenum, New York, p Google Scholar. Butz EA, Southern PJ Lymphocytic choriomeningitis virus-induced immune dysfunction: induction of and recovery from T-cell anergy in adult infected mice. This article reports the high-resolution X-ray crystal structure of the rotavirus polymerase in the presence and absence of RNA template, informing an understanding of genome segment packaging and replication. Ogden, K. Rotavirus RNA polymerases resolve into two phylogenetically distinct classes that differ in their mechanism of template recognition.

Virology , 50—57 Yang, H. Comparison of polymerase subunits from double-stranded RNA bacteriophages. Nelson, M. Dugan, V. The evolutionary genetics and emergence of avian influenza viruses in wild birds. Lindstrom, S. Genetic analysis of human H2N2 and early H3N2 influenza viruses, — evidence for genetic divergence and multiple reassortment events. Multiple reassortment events in the evolutionary history of H1N1 influenza A virus since Rambaut, A.

The genomic and epidemiological dynamics of human influenza A virus. Holmes, E. Whole-genome analysis of human influenza A virus reveals multiple persistent lineages and reassortment among recent H3N2 viruses. PLoS Biol. This first large-scale comparative genomics study of influenza A viruses shows that multiple co-circulating lineages exist and documents reassortment events. Ghedin, E.

Large-scale sequencing of human influenza reveals the dynamic nature of viral genome evolution. Westgeest, K. Genome-wide analysis of reassortment and evolution of human influenza A H3N2 viruses circulating between and Evolutionary dynamics of human rotaviruses: balancing reassortment with preferred genome constellations.

This first large-scale comparative genomics study of human rotaviruses shows that multiple co-circulating lineages exist and documents reassortment events. Diversity and relationships of cocirculating modern human rotaviruses revealed using large-scale comparative genomics. Zhang, S. Analysis of human rotaviruses from a single location over an year time span suggests that protein coadaption influences gene constellations. This comparative genomics study of human rotavirus identifies persistent lineages and suggests that co-adaptation of functionally interacting viral proteins may restrict reassortment over time.

Dennis, A. Molecular epidemiology of contemporary G2P[4] human rotaviruses cocirculating in a single U. Nomikou, K. Widespread reassortment shapes the evolution and epidemiology of bluetongue virus following European invasion.

Phylogenetic analysis reveals the global migration of seasonal influenza A viruses. Simonsen, L. Li, C. Compatibility among polymerase subunit proteins is a restricting factor in reassortment between equine H7N7 and human H3N2 influenza viruses. This is the first investigation to reveal how incompatibilities among polymerase subunits can restrict reassortment among divergent influenza A viruses.

Hara, K. Co-incorporation of the PB2 and PA polymerase subunits from human H3N2 influenza virus is a critical determinant of the replication of reassortant ribonucleoprotein complexes. Octaviani, C. Reassortment between seasonal H1N1 and pandemic H1N1 influenza viruses is restricted by limited compatibility among polymerase subunits. Shared and group-specific features of the rotavirus RNA polymerase reveal potential determinants of gene reassortment restriction.

This is the first report to demonstrate how incompatibilities between the rotavirus polymerase and core shell protein may restrict reassortment among divergent strains. Rotavirus VP2 core shell regions critical for viral polymerase activation.

Taraporewala, Z. Structure-function analysis of rotavirus NSP2 octamer by using a novel complementation system. Ilyushina, N. Kaverin, N. This article reports that compensatory mutations can correct mismatched protein interactions that were due to reassortment for influenza A viruses in cell culture experiments. Intergenic HA—NA interactions in influenza A virus: postreassortment substitutions of charged amino acid in the hemagglutinin of different subtypes. Rudneva, I.

Effect of gene constellation and postreassortment amino acid change on the phenotypic features of H5 influenza virus reassortants. Neverov, A. Intrasubtype reassortments cause adaptive amino acid replacements in H3N2 influenza genes. This study shows that influenza A virus reassortment in nature causes a temporary increase in the rate of amino acid changes as the viral proteins adapt to a new genetic environment.

