RNA Silencing May Play a Role in but Is Not the Only Determinant of the Multiplicity of Infection

Abstract

The multiplicity of infection (MOI), i.e., the number of viral genomes that infect a cell, is an important parameter in virus evolution, which for each virus and environment may have an optimum value that maximizes virus fitness. Thus, the MOI might be controlled by virus functions, an underexplored hypothesis in eukaryote Strong evidence supports the fact that, in nature, mixed rather than single viral infections may predominate in both plant and animal hosts (1, 2). Mixed infections result in a variety of virusvirus interactions, from cooperation to competition for host resources, which affect each virus's fitness. Thus, mixed infections are a factor in virus evolution, and there is evidence supporting the prediction that the within-host dynamics of microparasites in mixed infections affect virulence evolution (3-5). Mixed infections may also affect the genetic diversity and structure of virus populations, as coinfection is required for genetic exchange to occur, either by recombination or by genome segment reassortment between different virus species or genotypes (6, 7). Accordingly, interactions between viruses are relevant to understand virus evolution and epidemiology, as well as for the development of efficient control strategies against viral infections (7). At the cellular level, the extent of these interactions is mostly influenced by the number of viral genomes that infect the same cell, a parameter called the multiplicity of infection (MOI) (8-11).The MOI is a key parameter in virus evolution, because the extent of cell coinfection determines the extent of competition among virus variants and, hence, their fitness compared with single infections. Also, as the MOI is equivalent to the ploidy level, it determines the rates of genetic exchange, and thus genetic diversity, and of trans-complementation of defective mutants, slowing down selection against them (9, 12, 13). Despite its relevance, there are very few experimental estimates of the MOI. For plantinfecting viruses, six estimates have been reported. The first was presented by for the colonization of Nicotiana benthamiana Domin. by Tobacco mosaic virus (TMV) (genus Tobamovirus). The numbers of singly and doubly infected cells were monitored in inoculated and systemically infected leaves us-

When Viruses Play Team Sports: Mixed Infections in Plants

“…The interaction between viruses inside a host cell (as represented schematically in figure 2) can be highly influenced by the multiplicity of infection (MOI) that indicates the number of viral genomes present in the same cell (Gutiérrez et al, 2010). There are some indications that the MOI is controlled by virus-encoded functions, such as the suppression of RNA silencing mechanisms (Donaire et al, 2016). In mixed infections of N. benthamiana with two genotypes of TMV, it was observed that the MOI was higher at initial stages, and then changed (Gonzalez-Jara et al, 2009).…”

The role of co-opted ESCRT proteins and lipid factors in protection of tombusviral double-stranded RNA replication intermediate against reconstituted RNAi in yeast

“…A long-standing unanswered question is that which co-opted host components are involved in VRC assembly that protect (+)RNA viruses during replication from the potent RNAi response. The protection provided by VRCs seems significant, because plant (+)RNA viruses could replicate and accumulate even in the absence of RNAi suppressors [ 51 , 52 ]. Moreover, the Dicer-like enzymes could not completely degrade the viral dsRNA in infected cells, indicating that the viral dsRNA enjoys significant protection during replication.…”

Bottleneck, Isolate, Amplify, Select (BIAS) as a mechanistic framework for intracellular population dynamics of positive-sense RNA viruses

“…2009 ; Tromas et al. 2014 ; Donaire, Burgyán, and García-Arenal 2016 ). These authors infected plants with paired viral variants derived from three viruses: TEV, tobacco mosaic virus (TMV), and tomato bushy stunt virus (TBSV); and isolated single protoplast cells from infected leaves at multiple time points.…”

“…2009 ; Tromas et al. 2014 ; Donaire, Burgyán, and García-Arenal 2016 ). The authors established that, in the systemically infected plant leaves, successfully infected cells were mostly colonized by fewer than three founding genomes.…”