bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prospective study on the development of antibodies against human papillomavirus type 6 among patients with condyloma acuminata or new asymptomatic infection
Authors: Wikström A. , van Doornum G. J. J. , Kirnbauer R. , Quint W. G. V. , Dillner J. 
Published: March 2007

AbstractThe development over time of antibodies to human papillomavirus type 6 (HPV 6) was studied prospectively in a group of 26 condyloma patients receiving multiple treatments, as well as in 17 healthy subjects with a new HPV 6 infection. The condyloma patients provided serum samples during 2–12 visits over a period of 1–20 months, and the levels of IgA, IgG and IgM antibodies to HPV 6, 11 and 16 capsids, and to HPV 6‐derived peptide antigens were determined. Among the capsid antibodies, the IgG and IgA responses against HPV 6 were the most prominent, whereas IgM was detected only in a few patients. During follow‐up, seroconversion to HPV capsids was found in six patients and antibody peaks disappeared during follow‐up in nine patients. There was no association between serology and cure of the wart.One hundred twenty subjects who reported multiple sexual partners, but found negative for HPV DNA at multiple anogenital and oral sites, provided serum samples and swabs for HPV DNA analysis at 2–7 visits during 4–74 months. Seventeen subjects acquired HPV 6 DNA and were included in the study. Serum IgA, IgG and IgM antibodies to HPV 6 capsids were induced concomitantly with the acquisition of viral DNA (P = 0.02, 0.002 and 0.006, respectively), and declined again when the viral DNA was no longer detectable.In conclusion, antibodies to HPV 6 did not predict the clinical course of condylomatous disease, but appear to be useful mainly as epidemiological markers of viral exposure. © 1995 Wiley‐Liss, Inc.
Rapid genotyping of hepatitis C virus RNA‐isolates obtained from patients residing in Western Europe
Authors: Kleter G. E. M. , van Doorn L. J. , Stuyver L. , Maertens G. , Brouwer J. T. , Schalm S. W. , Heijtink R. A. , Quint W. G. V. 
Published: March 2007

AbstractTwo rapid genotyping methods for hepatitis C virus (HCV), the line probe assay (Inno‐LiPA) and the subtype‐specific core amplification system [Okamoto et al., (1992b) Journal of General Virology 73:673‐679], were applied to 58 HCV isolates which were typed as type 1 (n=37) and type 2 (n=21) by sequence analysis of the 5′ untranslated region (5′UTR). The line probe assay targets the 5′UTR and recognized 12 subtype 1a, 25 subtype 1b, 18 subtype 2a, 2 subtype 2b and 1 subtype 2d in accordance with sequence analysis of this region. Subtype‐specific core amplification revealed 7 discrepancies among the 37 type 1 isolates when compared to LiPA. A different subtype was observed in 3 isolates (la versus 1b), 2 isolates remained untyped and 2 isolates showed a coinfection of subtype la and 1b. The first 5 discrepancies were confirmed by sequence analysis of the core region whereas the coinfection could not be confirmed. Of the 21 type 2 isolates only one could be typed by subtype‐specific core amplification. HCV RNA was detected in all 21 cases after the general first round of polymerase chain reaction (PCR). Direct sequencing of the core region indicated sequence variation as a source of failure.It is concluded that LiPA results are conclusive for typing of HCV. However, LiPA is hampered occasionally for subtyping by lack of subtype specific sequence variation in 5′UTR. Subtyping results by subtype‐specific core amplification were accurate. However, it seems that this assay is not suitable for the identification of genotype 2 isolates that circulate in patients living in Western Europe. © 1995 Wiley‐Liss, Inc.
Quantitation of human cytomegalovirus genomes in the brain of AIDS patients
Authors: Kühn J. E. , Wendland T. , Eggers H. J. , Lorentzen E. , Wieland U. , Eing B. , Kiessling M. , Gass P. 
Published: March 2007

