bluuebunny/crossref_metadata_2025_split huggingface dataset:
A non‐invasive method for assessing adrenal activity in the chinchilla (chinchilla lanigera)
Authors: Ponzio Marina F. , Monfort Steven L. , Busso Juan M. , Dabbene Viviana G. , Ruiz Rubén D. , De Cuneo Marta Fiol 
Published: February 2004

AbstractThe Chinchilla is a rodent that was once abundant in the central Andes of South America. Excessive hunting for fur greatly reduced its distribution at the beginning of the twentieth century, and today Chinchilla species are nearly extinct in the wild. Although protected, wild populations of chinchilla are still declining. In general, this species has received little research attention and its biology is poorly understood. Improvements in captive breeding, husbandry, and genetic management are needed to ensure the conservation of the species. In this study, a noninvasive corticosteroid hormone monitoring technique was validated for use in Chinchilla lanigera. Two male domestic chinchillas were administered 3H‐corticosterone (i.m.) to determine the time course and relative proportion of urinary and fecal steroid metabolites. Most radioactivity was detected in urine and feces 5–10 and ∼30 h post‐isotope administration, respectively. Corticosteroid immunoreactivity was assessed by corticosterone radioimmunoassay (RIA) and cortisol enzyme immunoassay (EIA). High‐pressure liquid chromatography (HPLC) separation of corticosteroid metabolites in unprocessed urine revealed the presence of highly polar corticosteroid metabolites, but after enzymatic hydrolysis and diethyl ether extraction, most immunoreactivity co‐eluted with unconjugated cortisol. A ‘cause‐and‐effect’ relationship between the administration of exogenous adrenocorticotrophic hormone (ACTH), and the appearance of increased urinary corticosteroid metabolites demonstrated the physiological relevance of these measures for evaluating adrenal status in male chinchillas. From a conservation perspective, these methods can aid in situ and ex situ initiatives designed to evaluate how environmental conditions and management strategies affect overall animal health, well‐being and reproduction. J. Exp. Zool. 301A:218–227, 2004. © 2004 Wiley‐Liss, Inc.
Temporal expression of thyroid hormone receptor α1 in the liver of the lizard Podarcis sicula
Authors: Virgilio Francesca , Sciarrillo Rosaria , De Falco Maria , Comitato Raffaella , Laforgia Vincenza , Varano Lorenzo , Cardone Anna 
Published: February 2004

AbstractThe effects of thyroid hormones on metabolism and development are mediated by thyroid hormone receptors (TRs). To gain a better understanding of the potential role of thyroid hormone receptors in the liver of the lizard Podarcis sicula, we have evaluated the expression of TRs during the more critical periods of the annual variations of thyroid activity. The results obtained have indicated that in the liver of the lizard P. sicula there are three transcripts: mRNA of 5.0 kb for TRα1, mRNA of 2.6 kb for TRα2, and 6.0 kb band, which represent unprocessed heteronuclear RNA, encoding unspliced primary transcripts of RNA prior to their processing into the mature TRα1 and TRα2. By means of slot‐blot, we are able to determine that there is a change in the expression of TRs that occurs in the liver during the annual cycle of thyroid activity. A major expression registers in May, when the lizard thyroid gland shows the maximal activity. The combination of molecular biology with immunohistochemistry revealed that hepatic cells were also TRα IR positive. Particularly intense immunostaining was present in the cell nuclei of animals sacrified in May. These observations suggest that in lizard P. sicula the thyroid hormone (T3) might regulate hepatic activity, modulating TR mRNA levels. J. Exp. Zool. 301A:212–217, 2004. © 2004 Wiley‐Liss, Inc.
Are enterovirus infections a co‐factor in sudden hearing loss?
Authors: Mentel Renate , Kaftan H. , Wegner U. , Reißmann A. , Gürtler L. 
Published: February 2004

