Co-infection weakens selection against epistatic mutations in RNA viruses.
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Co-infection may be beneficial in large populations of viruses because it permits sexual exchange between viruses that is useful in combating the mutational load. This advantage of sex should be especially substantial when mutations interact through negative epistasis. In contrast, co-infection may be detrimental because it allows virus complementation, where inferior genotypes profit from superior virus products available within the cell. The RNA bacteriophage phi6 features a genome divided into three segments. Co-infection by multiple phi6 genotypes produces hybrids containing reassorted mixtures of the parental segments. We imposed a mutational load on phi6 populations by mixing the wild-type virus with three single mutants, each harboring a deleterious mutation on a different one of the three virus segments. We then contrasted the speed at which these epistatic mutations were removed from virus populations in the presence and absence of co-infection. If sex is a stronger force, we predicted that the load should be purged faster in the presence of co-infection. In contrast, if complementation is more important we hypothesized that mutations would be eliminated faster in the absence of co-infection. We found that the load was purged faster in the absence of co-infection, which suggests that the disadvantages of complementation can outweigh the benefits of sex, even in the presence of negative epistasis. We discuss our results in light of virus disease management and the evolutionary advantage of haploidy in biological populations. (+info)
Important disease conditions of newly cultured species in intensive freshwater farms in Greece: first incidence of nodavirus infection in Acipenser sp.
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We describe here the main pathological conditions of freshwater fish recently introduced for intensive rearing (open ponds and recirculating freshwater systems) in Greece. Sturgeon were susceptible to skeletal abnormalities of the spine (scoliosis and lordosis) of unknown aetiology. Horizontal transmission of nodavirus from infected sea bass to sturgeon was detected for the first time. This caused serious pathology and clinical signs, such as lethargy and imbalance, leading to secondary infections with Aeromonas hydrophila and Trichodina sp. and chronic, but steady, mortality. Sea bass were very susceptible to nodavirus infection, monogenean infections and gas bubble disease. Mullet reared under recirculated and open-flow conditions were very sensitive to Chilodonella sp. infection, whereas catfish were susceptible to infection with Ichthyophthirius sp. leading to secondary infections with A. hydrophila, Saprolegnia sp. and Myxobacteria spp. Tilapia were very susceptible to gas bubble disease and A. hydrophila. This bacterium was associated with management manipulations for all species and fully responsive to corrective hygiene methods. (+info)
Molecular detection and characterization of nodavirus in several marine fish species from the northeastern Atlantic.
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Nodaviruses (NNV) are responsible for causing disease outbreaks mainly in hatchery-reared larvae and juveniles of a wide variety of fishes throughout the world. This disease has seriously limited the culture of marine fishes over the last decade. In the Atlantic provinces of Canada, disease caused by a nodavirus was first reported in juvenile Atlantic cod being reared in Nova Scotia, in 1999. More recently, disease outbreaks caused by nodavirus have been identified in hatchery-reared Atlantic cod and haddock in Newfoundland and New Brunswick, respectively, and along the east coast of the USA. The presence of NNV in wild Atlantic cod adults and wild winter flounder has also been reported. Nodaviruses were isolated from cultured Atlantic cod and haddock, as well as from wild winter flounder from a variety of geographical localities, and their virus coat (capsid) protein genes were partially sequenced. An analysis of the data indicates that all of the nodaviruses isolated from eastern North America were closely related to one another, but that they were distinct from the European isolates already sequenced. Regardless of host species, isolates from close geographical localities were more similar than those from distant geographical areas. At the protein level, differences in coat protein sequences were seen only for strains isolated from Atlantic cod originating from Newfoundland. Our results suggest that NNV may have been present in the Atlantic off Canada and on the east coast of the USA for some time, and has evolved to form a monophyletic group, distinct from other isolates found in cold-water species. Non-lethal methods for detection of NNV are necessary to develop management strategies for this disease, and would be an asset to diagnosticians and producers. Based on the results of this study, new primers were designed and developed for an improved RT-PCR assay able to detect North Atlantic nodaviruses in ovarian fluids, eggs and other tissues. The application of this test to field samples is discussed. (+info)
Nodavirus infection causes mortalities in hatchery produced larvae of Lates calcarifer: first report from India.
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Larvae (15 to 21 d post hatch, dph) of the Asian sea bass Lates calcarifer (Bloch) suffered heavy mortalities (60 to 90%) during the hatchery-rearing phase. Darkened and moribund larvae showed no evidence of bacterial or parasitic infections. Tissue sections of brain and spinal cord showed clear necrotic vacuolation. Electron microscopy revealed membrane-bound viral particles in the cytoplasm of the nerve cells. The viral particles measured 28 to 30 nm in diameter. Primer sets, designed for the amplification of the RNA2 segment of the piscine nodavirus coat protein gene, were used in the RT-PCR analysis of moribund larvae of 20 and 21 dph which produced the amplified product of 430 bp. The clinical manifestations, pathology and electron microscopy observations supported by the RT-PCR analysis suggest that the nerve necrosis was due to nodavirus infection in the larvae. This is the first report of piscine nodavirus infection from the Indian sub-continent. (+info)
Cell type-specific involvement of RIG-I in antiviral response.
