Andreas Sauerbrei

Universitätsklinikum Jena, Jena, Thuringia, Germany

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Publications (156)349.47 Total impact

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    ABSTRACT: In this study, approaches were developed to examine the phenotype of non-viable clinical VZV strains with amino acid (aa) substitutions in the thymidine kinase (TK, ORF36) and/or DNA polymerase (Pol, ORF28) suspected to cause resistance to antivirals. Initially, recombinant TK proteins containing aa substitutions described as known or suspected cause of antiviral resistance were analyzed by measuring the TK activity applying a modified commercial enzyme immunoassay. To examine the effect of these TK and several Pol substitutions on the replication of recombinant virus strains, the method of en-passant mutagenesis was used. Targeted mutations within the ORF36 and/or ORF28 and an autonomously expressed gene of the monomeric red fluores-cent protein for plaque identification were introduced into the European wild-type VZV strain HJO. Plaque reduction assays revealed that the aa substitutions with unknown function in TK, Q303stop, N334stop, A163stop, and aa Δ7-74, were associated with resistance against acyclovir (ACV), penciclovir, or brivudin, whereas L73I and the Pol substitutions T237K and A955T revealed sensitive viral phenotypes. The results were confirmed by quantitative PCR measuring the viral load under increasing ACV concentrations. In conclusion, analyzing the enzymatic activity of recombinant TK proteins represents a useful tool to evaluate the significance of aa substitutions for antiviral resistance of clinical VZV strains. However, direct testing of replication-competent viruses by the introduction of non-synonymous mutations in a VZV bacterial artificial chromosome using en-passant mutagenesis led to reliable phenotypic results. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Antimicrobial Agents and Chemotherapy 02/2015; 59(5). DOI:10.1128/AAC.05115-14 · 4.45 Impact Factor
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    ABSTRACT: The administration of drugs to inhibit metabolic pathways not only reduces the risk of obesity-induced diseases in humans but may also hamper the replication of different viral pathogens. In order to investigate the value of the US Food and Drug Administration-approved anti-obesity drug orlistat in view of its anti-viral activity against different human-pathogenic viruses, several anti-viral studies, electron microscopy analyses as well as fatty acid uptake experiments were performed. The results indicate that administrations of non-cytotoxic concentrations of orlistat reduced the replication of coxsackievirus B3 (CVB3) in different cell types significantly. Moreover, orlistat revealed cell protective effects and modified the formation of multi-layered structures in CVB3-infected cells, which are necessary for viral replication. Lowering fatty acid uptake from the extracellular environment by phloretin administrations had only marginal impact on CVB3 replication. Finally, orlistat reduced also the replication of varicella-zoster virus moderately but had no significant influence on the replication of influenza A viruses. The data support further experiments into the value of orlistat as an inhibitor of the fatty acid synthase to develop new anti-viral compounds, which are based on the modulation of cellular metabolic pathways.
  • Future Virology 02/2015; 10(2):77-88. DOI:10.2217/fvl.14.97 · 1.00 Impact Factor
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    ABSTRACT: Streptococcus (S.) pneumoniae is a major cause of secondary bacterial pneumonia during influenza epidemics. Neuraminidase is a virulence factor of both pneumococci and influenza viruses. Bacterial neuraminidases are structurally related to viral neuraminidases and susceptible to oseltamivir, an inhibitor designed to target viral neuraminidases. This prompted us to evaluate the antipneumococcal potential of two neuraminidase inhibiting natural compounds, the diarylheptanoid katsumadain A and the isoprenylated flavone artocarpin. Chemiluminescence, fluorescence-, and hemagglutination-based enzyme assays were applied to determine the inhibitory efficiency (IC50 value) of the tested compounds towards pneumococcal neuraminidase. The mechanism of inhibition was studied via enzyme kinetics with recombinant NanA neuraminidase. Unlike oseltamivir, which competes with the natural substrate of neuraminidase, artocarpin exhibits a mixed-type inhibition with a Ki value of 9.70 μM. Remarkably, artocarpin was the only neuraminidase inhibitor for which an inhibitory effect in pneumococcal growth (MIC: 0.99–5.75 μM) and biofilm formation (MBIC: 1.15–2.97 μM) was observable. In addition, we discovered that the bactericidal effect of artocarpin can reduce the viability of pneumococci by a factor of >1000, without obvious harm to lung epithelial cells. This renders artocarpin a promising natural product for further investigations.