AbstractHuman cytomegalovirus (HCMV) is one of the major pathogens causing neurologic disease in the immunocompromised host. A competitive nested polymerase chain reaction (PCR) was used to determine DNA load, distribution, and sequence variability of HCMV genomes in the brain of AIDS patients with and without HCMV encephalitis confirmed by histology and immunocytochemistry. By quantitative PCR, HCMV genomes were found to be distributed diffusely in the central nervous system (CNS) of all five patients with histologically proven HCMV encephalitis, but also in the brain of five of eight AIDS patients without neuropathological evidence of HCMV encephalitis. The viral DNA load in cases with HCMV encephalitis was increased 10‐ to 1, 000‐fold as compared to patients without evidence of encephalitis. A viral load above 6, 000 copies HCMV/106 copies β‐globin was found to be highly suggestive for HCMV encephalitis. Characterization of PCR products by temperature gradient gel electrophoresis (TGGE) and direct sequencing allowed us to detect a sequence variability of the amplified fragment of HCMV glycoprotein B (gB) among different patients, but also among different HCMV foci within the same patient. Furthermore, two of five AIDS patients with HCMV encephalitis most likely experienced double infections with different HCMV strains. The experimental procedure described in this study should also be applicable to the detection of significant HCMV DNA levels in biopsy samples. © 1995 Wiley‐Liss, Inc.
Comparison of human immunodeficiency virus biological phenotypes isolated from cerebrospinal fluid and peripheral blood
Authors: Peeters Martine F. , Colebunders Robert L. , Van Den Abbeele Koen , Nys Patrick C. , Goeman Johan , Colans Philippe , Geerts Yvette , Van der Groen Guido 
Published: March 2007

AbstractQuantitative human immunodeficiency virus (HIV) cultures were carried out on cerebrospinal fluid (CSF), peripheral blood mononuclear cells (PBMCs), and plasma from patients with HIV in order to compare the infectious HIV load. The HIV strains isolated were studied for syncytiuminducing (SI) capacity, using the MT‐2 cell line, in order to compare the HIV strain phenotype of blood and CSF isolates.Forty‐two patients with HIV‐1 infection were enrolled in the study, 33 of whom had neurological symptoms and 9 of whom were without neurological symptoms. HIV was isolated from 16 (38%) of the 42 CSF cultures, with a low mean titer of 6.3 ± 3.4 tissue‐culture‐infective doses (TCID) per milliliter. Patients with HIV‐positive CSF culture had a viral load in PBMCs of 40.5 ± 15.5 TCID per 106 PBMC and in plasma of 104.7± 9.3 per milliliter. Two (15%) of the 13 CSF isolates were Sl strains, compared to 17 (56.6%) of the 30 PBMC isolates and 13 (54%) of the 24 plasma isolates (P<0.05). Five of the nine patients from whom CSF and blood strains were obtained had the same viral biological phenotype.This study suggests that different HIV variants may be found in different body fluids and/or cells. © 1995 Wiley‐Liss, Inc.
Base changes at positions 1014 and 578 of delta virus RNA in greek isolates maintain base pair in rod conformation with efficient RNA editing
Authors: Yang Ailing , Papaioannou Christos , Hadzyannis Stephanos , Thomas Howard , Monjardino John 
Published: March 2007

AbstractAnalysis of delta hepatitis virus (HDV) genomic RNA, derived from Greek patients from an area where HDV infection is associated with low pathogenicity, is described. In all isolates sequenced, which included 18/18 HDV cDNA clones derived from 6 different patients, irrespective of pathogenicity, a base change (T→C) was found in position 1014. No significant differences in editing efficiency were found between isolates from inactive and active forms of the disease, although L‐antigen was present in low to undetectable levels in the serum of 5/6 patients. An additional mutation was identified at position 578 (A→G), which reestablishes the canonical base pair G/C with the mutated 1014 when the genome adopts the “rod‐like” conformation. This finding supports the presence of this genome conformation in vivo and the requirement for the Watson‐Crick base pair 10141/578. A mutation, found at amino acid position 170 (serine → asparaginel, appears to segregate with patients with inactive disease. © 1995 WiIey‐Liss, Inc.
Epidemiologic applications of novel molecular methods to detect and differentiate small round structured viruses (Norwalk‐like viruses)
Authors: Ando Tamie , Jin Qi , Gentsch Jon R. , Monroe Stephan S. , Noel Jacqueline S. , Dowell Scott F. , Cicirello Helen G. , Kohn Melvin A. , Glass Roger I. 
Published: March 2007