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Download references. You can also search for this author in PubMed Google Scholar. Correspondence to Sarah M. Viruses in which the genome consists of more than one RNA molecule that is, segments. The genome segments can be packaged within a single virion particle or into separate particles. A representative viral strain that is studied to understand the biology of an entire viral genus or family.

A process of genetic exchange whereby two or more parental viruses co-infect a single host cell and exchange genome segments. The outcome is the formation of hybrid viral progeny with genome segments derived from multiple parental strains. The mechanism by which a segmented virus packages one of each genome segment into a virion particle. The capacity of an individual virus to generate infectious progeny, relative to other virus genotypes in the population.

A simplified experimental system in which viral genome segments are incorporated into a virion particle; this occurs in a test tube and outside the context of an infected host cell.

Spontaneously generated mutant RNA molecules that usually contain large gene deletions but maintain sequences that are crucial for their replication and packaging. These RNAs reduce the fitness of full-length viruses during cellular co-infection.

A binomial system of classification for influenza A viruses that is based on the neutralizing antibody response to the virion structural proteins haemagglutinin HA and neuraminidase NA.

In virology: when an individual virus encapsidates two diploidy or more polyploidy copies of the genome into a single virus particle. Reprints and Permissions. Reassortment in segmented RNA viruses: mechanisms and outcomes. Nat Rev Microbiol 14, — Download citation. Published : 23 May Issue Date : July Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative.

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Skip to main content Thank you for visiting nature. Subjects Influenza virus Rotavirus Viral evolution Viral pathogenesis. Abstract Segmented RNA viruses are widespread in nature and include important human, animal and plant pathogens, such as influenza viruses and rotaviruses. Access through your institution. Buy or subscribe. Rent or Buy article Get time limited or full article access on ReadCube. Figure 1: Reassortment, sexual reproduction and recombination.

Figure 3: Direct restrictions on the generation of reassortants. Figure 4: Fitness consequences of reassortment. References 1 Tate, J. Google Scholar 2 Klepser, M. Google Scholar 29 Emori, Y. Google Scholar 38 Dushoff, J.

Google Scholar 39 Johnson, N. Google Scholar 40 Parrish, C. Google Scholar 66 Lobo, P. Google Scholar 69 Lahon, A. Google Scholar 99 Lu, X. Among viruses that infect vertebrates, those that carry segmented genomes belong to the Arenaviridae, Birnaviridae, Bunyavirales, Orthomyxoviridae, Picobirnaviridae, and Reoviridae.

Reassortment has been documented to occur in nature for each of these viral taxa [ 1 — 6 ]. Nevertheless, both the frequency of reassortment and its evolutionary implications for this highly diverse set of viruses are likely to vary greatly. Since reassortment takes place in coinfected cells, a critical factor governing reassortment is the frequency of coinfection Fig 1.

When thinking about a single virus population within a host, infection of individual cells with multiple viral genomes is likely to be enhanced through aggregation of virus particles and spread of virus within foci rather than dispersal throughout a tissue.

In addition, if productive viral infection is fully or partially dependent on multiple infection for example, because some viral genomes lack one or more segments , this dependency would be expected to augment reassortment.

Indeed, abundant reassortment in influenza A virus IAV family Orthomyxoviridae infections occurs because fewer than eight segments are replicated in many singly infected cells [ 7 — 9 ]. Because all eight segments of IAV encode essential gene products, such semi-infected cells can produce progeny viruses only if the missing segments are introduced through coinfection.

As a result, a high proportion of productively infected cells are coinfected [ 7 , 8 ]. Although not formally demonstrated to date, this phenomenon is also expected to occur for bunyaviruses order Bunyavirales , which are thought to package less than the full complement of three genome segments into most virus particles [ 10 , 11 ]. Of course, reassortment has a greater impact on viral genotype if coinfecting viruses are not derived from the same population but rather represent two distinct lineages.

The likelihood of such a mixed infection occurring depends on numerous factors, including prevalence of the viral lineages in circulation, likelihood of dual exposure, and the spatial dynamics of the two viruses within a coinfected host.