    International Journal of Medical Microbiology 12/2014; 305(3). DOI:10.1016/j.ijmm.2014.12.004 · 3.42 Impact Factor
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    ABSTRACT: The amino acid substitution of aspartic acid to glycine in hemagglutinin (HA) in position 222 (HA-D222G) as well as HA-222D/G polymorphism of pandemic (H1N1) 2009 influenza viruses (A(H1N1)pdm09) were frequently reported in severe influenza in humans and mice. Their impact on viral pathogenicity and the course of influenza has been discussed controversially and the underlying mechanism remained unclarified. In the present study, BALB/c mice, infected with the once mouse lung- and cell-passaged A(H1N1)pdm09 isolate A/Jena/5258/09 (mpJena/5258), developed severe pneumonia. From day 2 to 3 or 4 post infection (p.i.) symptoms (body weight loss and clinical score) continuously worsened. After a short disease stagnation or even recovery phase in most mice, severity of disease further increased on days 6 and 7 p.i. Thereafter, surviving mice recovered. A 45 times higher virus titer maximum in the lung than in the trachea on day 2 p.i. and significantly higher tracheal virus titers compared to lung on day 6 p.i. indicated changes in the organ tropism during infection. Sequence analysis revealed an HA-222D/G polymorphism. HA-D222 and HA-G222 variants co-circulated in lung and trachea. Whereas, HA-D222 variant predominated in the lung, HA-G222 became the major variant in the trachea after day 4 p.i. This was accompanied by lower neutralizing antibody titers and broader receptor recognition including terminal sialic acid α-2,3-linked galactose, which is abundant on mouse trachea epithelial cells. Plaque-purified HA-G222-mpJena/5258 virus induced severe influenza with maximum symptom on day 6 p.i. These results demonstrated for the first time that HA-222D/G quasispecies of A(H1N1)pdm09 caused severe biphasic influenza because of fast viral intra-host evolution, which enabled partial antibody escape and minor changes in receptor binding.
    PLoS ONE 08/2014; 9(8):e104233. DOI:10.1371/journal.pone.0104233 · 3.53 Impact Factor
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    ABSTRACT: The avian-like swine influenza viruses emerged in 1979 in Belgium and Germany. Thereafter, they spread through many European swine-producing countries, replaced the circulating classical swine H1N1 influenza viruses and became endemic. Serological and subsequent molecular data indicated an avian source, but details remained obscure due to a lack of relevant avian influenza virus sequence data. Here, the origin of the European avian-like swine influenza viruses was analyzed using a collection of sixteen European swine H1N1 influenza viruses sampled in 1979-1981 in Germany, the Netherlands, Belgium, Italy and France as well as several contemporaneous avian influenza viruses of various serotypes. The phylogenetic trees suggest a triple reassortant with a unique genotype constellation. Time-resolved maximum clade credibility trees indicate times to the most recent common ancestors of 34-46 years (before 2008) depending on the RNA segment and the method of tree inference.
