WWW.WA S .ORG • WORLD AQUACULTURE • SEP TEMBER 2022 29 ( C O N T I N U E D O N P A G E 3 0 ) the interfering virus g at longer times (4 - 6 min) after inoculation of a resulted in lower interference (Delbrück and Luria 1942). Mechanisms of Virus Interference Because these earliest studies, it was thought that more than one mechanism of virus interference may be at play. At present, knowledge on virus interactions have greatly increased and various types have been reported. Many of the known virus-virus interactions have been grouped into different types (DaPalma et al. 2010) of which the set of direct interactions of viral genes or gene products may be the type of interaction that include some of the known virus interference mechanisms. SuperinfectionExclusion Superinfection exclusion is one mechanism of virus interference that consists of a primary virus infection (interfering), inducing resistance to a subsequent infection by another virus (superinfecting), which may be similar or different from the interfering one. This type of interference has been reported in several types of viruses, including bacteriophages, flaviviruses, orthomyxoviruses, paramyxoviruses, retroviruses, hepadnaviruses, arboviruses and plant viruses. Here, a host cell simultaneously infected with two different viruses shows interference, as one single interfering virus particle is able to inhibit replication of a superinfective virus in any interfered cell. In experiments done with bacterial cells exposed to two different bacteriophages, some features of the mechanism of virus interference were unraveled: 1) interference did not depend on virus adsorption to cells, penetration into the host cell or competition for a key enzyme (Delbrück 1945, Wagner 1960), 2) interference did not induce cross-immunity and 3) one cell never released both virus types, only one. This was called the mutual exclusion effect (Delbrück 1945, Wagner 1960), as it is an all-or-nothing event. An alternative outcome to the mutual exclusion effect was called “the depressor effect,” indicating a reduced yield of both viruses compared to their normal replication yield upon an interference event. Later, it was proposed that both the mutual exclusion and depressor effect were the result of the superinfecting virus not getting access to the cell division machinery (Wagner 1960). It is possible that the “mutual exclusion effect” described in bacterial cells may be analogous to the superinfection exclusion reported in viruses infecting animals, provided that the two viruses replicate in the same cellular compartment. Examples of superinfection exclusion in animal hosts include various strains of viruses of the same species, such as influenza virus, strains of yellow fever virus with different tissue affinities, interference caused by many other viruses of different species and even between viruses of different families (Fig. 2). Interference between viruses of the same species (strains) is related to changes in virulence between those virus variants. This can be evaluated by protection of the host against the virulent variant or by determining the presence of viral progeny of the virulent strain. Here, the interfering agent always is an active virus. Defective Interfering Particles (DIPs) An alternative virus interference mechanism is caused by Defective Interfering Particles (DIPs). This mechanism is different from superinfection exclusion because DIPs are not fully replicating viruses. DIPs or their genomes may constrain different stages of the virus replication cycle, thus inducing an antiviral effect (Fig. 4). DIPs of rabies, hepatitis A, West Nile, coxsackie, rubella and Dengue viruses can block adsorption and penetration steps of native virus particles, thus preventing virus entry to cells. DIPs of influenza virus interfere with replication of the native virus rather than transcription of viral RNA synthesis. DIPs or their genomes FIGURE 3.Virus interference in bacterial host. Bacteriophage species T2 [γ] and T1 [α] were simultaneously inoculated in equal amounts into E. coli cultures. interfering virus γ inhibited replication of virus α by 67 percent. FIGURE 4.Virus interference caused by Defective Interfering Particles (DIPs). DIPs can block the adsorption and/or penetration steps of normal virus particles, preventing virus entry and thus inducing virus interference. Also, their genomes may hinder various stages of the virus replication cycle, inducing an antiviral effect.
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