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Toll-like receptors (TLRs) play an important role in antiviral response by recognizing viral components. Recently, a RNA helicase, RIG-I, was also suggested to recognize viral double-stranded RNA. However, how these molecules contribute to viral recognition in vivo is poorly understood. We show by gene targeting that RIG-I is essential for induction of type I interferons (IFNs) after infection with RNA viruses in fibroblasts and conventional dendritic cells (DCs). RIG-I induces type I IFNs by activating IRF3 via IkappaB kinase-related kinases. In contrast, plasmacytoid DCs, which produce large amounts of IFN-alpha, use the TLR system rather than RIG-I for viral detection. Taken together, RIG-I and the TLR system exert antiviral responses in a cell type-specific manner. (+info)
Persistent infection of betanodavirus in a novel cell line derived from the brain tissue of barramundi Lates calcarifer.
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In order to obtain an in vitro system for studying the mechanism of persistent infection of fish nodavirus, a novel cell line (BB) was established from the brain tissue of a barramundi, Lates calcarifer, which had survived viral nervous necrosis disease. The cell line has been subcultured > 100 times. The persistence of fish nodavirus designated as barramundi brain nervous necrosis virus (BBNNV) in the BB cells was demonstrated by: (1) the detection of the infectious virus in the culture supernatants, (2) the detection of NNV nucleic acids extracted from the BB cells, (3) the positive result of immunochemical staining using an NNV-specific monoclonal antibody and (4) their resistance to infection by another fish nodavirus grouper NNV (GNNV). No temperature-sensitive mutants were detected in the culture supernatant of the BB cells. Neither truncated genome (RNA1 or RNA2) nor smaller coat protein was found in the purified BBNNV particles, suggesting that defective interfering particles were unlikely to be important in the NNV-persistent infection in the BB cells. The result of the neutralization test indicated that the 5 antigenic determinants, recognized by GNNV-specific neutralizing antibodies, also existed on the coat protein of BBNNV. The BB cell line is the first cell line reported to be persistently infected with NNV, and would be a useful model for understanding the mechanisms of NNV-persistent infection in vitro and in vivo. (+info)
We estimated for Australia the number of cases, hospitalizations, and deaths due to foodborne gastroenteritis in a typical year, circa 2000. The total amount of infectious gastroenteritis was measured by using a national telephone survey. The foodborne proportion was estimated from Australian data on each of 16 pathogens. To account for uncertainty, we used simulation techniques to calculate 95% credibility intervals (CrI). The estimate of incidence of gastroenteritis in Australia is 17.2 million (95% confidence interval 14.5-19.9 million) cases per year. We estimate that 32% (95% CrI 24%-40%) are foodborne, which equals 0.3 (95% CrI 0.2-0.4) episodes per person, or 5.4 million (95% CrI 4.0-6.9 million) cases annually in Australia. Norovirus, enteropathogenic Escherichia coli, Campylobacter spp., and Salmonella spp. cause the most illnesses. In addition, foodborne gastroenteritis causes approximately 15,000 (95% CrI 11,000-18,000) hospitalizations and 80 (95% CrI 40-120) deaths annually. This study highlights global public health concerns about foodborne diseases and the need for standardized methods, including assessment of uncertainty, for international comparison. (+info)
Innate signals compensate for the absence of PKC-{theta} during in vivo CD8(+) T cell effector and memory responses.
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PKC- is central to T-helper (Th) 2 cell differentiation and effector function; however, its importance for antiviral effector, and in particular memory CD8(+) T cell responses, remains unclear. We have investigated the role of PKC- during in vivo and in vitro responses against influenza virus, lymphocytic choriomeningitis virus, vaccinia virus, and replication-deficient virus-like particles. In the absence of PKC-, antiviral CD8(+) T cells presented an unresponsive phenotype in vitro, which could be restored with exogenous IL-2 or by Toll-like receptor ligand-activated dendritic cells. In striking contrast, PKC- appeared to be superfluous for in vivo antiviral responses irrespective of whether the virus infected systemically, was localized to the lung, or did not replicate. In addition, CD8(+) CCR7-effector memory responses were normal in PKC--deficient mice, both in lymphoid and peripheral tissues. Our data show that increased activation signals delivered in vivo by highly activated dendritic cells, as present during viral infections, overcome the requirement for PKC- during CD8(+) T cell antiviral responses. (+info)