    Journal of General Virology 07/2014; 95. DOI:10.1099/vir.0.068569-0 · 3.53 Impact Factor
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    ABSTRACT: An increase in acute autochthonous hepatitis E virus (HEV) infections has been recorded in Germany. These are suspected to be zoonotically transmitted from wild boar, deer and domestic pig. The latter may represent a major reservoir for HEV. In this study, 537 sera from humans living in Westphalia and Lower Saxony, representing areas of high pig density in Germany, were tested for the presence of HEV-specific antibodies. Among them were 302 individuals with occupational, direct contact to pigs and 235 individuals without direct contact to pigs. Two commercial tests and one in-house assay were applied for the detection of HEV-specific immunoglobulin G (IgG) antibodies. Sera were also tested in an assay that detects all classes of HEV-specific antibodies. Depending on the test used, the seroprevalence ranged from 4.1 to 27.9 %. Exposition to pigs was found to be associated with a significantly higher seroprevalence in subjects with contact to pigs (13.2-32.8 %) compared with that in non-exposed humans (7.7-21.7 %). In particular, individuals younger than 40 years with occupational exposure exhibited a markedly higher HEV seroprevalence compared with non-exposed individuals of that age group. In general, HEV seroprevalence increased with age resulting in a similar prevalence level in the age group of ≥50 years for exposed and non-exposed individuals. Analysis of all sera by a commercial anti-HEV IgM ELISA revealed 35 positive and 25 borderline samples. However, only one positive serum could be confirmed by an IgM line assay. Selected samples from IgM and/or IgG as well as total HEV antibody-positive individuals were also tested for the presence of HEV RNA. In one of the 78 samples, the only IgM ELISA positive and IgM line assay confirmed sample, RNA of HEV genotype 3 was detected. This sequence has high similarity to HEV sequences obtained from wild boars and domestic pigs from Germany and The Netherlands. This study demonstrates that in addition to the consumption of raw or undercooked meat, direct contact to pigs has to be considered as an additional risk factor for HEV infection.
    Medical Microbiology and Immunology 04/2014; 203(4). DOI:10.1007/s00430-014-0336-3 · 2.43 Impact Factor
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    ABSTRACT: The role of mutations in the thymidine kinase (TK, UL23) and DNA polymerase (pol, UL30) genes of herpes simplex virus (HSV) for development of different resistance phenotypes has to be exactly determined before genotypic resistance testing can be implemented in patient's care. Furthermore, the occurrence of cross-resistance is of utmost clinical importance. In this study, clinical HSV-1 isolates obtained between 2004 and 2011 from 26 patients after stem cell transplantation were examined in parallel by phenotypic and genotypic resistance testing. Thirteen isolates, which were phenotypically cross-resistant to acyclovir (ACV), penciclovir (PCV) and brivudin (BVDU), exhibited consistently frameshift or non-synonymous mutations in the TK gene known to confer resistance. One of these mutations (insertion of C at the nucleotide positions 1061-1065) has not been described before. Seven strains, phenotypically resistant to ACV and PCV and, except one each, sensitive to BVDU and resistant to foscarnet (FOS), carried uniformly resistance-related substitutions in the DNA pol gene. Finally, 3 isolates, resistant to ACV, PCV and 2 out of these also resistant to BVDU, had known but also unclear substitutions in the TK and DNA pol genes, and 3 isolates were completely sensitive. In conclusion, clinical ACV-resistant HSV-1 isolates, carrying resistance-associated mutations in the TK gene, can be regarded as cross-resistant to other nucleoside analogs such as BVDU. In contrast, clinical FOS-resistant HSV-1 strains which are cross-resistant to ACV may be sensitive to BVDU. This has to be considered for drug changes in antiviral treatment in case of ACV resistance.
    Antiviral research 04/2014; DOI:10.1016/j.antiviral.2014.03.015 · 3.43 Impact Factor
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    ABSTRACT: Influenza virus A/whale/Maine/328B/1984 (H13N2) was isolated from a diseased pilot whale. Since only a partial sequence was available, its complete genome was sequenced and compared to the sequences of subtype H13 influenza viruses from shorebirds and various influenza viruses of marine mammals. The data reveal a rare genotype constellation with all gene segments derived of an influenza virus adapted to gulls, terns and waders. In contrast, the phylogenetic trees indicate that the majority of influenza viruses isolated from marine mammals derived from influenza viruses adapted to geese and ducks. We conclude that A/whale/Maine/328B/1984 is the first record of an infection of a marine mammal from a gull-origin influenza virus.
