Retroviral superinfection resistance

Superinfection exclusion (SIE) is an antagonistic virus-virus interaction whereby initial infection by one virus prevents subsequent infection by closely related viruses. Although SIE has been described in diverse viruses infecting plants, humans, and animals, its mechanisms, including involvement of specific viral determinants, are just beginning to be elucidated. In this study, SIE determinants encoded by two economically important wheat viruses, Wheat streak mosaic virus (WSMV; genus Tritimovirus, family Potyviridae) and Triticum mosaic virus (TriMV; genus Poacevirus, family Potyviridae), were identified in gain-of-function experiments that used heterologous viruses to express individual virus-encoded proteins in wheat. Development of reverse genetics systems for viruses has revolutionized the understanding of viral replication, infection, and disease development through identification of viral determinants involved in these processes as well as the elucidation of interactions between viral and host factors (1-3). However, virusvirus interactions in hosts that facilitate superinfection exclusion (SIE) between related viruses or synergistic interactions between unrelated viruses have received less attention (4, 5). Synergistic interactions are facilitative virus-virus interactions between two or more unrelated viruses, and these interactions often cause increased virus accumulation of one or both viruses that could lead to severe disease compared to infection by individual viruses (4). In contrast, SIE is the result of antagonistic virus-virus interactions between closely related viruses (5-7).SIE, often referred to as "cross-protection" or "homologous interference," is defined as the phenomenon whereby initial infection by one virus prevents subsequent infection of preinfected cells by closely related viruses. SIE was originally observed between two strains of Tobacco mosaic virus (TMV) (6, 7), followed by observations with bacteriophages (8, 9). In TMV, cross-protection was used to examine the relatedness of newly collected virus isolates as being strains of, or distinct from, existing virus isolates (7, 10). Subsequently, cross-protection has been used for the management of plant viruses by purposefully infecting plants with mild isolates of a virus to prevent infection by severe isolates (11,12).The SIE phenomenon has been observed in diverse groups of plant-, human-, and animal-infecting viruses belonging to the reverse transcribing viruses such as Human immunodeficiency virus

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

The Coat Protein and NIa Protease of Two Potyviridae Family Members Independently Confer Superinfection Exclusion

Satyanarayana

French

2016

“…It is remarkable that many unrelated viruses can prevent secondary infections of cells by closely related genotypes (9)(10)(11)(12)(13)(14)(15)(16)(17)(18). In these cases of "superinfection exclusion," different viral genotypes coinfecting a host are rarely found coinfecting cells, and they sometimes segregate into distinct groups of cells or tissues within which only one genotype is observed (19)(20)(21)(22)(23)(24)(25).…”

Section: Importancementioning

confidence: 99%

The Multiplicity of Cellular Infection Changes Depending on the Route of Cell Infection in a Plant Virus

Gutiérrez

Pirolles

Yvon

et al. 2015

The multiplicity of cellular infection (MOI) is the number of virus genomes of a given virus species that infect individual cells. This parameter chiefly impacts the severity of within-host population bottlenecks as well as the intensity of genetic exchange, competition, and complementation among viral genotypes. Only a few formal estimations of the MOI currently are available, and most theoretical reports have considered this parameter as constant within the infected host. Nevertheless, the colonization of a multicellular host is a complex process during which the MOI may dramatically change in different organs and at different stages of the infection. IMPORTANCEThe MOI is the size of the viral population colonizing cells and defines major phenomena in virus evolution, like the intensity of genetic exchange and the size of within-host population bottlenecks. However, few studies have quantified the MOI, and most consider this parameter as constant during infection. Our results reveal that the MOI can depend largely on the route of cell infection in a systemically infected leaf. The MOI is usually one genome per cell when cells are infected from virus particles moving long distances in the vasculature, whereas it is much higher during subsequent cell-to-cell movement in mesophyll. However, a fast-acting superinfection exclusion prevents cell coinfection by merging populations originating from different primary foci within a leaf. This complex colonization pattern results in a situation where within-cell interactions are occurring almost exclusively among kin and explains the common but uncharacterized phenomenon of genotype spatial segregation in infected plants.V iral populations can evolve rapidly, even during a single host infection, and the resulting changes in the population ultimately can affect the outcome of viral diseases. A clear example of this is the emergence of drug-resistant mutants of animal/human viruses, of resistance-breaking variants of plant viruses, or of recombinant genotypes with an enlarged host range. Therefore, it is not surprising that increasing efforts are being made to characterize parameters defining within-host evolution of viral populations.Since viruses are obligate intracellular parasites, a fundamental parameter determining their within-host population dynamics/ genetics is the multiplicity of cellular infection (MOI), defined as the number of genomes of a given virus species that infects a cell. The MOI influences two major processes in viral evolution, namely, the population bottlenecks and the interactions among genotypes. Within-host bottlenecks are linked to the number of infected cells during host colonization and to the MOI at which these cells are infected. The overall intensity of interactions among viral genomes, i.e., competition, genetic exchange, functional complementation, and collective action, depends to a large extent on the probability of encountering different genotypes within host cells, a probability that is directly linked to the MOI. Given the ...

“…This allows the first virus to maximize the production of progeny virus particles once the cell has been infected. Although superinfection exclusion is a recognized effect for different virus species, several mechanisms for the phenomenon have been described (2,3,(6)(7)(8). However, total exclusion brings potential disadvantages for the virus, as it reduces or abolishes the possibility of generation of recombinants in situations in which the generation of genetic diversity is advantageous for virus survival.…”

mentioning

confidence: 99%

Superinfection Exclusion in Alphabaculovirus Infections Is Concomitant with Actin Reorganization

Beperet

Irons

Simón

et al. 2014

Superinfection exclusion is the ability of an established virus to interfere with a second virus infection. This effect was studied in vitro during lepidopteran-specific nucleopolyhedrovirus (genus observed following inoculation with mixtures of these two phylogenetically distant nucleopolyhedroviruses-AcMNPV and SfMNPV-but at a frequency lower than predicted, suggesting interspecific virus interference during infection or replication. The temporal window of infection is likely necessary to maintain genotypic diversity that favors virus survival but also permits dual infection by heterospecific alphabaculoviruses.IMPORTANCE Infection of a cell by more than one virus particle implies sharing of cell resources. We show that multiple infection, by closely related or distantly related baculoviruses, is possible only during a brief window of time that allows additional virus particles to enter an infected cell over a period of ca. 16 h but then blocks multiple infections as newly generated virus particles begin to leave the infected cell. This temporal window has two important consequences. First, it allows multiple genotypes to almost simultaneously infect cells within the host, thus generating genetically diverse virus particles for transmission. Second, it provides a mechanism by which different viruses replicating in the same cell nucleus can exchange genetic material, so that the progeny viruses may be a mosaic of genes from each of the parental viruses. This opens a completely new avenue of research into the evolution of these insect pathogens.