AbstractSince viral infections are believed to be one of the causes of sudden hearing loss we have used serological assays for herpes simplex virus (HSV), varicella zoster virus (VZV), and enterovirus as well as polymerase chain reaction for enterovirus to test 55 sudden hearing loss patients for viral infections. Serological screening of these patients for HSV and VZV failed to reveal significant differences between the patient group and the controls. In contrast, enterovirus sequences were detected by RT‐PCR in 40% of the patient group, but in none of the controls, suggesting that enterovirus infections may be associated with sudden hearing loss. J. Med. Virol. 72:625–629, 2004. © 2004 Wiley‐Liss, Inc.
Possible involvement in oncogenesis of a single base mutation in an internal ribosome entry site of Epstein–Barr nuclear antigen 1 mRNA
Authors: Endo Rika , Kikuta Hideaki , Ebihara Takashi , Ishiguro Nobuhisa , Kobayashi Kunihiko 
Published: February 2004

AbstractIt has been reported recently that the U leader exon located within the 5′ untranslated region of Epstein–Barr nuclear antigen 1 (EBNA1) gene contains an internal ribosome entry site (IRES) element. Sequence analysis of the U leader exon was undertaken in samples from 19 patients with infectious mononucleosis and 19 patients with lethal lymphoproliferative diseases and in 15 spontaneously established lymphoblastoid cell lines. The sequence was conserved except for a single base substitution (T‐C) at position 67,585. Although the mutation was detected in only one case of infectious mononucleosis, it was found in more than half of the lethal lymphoproliferative diseases and all lymphoblastoid cell lines. The results suggest that a mutation in the IRES element affects EBNA1 gene expression at the translational level and provides Epstein–Barr virus (EBV)‐infected cells with a growth advantage, leading to immortalization of cells in vitro and to the development of lethal lymphoproliferative diseases in vivo. J. Med. Virol. 72:630–634, 2004. © 2004 Wiley‐Liss, Inc.
Sustained CD8+ T‐cell immune response to a novel immunodominant HLA‐B*0702‐associated epitope derived from an Epstein–Barr virus helicase‐primase‐associated protein
Authors: Turčanová Vanda , Höllsberg Per 
Published: February 2004

AbstractGeneration of a peptide‐based vaccine against persistent viral infections, such as Epstein–Barr virus (EBV), requires identification of immunodominant epitopes recognized by anti‐viral cytotoxic T‐cells. Using available computer algorithms, we have screened the entire translated EBV genome for potential HLA‐B7‐binding peptides. The binding to HLA‐B7 of 18 selected peptides was assessed by competitive binding assays and was found to correlate with the computer‐assigned scores, confirming the predictive value of these algorithms in selection of HLA‐B7‐associated peptides. Screening of the immune responses to these peptides by ELISpot assays identified a novel immunodominant epitope, termed LPRA, derived from an EBV helicase‐primase‐associated protein encoded by BBLF2/3. Peptide‐specific cells constituted up to 0.8% LPRA‐specific CD8+ T‐cells in the matured anti‐viral response. Cytotoxic and proliferative cytotoxic T lymphocytes (CTL) responses to the LPRA peptide were readily demonstrated ex vivo. In addition, mutational studies of this epitope demonstrated a highly specific recognition by LPRA‐specific CD8+ T‐cells. Taken together, our data suggest that the novel lytic‐phase HLA‐B7‐associated epitope contains essential features required of a component in an EBV peptide‐based vaccine. J. Med. Virol. 72:635–645, 2004. © 2004 Wiley‐Liss, Inc.
Precore/core promoter mutations and genotypes of hepatitis B virus in chronic hepatitis B patients with fulminant or subfulminant hepatitis
Authors: Liu Chun‐Jen , Kao Jia‐Horng , Lai Ming‐Yang , Chen Pei‐Jer , Chen Ding‐Shinn 
Published: February 2004