    Infection, genetics and evolution: journal of molecular epidemiology and evolutionary genetics in infectious diseases 04/2014; 24. DOI:10.1016/j.meegid.2014.03.026 · 3.26 Impact Factor
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    ABSTRACT: The emergence of new influenza viruses like the pandemic H1N1 influenza A virus in 2009 (A(H1N1)pdm09) with unpredictable difficulties in vaccine coverage and established antiviral treatment protocols emphasizes the need of new murine models to prove the activity of novel antiviral compounds in vivo. The aim of the present study was to develop a small-scale mathematical model based on easily attainable experimental data to explain differences in influenza kinetics induced by different virus strains in mice. To develop a three-dimensional ordinary differential equation model of influenza dynamics, the following variables were included: (i) viral pathogenicity (P), (ii) antiviral immune defense (D), and (iii) inflammation due to pro-inflammatory response (I). Influenza virus-induced symptoms (clinical score S) in mice provided the basis for calculations of P and I. Both, mono- and biphasic course of mild to severe influenza induced by three clinical A(H1N1)pdm09 strains and one European swine H1N2 virus were comparatively and quantitatively studied by fitting the mathematical model to the experimental data. The model hypothesizes reasons for mild and severe influenza with mono- as well as biphasic course of disease. According to modeling results, the second peak of the biphasic course of infection is caused by inflammation. The parameters (i) maximum primary pathogenicity, (ii) viral infection rate, and (iii) rate of activation of the immune system represent most important parameters that quantitatively characterize the different pattern of virus-specific influenza kinetics.
    Bio Systems 04/2014; DOI:10.1016/j.biosystems.2014.02.004 · 1.47 Impact Factor
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    ABSTRACT: After successful invasion of susceptible hosts, systemic distribution of coxsackievirus B3 (CVB3) most likely requires interactions with the endothelial system. Thereby, infection of endothelial cells occurs directly or viruses and/or virus-infected leukocytes migrate through the endothelial barrier. Many of these processes have not been studied so far. In order to analyze viral replication in the endothelium, human umbilical vein endothelial cells (HUVEC) were isolated and infected with CVB3. Time-course experiments revealed maximal viral replication at 10-24 h and viral RNA persistence up to 120 h post-infection (p. i.) without the induction of obvious general cytopathic effects or the loss of cellular viability. However, the application of the EGFP-expressing recombinant virus variant CVB3/EGFP revealed shrinkage and death of individual cells. Using infectious center assays, a noticeable CVB3 replication occurred on an average of 20 % of HUVEC at 10 h p. i. This may be in part due to a higher coxsackievirus/adenovirus receptor expression in a small subgroup of HUVEC (5-7 %) as analyzed by flow cytometry. Interestingly, CVB3 replication escalated and cellular susceptibility increased significantly after reversal of cell cycle arrest caused by serum deprivation indicating that reactivation of cellular metabolism may help to promote CVB3 replication. Finally, CVB3-infected HUVEC cultures revealed increased DNA fragmentation, and inhibition of caspase activity caused an accumulation of intracellular virus particles indicating that apoptotic processes are involved in virus release mechanisms. Based on these observations, it is assumed that CVB3 replicates efficiently in human endothelial cells. But how this specific infection of the endothelium may influence viral spread in the infected host needs to be investigated in the future.
