The majority of duck hepatitis B virus reverse transcriptase in cells is nonencapsidated and is bound to a cytoplasmic structure.
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The hepadnavirus reverse transcriptase binds cotranslationally to the viral pregenomic RNA. This ribonucleoprotein complex is then encapsidated into nascent viral core particles, where the reverse transcriptase copies the viral RNA into DNA. Here we report that 75% of the duck hepatitis B virus reverse transcriptase present in transfected LMH cells does not follow this well-known pathway but rather exists in the cell separate from the core protein or nucleocapsids. The nonencapsidated reverse transcriptase is also abundant in infected duck liver. The nonencapsidated reverse transcriptase exists as a complex set of isoforms that are most likely produced by posttranslational modification. Interestingly, only the smallest of these isoforms is encapsidated into viral core particles. The nonencapsidated reverse transcriptase is bound to a large cellular cytoplasmic structure(s) in a detergent-sensitive complex. The cellular distribution of the reverse transcriptase only partially overlaps that of the core protein, and this distribution is unaffected by blocking encapsidation. These observations raise the possibilities that the metabolic fate of the reverse transcriptase may be posttranscriptionally regulated and that the reverse transcriptase may have roles in the viral replication cycle beyond its well-known function in copying the viral genome. (+info)
Amplified fragment length polymorphism analysis of Campylobacter jejuni strains isolated from chickens and from patients with gastroenteritis or Guillain-Barre or Miller Fisher syndrome.
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The high-resolution genotyping method of amplified fragment length polymorphism (AFLP) analysis was used to study the genetic relationships between Campylobacter jejuni strains infecting chickens (n = 54) and those causing gastroenteritis in humans (n = 53). In addition, C. jejuni strains associated with the development of Guillain-Barre syndrome (GBS) (n = 14) and Miller Fisher syndrome (MFS) (n = 4), two related acute paralytic syndromes in human, were included. Strains were isolated between 1989 and 1998 in The Netherlands. The AFLP banding patterns were analyzed with correlation-based and band-based similarity coefficients and UPGMA (unweighted pair group method using average linkages) cluster analysis. All C. jejuni strains showed highly heterogeneous fingerprints, and no fingerprints exclusive for chicken strains or for human strains were obtained. All strains were separated in two distinct genetic groups. In group A the percentage of human strains was significantly higher and may be an indication that genotypes of this group are more frequently associated with human diseases. We conclude that C. jejuni from chickens cannot be distinguished from human strains and that GBS or MFS related strains do not belong to a distinct genetic group. (+info)
A model for evaluating intervention strategies to control salmonella in the poultry meat production chain.
(51/1831)
A model of the transmission of salmonella through the poultry meat production chain is developed, to predict the effects of intervention strategies for salmonella control. The model first describes the situation before intervention in terms of salmonella prevalences at flock level and some transmission parameters. After single control measures are translated into effects on these transmission parameters, the effects of sets of control measures (intervention strategies), can be calculated with the model. As research data are lacking, the model input parameters were derived from expert opinion. As an example, the effects of two intervention strategies proposed for the Dutch poultry industry are predicted. A sensitivity analysis is performed to indicate where the most effective control measures may be expected. Additionally, the reliability of the model predictions is studied by an uncertainty analysis. The use of the model as a tool for policy makers deciding about salmonella control strategies is discussed. (+info)
Heritabilities of and genetic relationships between salmonella resistance traits in broilers.
(52/1831)
Using experimental infections, three traits for salmonella resistance were studied: mortality, survival time (in animals that died by infection), and quantitative cecal salmonella carriage at the end of the rearing period (in animals that did not die). In total, 548 animals were used; mortality was 29.2%, mean survival time was 5.97 d (n = 160), and the mean 10log of colony forming units per gram of cecal contents was 1.62 (n = 387). Genetic parameters were evaluated in bivariate threshold-linear models to account for the selective measurement of survival time and cecal carriage. Heritabilities were .06 for survival time, .09 for cecal carriage, and .12 for mortality. The genetic correlation between mortality and cecal carriage was weak (.26), which suggests that these traits are largely controlled by different genes. The genetic correlation between mortality and survival time was relatively strong (-.68). Simultaneous study of multiple traits seems to be of particular importance in judging epidemiological consequences of a possible selection for resistance. Results here indicate that selection on decreased mortality could be unfavorable for the spread of salmonella because the resulting correlated increase in survival time, implying longer shedding by infected animals, is relatively stronger than the correlated decrease in level of cecal carriage. Selection to reduce the level of cecal salmonella carriage could be done while keeping survival time constant, if so desired, because the correlation between these traits is weak (-.15). (+info)
Characterization of fluoroquinolone resistance among veterinary isolates of avian Escherichia coli.