AbstractThe association of precore stop codon mutation (A1896), dinucleotide mutation (T1762/A1764) in the basic core promoter of hepatitis B virus (HBV) genome, and genotype of HBV with fulminant or subfulminant hepatitis remains controversial. We studied HBV genotypes as well as mutations in the precore and basic core promoter regions in 18 hepatitis B carriers with fulminant or subfulminant hepatitis. Genotyping of HBV was performed by polymerase chain reaction‐restriction fragment length polymorphism. The presence of A1896 in the precore gene and T1762/A1764 in the basic core promoter gene was determined by the polymerase chain reaction and by direct sequencing. Eighteen age‐ and sex‐matched patients with chronic active hepatitis B served as controls. The HBV was of genotype B in 14, genotype C in 3, and unclassified in 1. Precore A1896 mutation occurred in 12 (67%) of the 18 patients. In contrast, the prevalence of basic core promoter mutation was only 17%. Nevertheless, the distribution of HBV genotype and the prevalence of precore A1896 mutation in the fulminant and subfulminant hepatitis patients were similar to those in 18 control patients. In conclusion, the genomic variability of HBV does not seem to contribute to the fulminant and subfulminant exacerbation of chronic hepatitis B in Taiwanese HBV carriers. J. Med. Virol. 72:545–550, 2004. © 2004 Wiley‐Liss, Inc.
Differential binding efficiency between the envelope protein of Japanese encephalitis virus variants and heparan sulfate on the cell surface
Authors: Liu Hsiuan , Chiou Shyan‐Song , Chen Wei‐June 
Published: February 2004

AbstractJapanese encephalitis (JE) virus infects a number of host cells, either mosquitoes or vertebrates, in nature. The viral envelope (E) protein is known to interact with molecule(s) on the cell membrane during the early stage of virus infection. In this study, two sets of virus variants including T1P1‐L4/T1P1‐S1 and CJN‐L1/CJN‐S1 derived from two strains (T1P1 and CJN) of the JE virus were used to evaluate the effects of genomic variations on virus entry. Each set of virus variant (T1P1‐L4/T1P1‐S1 or CJN‐L1/CJN‐S1) possessed a single amino acid variation in the E protein. The variation of Glu/Lys at E‐306 was found between T1P1‐L4 and T1P1‐S1 whereas the same variation at E‐138 was seen between CJN‐L1 and CJN‐S1. The results showed that heparan sulfate (HS) differentially expressed on the surface of different types of host cells was essential for JE virus infection as shown in an evident difference in attachment efficiency between CHO‐K1 cells and its mutant with defects in GAG biosynthesis. Furthermore, differential interaction of heparin with the envelope protein of JE virus variants implies the significance of virus mutations (especially Lys for E‐138 and/or E306 in this case) that are rather likely involved in determining efficiencies of viral attachment, penetration, and eventual infection. J. Med. Virol. 72:618–624, 2004. © 2004 Wiley‐Liss, Inc.
Identification of rare polymerase variants of hepatitis B virus using a two‐stage PCR with peptide nucleic acid clamping
Authors: Ohishi Waka , Shirakawa Hiroo , Kawakami Yoshiiku , Kimura Sonoko , Kamiyasu Masaya , Tazuma Susumu , Nakanishi Toshio , Chayama Kazuaki 
Published: February 2004