    Medical Microbiology and Immunology 03/2014; 203(4). DOI:10.1007/s00430-014-0333-6 · 2.43 Impact Factor
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    Eurosurveillance: bulletin europeen sur les maladies transmissibles = European communicable disease bulletin 02/2014; 19(5). DOI:10.2807/1560-7917.ES2014.19.5.20687 · 4.66 Impact Factor
  • Andreas Sauerbrei
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    ABSTRACT: The hepatitis B virus (HBV) is considered to be a major public health problem worldwide, and a significant number of reports on nosocomial outbreaks of HBV infections have been reported. Prevention of indirect HBV transmission by contaminated objects is only possible through the use of infection-control principles, including the use of chemical biocides, which are proven to render the virus non-infectious. The virucidal activity of biocides against HBV cannot be predicted; therefore, validation of the virucidal action of disinfectants against HBV is essential. However, feasible HBV infectivity assays have not yet been established. Thus, surrogate models have been proposed for testing the efficacy of biocides against HBV. Most of these assays do not correlate with HBV infectivity. Currently, the most promising and feasible assay is the use of the taxonomically related duck hepatitis B virus (DHBV), which belongs to the same Hepadnaviridae virus family. This paper reviews the application of DHBV, which can be propagated in vitro in primary duck embryonic hepatocytes, for the testing of biocides and describes why this model can be used as reliable method to evaluate disinfectants for efficacy against HBV. The susceptibility levels of important biocides, which are often used as ingredients for commercially available disinfectants, are also described.
    World Journal of Gastroenterology 01/2014; 20(2):436-444. DOI:10.3748/wjg.v20.i2.436 · 2.43 Impact Factor
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    ABSTRACT: Serological methods are used widely for the determination of herpes simplex virus (HSV) IgG and IgM antibodies in virological laboratories. The present study evaluates the automated performance of the Virion\Serion (Würzburg, Germany) and Orgentec (Mainz, Germany) enzyme-linked immunosorbent assays (ELISA) for the determination of HSV type-common and type-specific IgG and IgM antibodies. Two hundred sixty-three sera from HSV-negative children, healthy blood donors as well as patients without and with acute HSV infections were included. The Serion ELISAs classic HSV 1+2, HSV 1 and HSV 2 IgG showed sensitivities between 89.1% and 98.0% and specificities from 82.8% to 100%. Sensitivities of the Orgentec ELISAs Anti-HSV-1 and Anti-HSV-2 IgG were calculated as 91.0-96.0% and 88.5-95.4% accompanied by specificities between 91.3% and 100%. The HSV type-common Serion IgM ELISA revealed also a high sensitivity and specificity. However, the single-type HSV-1 and HSV-2 IgM ELISAs from both companies did not detect reliably HSV-1- and HSV-2-specific IgM antibodies. In conclusion, the automated performance of Serion ELISAs classic HSV 1+2, HSV 1 and HSV 2 IgG as well Orgentec ELISAs Anti-HSV-1 and Anti-HSV-2 IgG provide highly dependable results for identifying HSV-1 and HSV-2 IgG-positive or -negative individuals. While HSV type-common IgM ELISAs can be useful to confirm acute newly acquired HSV infections, the use of single-type IgM ELISAs on the basis of whole-virus antigen is dispensable.
    Journal of virological methods 01/2014; 199. DOI:10.1016/j.jviromet.2014.01.001 · 1.88 Impact Factor
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    ABSTRACT: Influenza virus A/whale/Maine/328B/1984 (H13N2) was isolated from a diseased pilot whale. Since only a partial sequence was available, its complete genome was sequenced and compared to the sequences of subtype H13 influenza viruses from shorebirds and various influenza viruses of marine mammals. The data reveal a rare genotype constellation with all gene segments derived of an influenza virus adapted to gulls, terns and waders. In contrast, the phylogenetic trees indicate that the majority of influenza viruses isolated from marine mammals derived from influenza viruses adapted to geese and ducks. We conclude that A/whale/Maine/328B/1984 is the first record of an infection of a marine mammal from a gull-origin influenza virus.