AbstractThe molecular epidemiology of a large, multi‐state outbreak of oyster‐associated gastroenteritis [Kohn et al. (1995): Journal of the American Medical Association 273:466–471. Dowell et al. (1995): Journal of Infectious Diseases 171:1497–1503.] was examined using new methods to detect small round structured viruses (SRSVs) by reverse transcription‐polymerase chain reaction (RT‐PCR) and to characterize strains by Southern hybridization and nucleotide sequencing of 81‐bp of a PCR product amplified from the RNA polymerase gene. Of 37 stool specimens examined from patients in eight clusters of the multi‐state outbreak, 32 (86%) gave RT‐PCR products specific for SRSVs of PI‐A phylogenetic group. Nineteen PCR products from the eight clusters were confirmed to have the identical sequence, indicating that this large outbreak was attributed to a single strain of SRSV. In one of the eight clusters, five (63%) of eight patients had a mixed infection with a second SRSV strain that belonged to P2‐B phylogenetic group. Of 12 specimens from patients in five other outbreaks and one sporadic case which occurred at the same time as the multistate outbreak, 10 (83%) gave products specific for SRSVs representing four phylogenetic groups (PI‐A, PI‐B, P2‐A, and P2‐ B). The sequences of the PI‐A products from two outbreaks and that of the P2‐B product from another outbreak were identical to the P1‐A sequence from the eight clusters and the P2–6 sequence from the one cluster of the multistate outbreak, respectively. These results demonstrate the first application of these methods to enhance our understanding of the molecular epidemiology of SRSVs and provide answers of public health interest that could not have been obtained using classical epidemiologic methods alone. © 1995 Wiley‐Liss, lnc.This article is a US Government work and, as such, is in the public domain in the United States of America.
Large‐scale study suggests no direct link between human herpesvirus‐6 and primary Sjögren's syndrome
Authors: Ranger‐Rogez S. , Vidal E. , Labrousse F. , Riche A. , Vidal J. , Collineau M. , Liozon F. , Denis F. 
Published: March 2007

AbstractThe aim of this study was to evaluate the role of human herpesvirus‐6 (HHV‐6) in the development of primary Sjögren's syndrome (PSS). Serum HHV‐6 antibody levels, as measured by immunofluorescence assay (IFA) and the prevalence of HHV‐6 DNA in peripheral blood mononuclear cells (PBMCs) determined by poly‐merase chain reaction (PCR), were studied in 49 PSS patients and 50 control subjects, all in‐patients in the University Hospital Internal Medicine ward, Limoges, France. In addition, portions of labial salivary gland were obtained from 34 patients and 15 controls, the presence of viral DNA being detected by the same PCR technique. The results were then compared with clinical observations of systemic disease manifestations in patients and a histological study of salivary gland involvement. No significant difference in HHV‐6 seroprevalence was found between control subjects (50.0%) and patients (63.3%) nor was there any statistically significant difference between patient and control groups for total viral DNA in PBMCs (22.4%, 12.0%) and salivary glands (8.8%, 6.6%). Analysis of clinical and histological data revealed no detectable correlation between disease severity and viral involvement. Tests for HHV‐6A and HHV‐6B proved positive in patient and control groups, HHV‐6B being the most frequently encountered type in both groups. In conclusion, the results of this large‐scale trial does not confirm the suspected direct role of HHV‐6 in the etiology of PSS. © Wiley‐Liss, Inc.
Quantitation of anti‐hepatitic C virus antibodies in interferon‐treated patients by S29‐1/S4 ELISA
Authors: Sato Atsushi , Nakamura Haruji , Sho Yukihiko , Arima Terukatsu 
Published: March 2007

AbstractIn 23 patients with chronic hepatitis C who have undergone interferon (IFN) treatment, quantitation of anti‐hepatitis C virus IgG antibodies by a second‐generation assay S29‐1/S4 ELISA [Sato et al. (1993): Microbiology and Immunology 37: 295‐304]. (anti‐S29‐1/S4) was compared with that of anti‐HCV core IgG antibodies (C22‐3, anti‐core) and the presence of viral RNA confirmed by the reverse transcription‐nested polymerase chain reaction (RT‐nested PCR). In 12 complete responders with loss of HCV‐RNA and normal alanine aminotransferase (ALT) levels at 6 months after therapy, IgG antibodies quantified by a second‐generation assay have decreased significantly at the end of treatment (P < 0.05). Further significant reduction of anti‐S29‐1/S4 titers was observed at 6 months after therapy (P < 0.01) as well as anti‐core antibodies (P < 0.01). On the other hand, in 11 non‐responders with persistent or intermittent viremia at 6 months after therapy, no significant change in the level of anti‐S29‐l/S4 titers was observed, whereas anti‐core titers have decreased at the end of therapy (P < 0.01). In contrast, both levels of anti‐S29‐1/S4 and anti‐core have increased at 6 months after treatment (P < 0.05). It is concluded that, although it appears difficult to monitor the effect of virus clearance during IFN therapy, changes in anti‐S29‐l/S4 titers after IFN treatment correlate with virus clearance and with anti‐core titers. © Wiley‐Liss, Inc.
Quantitative measurement of HBeAg in chronic hepatitis B: A comparison between a radioimmunoassay a fluorescence ELISA and a chemiluminescence ELISA
Authors: Heijtink R. A. , Snobl J. , Kruining J. , Kerkhof‐Los C. , de Man R. A. , Janssen H. L. A. , Schalm S. W. 
Published: March 2007