AbstractEmergence of lamivudine‐resistant variants, with amino acid substitutions in the Tyr‐Met‐Asp‐Asp (YMDD) motif of hepatitis B virus (HBV) reverse transcriptase, is a serious problem in antiviral therapy. Presence of YMDD motif variants in patients who had never been treated with lamivudine has been reported recently. However, no analysis of nucleotide and amino acid sequences of these variants has been performed. In the present study, using polymerase chain reaction (PCR) with peptide nucleic acid (PNA) clamping, we detected many new variants, such as Tyr‐Arg‐Asp‐Asp (YRDD), Tyr‐Met‐Asp‐Asn (YMDN). Many of them had stop codon(s) in overlapping HBs gene. Although the biological activity of these HBV polymerase variants remains to be determined, our results showed that numerous quasispecies are created during virus replication. A typical lamivudine‐resistant Tyr‐Val‐Asp‐Asp (YVDD) variant was detected in only one of 62 (1.6%) anti‐HBe patients with HBV infection before administration of lamivudine. This variant did not have the L528M mutation, which is often associated with YVDD variants, and lamivudine therapy in this patient suppressed HBV replication. Thus, care should be taken when interpreting the results of detection of YMDD variants, especially when the sensitivity of the assay is very high. Amplification of rare variants by PCR with PNA seems a useful tool to examine the emergence of drug‐resistant variants as well as naturally occurring mutants, such as the hepatitis B e antigen (HBeAg) stop codon and vaccine escape mutants. Examination of rare variants should enhance the understanding of the mechanism for emergence of drug‐resistant HBV variants and help in developing strategies for new antiviral drugs. J. Med. Virol. 72:558–565, 2004. © 2004 Wiley‐Liss, Inc.
Persistence of rhinovirus and enterovirus RNA after acute respiratory illness in children
Authors: Jartti Tuomas , Lehtinen Pasi , Vuorinen Tytti , Koskenvuo Minna , Ruuskanen Olli 
Published: February 2004

AbstractThe persistence of rhinovirus and enterovirus RNAs was studied in the nasal secretions of children with acute expiratory wheezing (median age: 1.7 years). On admission, 84 samples from 161 (52%) children admitted to hospital were positive by reverse transcriptase‐polymerase chain reaction (RT‐PCR), which detects rhino‐ and enteroviruses simultaneously. Of the samples, 26 (16%) were positive for rhinovirus, 29 (18%) enterovirus and 29 (18%) nontypable rhino‐enterovirus. After 2 weeks, 16 of these 84 (19%) samples were still positive. Rhinovirus RNA remained positive in 13 of 26 (50%) cases, whereas enterovirus RNA remained positive only in 1 of 29 (3%) cases (P = 0.0001). Respiratory symptoms at 2 weeks or systemic glucocorticoid treatment during hospital stay were not related to the persistence of viral RNA. After 5 weeks, only one sample remained PCR‐positive. Thirteen of the 79 (16%) asymptomatic control children were PCR‐positive for respiratory picornavirus. Five of the 13 (38%) PCR‐positive children developed respiratory symptoms in the following week. The study shows that after the onset of symptomatic respiratory infection enterovirus RNA may take 2–3 weeks and rhinovirus RNA 5–6 weeks to disappear from nasal mucus. J. Med. Virol. 72:695–699, 2004. © 2004 Wiley‐Liss, Inc.
Hepatitis in Albanian children: Molecular analysis of hepatitis A virus isolates
Authors: Gabrieli Rosanna , Sanchez Gloria , Macaluso Alessia , Cenko Fabian , Bino Silva , Palombi Leonardo , Buonomo Ersilia , Pinto Rosa M. , Bosch Albert , Divizia Maurizio 
Published: February 2004

AbstractHepatitis A is a common disease in developing countries and Albania has a high prevalence of this disease associated to young age. In spite of the occurrence of a unique serotype there are different genotypes classified from I to VII. Genotype characterisation of HAV isolates circulating in Albania has been undertaken, as well as the study of the occurrence of antigenic variants in the proteins VP3 and VP1. To evaluate the genetic variability of the Albanian hepatitis A virus (HAV) isolates, samples were collected from 12 different cities, and the VP1/2A junction amplified and sequenced. These sequences were aligned and a phylogenetic analysis performed. Additionally, the amino half sequence of the protein VP3 and the complete sequence of the VP1 was determined. Anti‐HAV IgM were present in 66.2% of all the sera. Fifty HAV isolates were amplified and the analysis revealed that all the isolates were sub‐genotype IA with only limited mutations. When the deduced amino acid sequences were obtained, the alignment showed only two amino acids substitutions at positions 22 and 34 of the 2A protein. A higher genomic stability of the VP1/2A region, in contrast with what occurs in other parts of the world could be observed, indicating high endemicity of HAV in Albania. In addition, two potential antigenic variants were detected. The first at position 46 of VP3 in seven isolates and the second at position 23 of VP1 in six isolates. J. Med. Virol. 72:533–537, 2004. © 2004 Wiley‐Liss, Inc.
Seroprevalence of human herpesvirus‐8 in blood donors from different geographical regions of Argentina, Brazil, and Chile
Authors: Pérez Celeste , Tous Mónica , Gallego Sandra , Zala Norma , Rabinovich Oscar , Garbiero Susana , Martínez María José , Cunha Andrèa Mendonça Gusmão , Camino Sofía , Cámara Alicia , Costa Sandra Cecília Botelho , Larrondo Milton , Francalancia Verónica , Landreau Fernando , Bartomioli Miguel Angel 
Published: February 2004