  • Andreas Sauerbrei, Kathrin Bohn
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    ABSTRACT: Resistance testing of antivirals to herpes simplex virus type 1 can be done by phenotypic and genotypic methods. The determination of a resistant phenotype is based on the calculation of inhibitory concentrations for the antiviral drug, which should be tested. The main advantage is a clear interpretation of laboratory findings, but the method is time consuming and a considerable experience is required for handling infectious virus. Genotypic resistance testing is based on the detection of resistance-related mutations in viral genes encoding the thymidine kinase and DNA polymerase by means of amplification and sequencing. This approach has the advantage of being faster, but only frameshift mutations and stops of translation can be interpreted without doubt and numerous amino acid substitutions are diagnostically less conclusive.
    Methods in molecular biology (Clifton, N.J.) 01/2014; 1144:149-65. DOI:10.1007/978-1-4939-0428-0_10 · 1.29 Impact Factor
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    ABSTRACT: The complete genomes of two swine influenza viruses from England were sequenced. Phylogenetic analysis revealed classical swine H1N1 viruses, one of which, A/swine/London, is closely related to virus strains of the early 1930s. Both strains are also antigenically related to A/swine/Iowa/15/1930, the strain originally isolated by Richard Shope. The source of A/swine/London is unknown, but its relationship to early classical swine influenza viruses suggests that the emergence of these viruses in Europe has to be antedated by 15-20 years.
    Archives of Virology 12/2013; DOI:10.1007/s00705-013-1950-x · 2.28 Impact Factor
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    ABSTRACT: Influenza virus neuraminidase (iNA) is a homotetrameric surface protein of the influenza virus and an established target for antiviral drugs. In contrast to neuraminidases (NAs) of other biological systems (non-iNAs), enzymatic activity of iNA is only observed in a quaternary assembly and iNA needs the tetramerization to mediate enzymatic activity. Obviously, differences on a molecular level between iNA and non-iNAs are responsible for this intriguing observation. Comparison between protein structures and multiple sequence alignment allow the identification of differences in amino acid composition in crucial regions of the enzyme, such as next to the conserved D151 and the 150-loop. These differences in amino acid sequence and protein tetramerization are likely to alter the dynamics of the system. Therefore, we performed molecular dynamics simulations to investigate differences in the molecular flexibility of monomers, dimers, and tetramers of iNAs of subtype N1 (avian 2004, pandemic 1918 and pandemic 2009 iNA) and as comparison the non-iNA monomer from Clostridium perfringens. We show that conformational transitions of iNA are crucially influenced by its assembly state. The protein-protein interface induces a complex hydrogen-bonding network between the 110-helix and the 150-loop, which consequently stabilizes the structural arrangement of the binding site. Therefore, we claim that these altered dynamics are responsible for the dependence of iNA's catalytic activity on the tetrameric assembly. Only the tetramerization-induced balance between stabilization and altered local flexibility in the binding site provides the appropriate arrangement of key residues for iNA's catalytic activity.
    Journal of biomolecular Structure & Dynamics 11/2013; 33(1). DOI:10.1080/07391102.2013.855142 · 2.98 Impact Factor
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    ABSTRACT: Since asymptomatic hepatitis E virus (HEV) infections particularly affect children, there is a need for studies to determine the HEV seroprevalence among infants, children and adolescents. The prevalence of anti-HEV IgG antibodies was determined in sera taken in 2008 to 2010 from 1,646 children aged 0-17 years living in Germany. Antibody testing was carried out using the ELISA recomWell HEV IgG as well as the recomLine HEV IgG/IgM distributed by Mikrogen. Furthermore, the performance of MP Biomedicals ELISA HEV and the HEV-Ab ELISA from Axiom was analyzed in comparison to the recomWell/recomLine test system using a defined subset of sera. In children, the overall prevalence of antibodies was 1.0%. Starting with the 5-6 year-olds, there was a significant increase of HEV seroprevalence to 1.5% in the group of the 15-17 year-olds. There was no statistically significant difference between seroprevalences of boys (1.2%) and girls (0.7%). Passively transmitted maternal antibodies persisted for about 3 months. The strength of agreement between the recomWell/recomLine system and the ELISAs from MP Biomedicals or Axiom varied between 0.229 and 0.542 and was calculated at 0.111 when the assays from MP Biomedicals and Axiom were compared. In Germany, only a very small number of HEV infections occur in children. The majority of infections occur in adults with increasing age. Because of considerable variations in assay accordance, there is an urgent need for standardization of HEV serology.