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Fluoroquinolone-resistant avian Escherichia coli isolates from northern Georgia were investigated for gyrA and parC mutations. All isolates contained a mutation in GyrA replacing Ser83 with Leu; seven isolates also contained mutations replacing Asp87 with either Gly or Tyr. Random amplified polymorphic DNA analysis revealed that quinolone-resistant E. coli isolates were genetically diverse. (+info)
New fimbrial gene cluster of S-fimbrial adhesin family.
(54/1831)
Fimbrial adhesins that mediate attachment to host cells are produced by most virulent Escherichia coli isolates. These virulence factors play an important role in the initial stages of bacterial colonization and also in determination of the host and tissue specificity. Isolates belonging to serotype O78 are known to cause a large variety of clinical syndromes in farm animals and humans and have been shown to produce several types of adherence fimbriae. We studied the fimbrial adhesin from an avian septicemic E. coli isolate of serotype O78. Analysis of the genetic organization of the fac (fimbria of avian E. coli) gene cluster indicates that it belongs to the S-fimbrial adhesin family. Seven open reading frames coding for major and minor structural subunits were identified, and most of them showed a high degree of homology to the corresponding Sfa and Foc determinants. The least-conserved open reading frame was facS, encoding a protein known to play an important role in determining adherence specificity in other S-fimbrial gene clusters. (+info)
pMGA phenotypic variation in Mycoplasma gallisepticum occurs in vivo and is mediated by trinucleotide repeat length variation.
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Chickens were infected with a pathogenic strain of Mycoplasma gallisepticum, and the expression of pMGA, the major surface protein, was inferred by examination of colonies from ex vivo cells. Within 2 days postinfection, 40% of cells had ceased the expression of the original pMGA surface protein (pMGA1.1), and by day 6, the majority of recovered cells were in this category. The switch in pMGA phenotype which had occurred in vivo was reversible, since most colonies produced from ex vivo progenitors exhibited frequent pMGA1. 1(+) sectors. After prolonged in vivo habitation, increasing proportions of recovered cells gave rise to variant pMGA colonies which had switched from the expression of pMGA1.1 to another gene, pMGA1.2, concomitant with the acquisition of a (GAA)(12) motif 5' to its promoter. Collectively, the results suggest that changes in M. gallisepticum pMGA gene expression in vivo are normal, common, and possibly obligate events for successful colonization of the host. Surprisingly, the initial cessation of pMGA1.1 expression occurred in the absence of detectable pMGA antibodies and seemed to precede the adaptive immune response. (+info)
Adjuvanticity and inflammatory response following administration of water-in-oil emulsions prepared with saturated hydrocarbons in chickens.
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Water-in-oil emulsions containing bovine serum albumin (BSA) as a model antigen were prepared using aliphatic saturated hydrocarbons with carbon number from 12 to 18, and were tested in chickens. Straight-chain hydrocarbons induced higher antibody titers against BSA after administration than branched-chain hydrocarbons. n-C16H34 and n-C18H38 maintained high antibody titers even at 32 weeks after administration, compared with n-C12H26, n-C14H30 and n-C15H32. n-C12H26 and n-C14H30 raised concentrations of sialic acid and creatine kinase in plasma, both of which are important markers of inflammatory responses, immediately after administration. n-C16H34 and n-C18H38 did not raise the values of these markers. These results indicated that n-C16H34 and n-C18H38 induced elevated and sustained immune responses without severe adverse reactions in chickens. (+info)