AbstractHuman herpesvirus‐8 (HHV‐8) causes Kaposi's sarcoma (KS) and lymphoproliferative disorders in both HIV‐infected and uninfected patients. HHV‐8 has a worldwide occurrence but infection rates vary according to a combination of geographic and behavioral risks. The main transmission route seems to be sexual, nevertheless, nasal secretions, saliva, blood, and organ graft have been proposed. HHV‐8 was postulated as a new infectious agent for screening in blood donors. The aim of this study was to evaluate the prevalence of antibodies against HHV‐8 antigens in blood donors of South America. Serum samples from 2,470 blood donors from Argentina, Brazil, and Chile corresponding to five geographic regions were studied by indirect immunofluorescence assay (IFA). Seroprevalence rate was 3.7% (92/2,470; 95% CI 2.9–4.5) in the entire blood donor population distributed as follows: Argentina, 4.0% (Buenos Aires city, 4.3%; Bahia Blanca, 2.4%; and Córdoba, 4.0%), Campinas (Brazil), 2.8%; and Santiago de Chile, 3.0%. There was no difference (P > 0.05) between men and women or age related, except in Brazil where positive cases were 30–49‐year‐old males. The present study, which includes different geographical areas of multiple countries from South America, has not been done before. The results show similar prevalence rates among the studied zones corresponding to low‐prevalence regions. South America is a large sub‐continent with a wide spectrum of population and geographical characteristics, thus, more HHV‐8 prevalence studies should be necessary to establish possible regional differences. J. Med. Virol. 72:661–667, 2004. © 2004 Wiley‐Liss, Inc.
Decrease of replicative capacity of HIV isolates after genotypic guided change of therapy
Authors: Sarmati L. , Nicastri E. , Montano M. , Dori L. , Buonomini A.R. , d'Ettorre G. , Gatti F. , Parisi S.G. , Vullo V. , Andreoni M. 
Published: February 2004

AbstractA longitudinal study of the replication capacity of HIV strains isolated from 18 patients failing highly active antiretroviral therapy (HAART) was undertaken at the time of genotypic guided change of therapy and after 12 months. Patients were divided in two groups according to the response to therapy: immune responders (12 patients with immune recovery defined as having more than 100 CD4 cells compared to baseline value), and failing patients (six patients without immune recovery). At enrolment no significant difference in terms of CD4 cell count and HIV plasma viremia was detected between the two groups. One year after change of therapy, all patients experienced a decrease in the replication capacity of HIV strains. The HIV replication capacity of the failing and of immune‐responder patients decreased from 60% (range 14–96%) to 26.4% (range 0.4–74.5) and from 46.8% (range 15–98%) to 3.6% (range 0.1–26.8%), respectively. At month 12, the difference of HIV replication capacity between the two groups reached a statistical significance (P < 0.03). After the change of therapy, an increase in the number of drug resistance mutations in the protease gene was detected in both groups with a higher prevalence of M36I mutation in immune responders. The HIV strains of patients failing HAART showed a progressive impaired replication capacity. The degree of the impairment in viral replication correlated with the viro‐immunological discordant response to HAART and with the acquisition of new drug resistant mutations in the protease gene. In patients failing HAART, the impaired replication capacity of HIV strains could justify the persistence of an immune recovery. J. Med. Virol. 72:511–516, 2004. © 2004 Wiley‐Liss, Inc.
Antibody response to B19 parvovirus VP1 and VP2 linear epitopes in patients with haemophilic arthritis
Authors: Azzi A. , Manaresi E. , Zakrzewska K. , De Santis R. , Musiani M. , Zerbini Marialuisa 
Published: February 2004

