28 SEP TEMBER 2022 • WORLD AQUACULTURE • WWW.WA S .ORG related to the brain or central nervous system were resistant to an infection by another herpesvirus strain that replicated better in the brain and other cell types of the central nervous system. This experiment showed interference between strains of the same virus species. In a 1935 experiment by Hoskins, monkeys were infected with two strains of yellow fever virus with different tissue affinities. Monkeys infected by a strain that replicated better in brain tissues were protected against lethal infection by a strain that replicated better in other tissues except brain (Lennette and Koprowski 1946). This experiment showed that two strains of the same virus species induced virus interference observed as the resistance of the host to infection/mortality caused by a highly pathogenic virus. In another study, rhesus monkeys infected by Rift Valley fever virus were protected from infection with the unrelated yellow fever virus (Findlay and MacCallum 1937, Fig. 2). In bacterial hosts, virus interference was first reported in 1942 using as host the bacterium Escherichia coli. Two different viruses infecting bacteria (bacteriophages) interfered with each other’s replication. The bacteriophage species (T2 [g] and T1 [a]) with distinct replication speed and inhibition halo size were evaluated. Equal amounts of these bacteriophages were inoculated into E. coli cultures, showing that T2 [g] inhibited replication of T2 [a] by 67 percent (Fig. 3). This study produced valuable information on the mechanism of virus interference, as interference was not due to differences in virus adsorption by the cells. Also, inoculating Virus interference is the result of a virus-virus interaction between either related or unrelated viruses within a host that modifies the infectivity or replication of at least one of the viruses, inducing host resistance to that virus, which normally would be superinfecting or highly pathogenic (Schlesinger 1959). The main characteristic of virus interference is its independence of any innate or specific host immune responses, either caused by humoral immunity, including the presence of interferons, neutralizing antibodies or cellular defense responses (Isaacs and Burke 1959, Laurie et al. 2018, Fig. 1). Virus interference has been reported to occur in plants, animals and bacteria, but also can occur under experimental conditions in tissue or cell cultures. Historical Background The first hints of the existence of this phenomenon were recorded in the 16th century, when it was noticed that sometimes one disease could be cured by another. In the 18th century, it was reported that children who suffered secondary yaws infection had a milder smallpox infection, and in the 19th century it was observed that cowpox scarification reduced the severity of smallpox infection (Lennette 1951). Virus interference was first reported in plants in 1929 by McKinney. He showed plants infected with the common mosaic virus were resistant to infection by the yellow tobacco mosaic virus. In 1935, virus interference was first recorded in animals. In rabbits, infection with a herpesvirus strain that replicated better in tissues that were not Virus Interference in Crustaceans Cesar M. Escobedo-Bonilla FIGURE 1.Viral interference independent of immune responses. Virus interference is not the result of activation of different immune responses such as interferons, natural antibodies or complement components. FIGURE 2.Virus interference between Rift Valley fever virus and yellow fever virus. Animals infected with the former virus were protected against a lethal infection with the latter virus. The mechanism of interference may be superinfection exclusion.
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