30 SEP TEMBER 2022 • WORLD AQUACULTURE • WWW.WA S .ORG lack an immune system with cells that remember and recognize foreign particles and pathogens or antibody-producing cells; instead, they have an efficient defense system able to recognize molecules related to microbial cell walls, thus eliminating foreign materials and microorganisms. Penaeid shrimp species such as Letopenaeus vannamei and Penaeus monodon are among the most cultured crustaceans in aquaculture. These animals are also susceptible to infectious diseases of diverse etiology, of which viruses may be among the most damaging (Lightner 2011). Since its beginnings, shrimp aquaculture has been affected by several viruses causing important damages to the industry. The first description of viral pathogens in a wild crustacean, the crab Liocarcinus depurator, dates to 1966 (Johnson 1977). Later, the virus Baculovirus penaei was found in the marine shrimp P. duorarum (Couch 1974). Simultaneous infection of two viruses in wild or farmed crustaceans was reported (Owens et al. 2010, Texeira-Lopes et al. 2011, Feijo et al. 2013, Senapin et al. 2013), suggesting the high probability of virus-virus interactions in these hosts. In fact, few events of heterologous virus interference have been reported in crustaceans. Virus interference may be relevant because it could prove to be a natural alternative aimed to reduce the impact of highly pathogenic viruses. This strategy may be applied in areas where some interfering viruses are endemic in crustacean populations. Thus, virus interference could become an aid against deadly virus epizootics. At present, more than 20 viruses have been reported to infect penaeid shrimp and most have caused huge losses. In time, some viruses have become less pathogenic to shrimp but others continue to be very damaging. The Penstylhamaparvovirus 1, formerly known as infectious hypodermal and haematopoietic necrosis virus (IHHNV) (Pénzes et al. 2020), has become an endemic virus in many shrimp farming countries and its pathogenicity apparently has declined. This virus has a small (» 20 nm) icosahedral naked virion with a single-stranded DNA genome of 3900 base pairs (bp) (Bonami et al. 1990). In contrast, white spot syndrome virus (WSSV) is a large (120 nm × 280 nm), bacilliform enveloped virion with a tail-like appendage at one end. Its genome is one of the largest in viruses that infect animals (292,000-308,000 bp). Both viruses infect multiple tissues and organs of mesodermal and ectodermal origin, including epithelial cells and connective tissues of gills, foregut, integument, haematopoietic tissues and antennal gland, among other tissues (Escobedo-Bonilla et al. 2008). may also hinder packaging steps, causing an antiviral effect. Also, DIPs of lymphocytic choriomeningitis virus promotes the release of DIPs and inhibits exit of native viral particles from cells in a process called viral budding, thus inducing an antiviral effect (Yang et al. 2019). Cell Receptor Blockade Another mechanism of virus interference is the cell receptor blockade (Lennette 1951, Fig. 5). This mechanism works by adsorption of virus to cellular receptors as the first step of infection, with subsequent destruction of the receptor by a viral enzyme. This creates a breach in the cellular defense that allows virus entry into the cell. Virus Interference and Host Response Interference between viruses of the same species (heterotypic) or family (homologous) may be more difficult to distinguish from immune responses and genetic interactions because both viruses have antigenic similarity. Nonetheless, interference between closely related viruses can be recognized from immune responses. The time interval between inoculation of interfering and superinfecting viruses must not be long to prevent the stimulation of immune responses by the first inoculated virus. Also, the dose of the superinfecting virus may not be large to prevent a further stimulation of a secondary immune response (Schlesinger 1959). In contrast, interference between viruses of different species or family (heterologous) can be better identified from immune responses because the viruses are antigenically distinct. Hence, lack of immunogenicity against the virus pairs by the host or the independence of interference to any relationship to antigenic reactions and antibody production is an important criterion in this type of interference. Many interference studies have been done using viruses of different families in a variety of hosts, including crustaceans. Important information about timing and dosing of interfering and superinfective viruses has been obtained, despite the fact that interference cannot always be quantified or clearly observed as inhibition of replication. Instead, interference has been shown as protection against disease and/or mortality caused by the superinfecting virus. The degree of protection is dependent on the host-virus system and the severity of disease leading to pathological manifestations of death, both in vivo and in vitro. Viral Infection of Crustaceans Crustaceans are a diverse group of arthropods, many of which have economic importance as food items and are major resources in fisheries and aquaculture operations worldwide. Crustaceans FIGURE 5.Virus interference caused by cell receptor blockade. In this mechanism, the interfering virus is adsorbed by cellular receptors, and subsequently, the neuraminidase (sialic acid-cleaving) activity destroys the cellular receptor preventing further virus entry into the cell.
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