AbstractParvovirus B19 infection occurs very frequently in patients with haemophilia on account of its transmission with plasma derivatives. In order to achieve a more defined serological pattern for the study of the role of B19 infection in haemophilic arthritis, 53 serum samples from 37 patients with haemophilic arthritis were investigated for the presence of IgG immune response against B19 VP2 and VP1 linear epitopes and VP2 conformational antigen compared to the serological reactivity against B19 NS1 and to the presence of B19 DNA in the synovial membranes. An IgG immune response against VP1 and VP2 linear epitopes was detected by immunoblot assay using recombinant proteins expressed in Escherichia coli. Specific IgG against VP2 and VP1 linear epitopes were present in 84.90 and 92.45% of haemophilic arthritis patients and in 28.0 and 64.0% of the controls (P < 0.001) respectively. All 53 sera of the haemophiliacs (100%) and 66.0% of the controls (P < 0.001) were IgG positive and IgM negative against VP2 structural epitopes. Specific IgG against VP2 linear epitopes, which are a serological marker of active or very recent B19 infection, proved to be significantly associated with the presence of anti‐NS1 antibodies and with the presence of B19 DNA in synovial tissue in patients with haemophilic arthritis. In conclusion, in these patients the presence of B19 IgG anti‐VP2 linear epitopes, in absence of IgM anti‐VP2 structural antigens, can be a useful serological marker to diagnose active, recent or persistent B19 infection. J. Med. Virol. 72:679–682, 2004. © 2004 Wiley‐Liss, Inc.
Risk factors and clinical consequences of human herpesvirus 7 infection in paediatric haematopoietic stem cell transplant recipients
Authors: Chan Paul K.S. , Li C.K. , Chik K.W. , Lee Vincent , Shing Matthew M.K. , Ng K.C. , Cheung Jo L.K. , Fok T.F. , Cheng Augustine F. 
Published: February 2004

AbstractHuman herpesvirus 7 (HHV‐7) is the least studied β‐herpesvirus in transplant settings. This prospective study examined the activity of HHV‐7 during the first 12 weeks post‐stem cell transplant in 59 paediatric patients. The presence of HHV‐7, human cytomegalovirus (HCMV) and human herpesvirus 6 (HHV‐6) in blood was monitored weekly by a multiplex nested polymerase chain reaction. Overall, 33 (55.9%) patients had one or more surveillance blood sample(s) positive for HHV‐7. In contrast to HCMV and HHV‐6, no obvious peak time of reactivation was observed for HHV‐7. The occurrence of HHV‐7 DNAaemia showed a significant negative association with HHV‐6 (P = 0.022), but with no association with HCMV. A significant higher positive rate for HHV‐7 was found in autologous versus allogeneic (P = 0.002), and in peripheral blood versus umbilical cord/marrow (P < 0.001) transplant. Acyclovir had no effect, whereas ganciclovir was associated with a lower rate of HHV‐7 reactivation (P = 0.009). One patient died of HHV‐7 associated brain stem encephalitis. The administration of colony stimulating factor, occurrence of acute graft versus host disease, time to neutrophil and platelet engraftment showed no significant association with the occurrence of HHV‐7 DNAaemia. J. Med. Virol. 72:668–674, 2004. © 2004 Wiley‐Liss, Inc.