Another important factor is the active exclusion of a second virus as a result of superinfection interference [ 12 , 13 ]. This phenomenon can result from direct effects of primary infection, such as viral destruction of cell surface receptors, or as a consequence of host innate immune responses, which render infected cells or an infected host refractory to further infection.

Superinfection interference has been documented for diverse viruses, but it is notable that this effect appears to be minimal for certain members of the Reoviridae and Arenaviridae [ 14 — 16 ].

In theory, coinfection does not necessarily lead to reassortment. The efficiency of reassortment within a coinfected cell depends on i the extent to which viral replication is compartmentalized within the cell and ii the stringency of genome packaging and compatibility of packaging signals between coinfecting viruses.

The first of these factors determines the level of mixing between coinfecting viral genomes, while the second dictates whether or not segments derived from differing parental strains can be coincorporated into nascent virus particles.

Most viral life cycles are characterized by a compartmentalization of viral functions into localized areas. These can take the form of cytoplasmic inclusion bodies, viral replication organelles associated with host cell membranes, or punctate accumulations of viral components within the nucleus. The concentration of viral genetic material, viral proteins, and necessary host factors within these inclusions is thought to increase the efficiency of viral functions.

However, reassortment is predicted to be limited by inclusions. If each incoming parental virus generates its own inclusion, the resultant constraint on the physical mixing of genome segments would restrict reassortment. Reoviruses family Reoviridae give an excellent example of a highly compartmentalized viral lifecycle.

Reovirus components accumulate in distinct inclusion bodies within the cytoplasm, which are the sites of viral transcription, translation, replication, and particle assembly [ 17 ].

In this context, viral genomes replicated within the same cytoplasm may nevertheless remain unmixed. Relatively inefficient mixing of coinfecting reovirus genomes is supported by the results of experimental coinfections in which the majority of progeny viruses from coinfected cells retained a parental genotype [ 18 ]. The fact that reovirus reassortment occurs, however, is likely attributable to the merging of heterologous viral inclusions within coinfected cells Fig 1.

Reovirus inclusions are known to be dynamic, and fusion between inclusions in singly infected cells has been documented [ 19 ]. Trafficking of viral RNAs between inclusions may also be possible. In contrast to reovirus, visualization of IAV RNAs within infected cells suggested that the gene segments remain colocalized only en route to the nucleus early in infection and that the segments disperse once in the nucleus, creating the potential for mixing when multiple genomes are present [ 20 ].

Viral mechanisms that evolved to ensure the coordinated packaging of genome segments into virus particles may also place constraints on reassortment. Incorporation of viral genomes into virions is typically directed by specific nucleic acid sequences, viral protein motifs, or a combination of both. For segmented viruses, these packaging signals must be present on all gene segments. In addition, some segmented viruses enforce a high fidelity of genome packaging to ensure that one of each segment is present, a process that relies on segment-specific signals and selective incorporation.

Divergence among related viruses in packaging signals may limit the potential for reassortant genotypes to form. For IAV, this form of constraint has been demonstrated experimentally [ 21 , 22 ]. Although the formation of viruses with heterologous packaging signals was disfavored, it was not entirely excluded. This degree of flexibility in IAV packaging gives the potential for large changes, or shifts, in viral genotype to occur when highly heterologous strains reassort.

In contrast to other forms of recombination, reassortment does not rely on template switching during replication and does not result in the formation of chimeric genes. Reassortment therefore does not give rise to nonfunctional genes. Nevertheless, most reassortment events are deleterious, even between similar viruses [ 23 ] Fig 2. The reason is that many viral components act in concert, and coevolution of these components optimizes their physical or functional interactions.

Reassortment, however, can abruptly pair divergent—often incompatible—viral genes. The polymerase of IAV is, for example, a tripartite complex composed of proteins encoded on three different segments.

Reassortment among these segments is frequently associated with suboptimal polymerase activity and reduced fitness of the reassortant viruses [ 24 , 25 ].