    The Pediatric Infectious Disease Journal 10/2013; 33(3). DOI:10.1097/INF.0000000000000077 · 3.14 Impact Factor
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    ABSTRACT: An increasing number of acute autochthonous human hepatitis E virus (HEV)-infections was noticed in Germany and other developed countries, most likely the result of a zoonotic virus transmission from pig, wild boar and deer. Currently there is still a lack of profound data concerning the actual prevalence of HEV-specific antibodies in domestic pig herds in Germany, in particular for regions with high pig density, and its age-dependency. 2273 domestic pig sera were collected in 2011 mainly from Bavaria, North Rhine-Westphalia and Lower Saxony from areas having a high pig density. Initially, 420 randomly selected pig sera were tested in three commercially available and in two in-house HEV-antibody ELISAs. 43.6% (183/420) to 65.5% (275/420) of the sera were demonstrated to be reactive against human pathogenic HEV genotypes 1 and/or 3. The majority of sera reacted only weakly or not at all with the rat HEV antigen with very few sera showing a stronger reactivity to this antigen compared to the genotype 3 antigen. The results of all three HEV-IgG tests, i.e. the PrioCHECK(®) HEV Ab porcine ELISA kit, the ID Screen(®) Hepatitis E Indirect Multi-species ELISA kit and the genotype 3 in-house ELISA were in good accordance. Therefore, the remaining sera were tested using the PrioCHECK(®) HEV Ab porcine ELISA kit. Samples with a borderline result were finally determined by application of the conjugate-modified recomLine HEV IgG assay. A total of 1065 of the 2273 sera (46.9%) were found to be anti-HEV IgG-positive. While 38.4% (306/796) of fatteners (age between 3 and 9 months) exhibited HEV-specific antibodies, 51.4% (759/1477) of sows (age older than 9 months) exhibited anti-HEV antibodies (P<0.001). Fatteners kept in Southern Germany had a significantly higher HEV IgG prevalence compared to fatteners kept in the high pig density federal states North Rhine-Westphalia and Lower Saxony but also in German federal states with a low pig density. In conclusion, the present study clearly demonstrates that a high percentage of domestic pigs in Germany have had contact with HEV. Seroprevalence depends on the pig's age and herd origin with the most significant regional variations for fatteners. The presence of anti-HEV-free herds may indicate that it is feasible to establish and sustain HEV-free pig herds. HEV seroprevalence still depends on the assay used for testing. This demonstrates an urgent need for test validation.
    Veterinary Microbiology 10/2013; 167(3-4). DOI:10.1016/j.vetmic.2013.10.001 · 2.73 Impact Factor

Publication Stats

2k Citations
349.47 Total Impact Points

Institutions

  • 2006–2014
    • Universitätsklinikum Jena
      • Institute of Virology and Antiviral Therapy
      Jena, Thuringia, Germany
  • 1996–2014
    • Friedrich Schiller University Jena
      • Institute of Virology and Antiviral Therapy
      Jena, Thuringia, Germany
  • 2012
    • Karolinska Institutet
      Solna, Stockholm, Sweden
  • 2011
    • Leibniz Institute for Age Research - Fritz Lipmann Institute
      • Genome Analysis
      Jena, Thuringia, Germany
  • 2008
    • Universität Hamburg
      • Institute of Organic Chemistry
      Hamburg, Hamburg, Germany
  • 2005
    • Centers for Disease Control and Prevention
      • National Center for Emerging and Zoonotic Infectious Diseases
      Atlanta, Michigan, United States
  • 2004
    • Leibniz Institute for Natural Product Research and Infection Biology - Hans Knöll Institute
      Jena, Thuringia, Germany