AbstractThe presence of the hepatitis B e antigen (HBeAg) in peripheral blood of chronic hepatitis B patients is a widely accepted marker of active replication of the hepatitis B virus. HBeAg determination during interferon therapy is a useful guide for the therapeutic regimen.The aim of the study was to compare the suitability of an HBeAg radioimmunoassay (RIA, Abbott Laboratories, North Chicago, IL, USA), the IMx‐HBeAg assay (IMx, Abbott Laboratories) and the HBeAg/anti‐HBe Amerlite assay (Amerlite, Johnson & Johnson Clinical Diagnostics, Cardiff, UK) for semiquantitative monitoring of HBeAg during therapy. HBeAg levels in serum samples obtained before and during interferon therapy were measured using an in‐house standard calibrated against the Paul Ehrlich Institute HBeAg reference preparation (PEI standard).When serial dilutions of pretreatment serum samples were assayed by the three methods, radioimmunoassay was found to be highly sensitive although it had a very limited working range (0.5 to 12 PEI U/ml). A broader linear working range was observed for Amerlite (0.5 to 50 PEI U/rnl) and the IMx assay (0.5 to 100 PEI U/ml). The intra‐assay and interassay variations did not differ significantly. Since the IMx assay was less susceptible to sample variation and had a broad working range, semiquantitative measurement of HBeAg in one diluted and one undiluted sample by this assay may justifiably be introduced as routine procedure. Routine semiquantitative HBeAg measurement may improve individual dose adjustments and thus the success of interferon therapy. © Wiley‐Liss, Inc.
Experimental myocarditis induced by two different coxsackievirus B3 variants: Aspects of pathogenesis and comparison of diagnostic methods
Authors: Arola Anita , Kalimo Hannu , Ruuskanen Olli , Hyypiä Timo 
Published: March 2007

AbstractThe ability of two coxsackievirus B3 (CBV3) variants to induce myocarditis in BALB/c mice was studied and plaque‐forming assay, polymerase chain reaction (PCR), in situ hybridization, and immunohistochemistry were compared for detecting viruses and viral components in the myocardium. The virological findings were related to histopathologic and ultrastructural changes in the myocardium. CBV3‐W induced severe myocarditis characterized by massive myocyte necrosis. Widely distributed myocyte damage clearly preceded modest inflammatory infiltrates in the myocardium. In contrast, CBV3‐MI induced mild myocardial injury. Both variants caused fulminant pancreatitis with nearly complete necrosis of the exocrine pancreas. CBV3 RNA was identified by PCR in the myocardium of CBV3‐W‐infected mice until the end of the follow‐up period of 14 days. Moreover, semiquantitative results were obtained when the PCR/ hybridization results were analyzed by a phosphor imaging system. lmmunohistochemistry and in situ hybridization from formaldehyde‐fixed, paraffin‐embedded specimens were highly similar in detecting viral components during the early stages of the myocardial injury. The results indicate that: (i) direct viral damage plays an essential role in acute murine CBV3‐induced myocarditis, (ii) PCR appears a useful and sensitive diagnostic method in acute myocarditis, and (iii) immunohistochemistry as a specific and relatively rapid method might be practicable also in studying the early stages of acute myocarditis from archival clinical material. © Wiley‐Liss, Inc.
Biological phenotypes of HIV‐1 subtypes A and B strains of diverse origins
Authors: Nkengasong John N. , Peeters Martine , Zhong Ping , Willems Betty , Janssens Wouter , Heyndrickx Leo , Fransen Katrien , Ndumbe Peter M. , Gershy‐Damet Guy‐Michel , Nys Patrick , Kestens Luc , Piot Peter , van der Groen Guido 
Published: March 2007

AbstractThe identification of specific biologic phenotypic traits that can be correlated with different HIV‐1 genetic subtypes was sought. The genetic subtypes were determined by either sequencing (Cameroonian strains, n = 18) or by the heteroduplex mobility assay (HMA) (Belgian strains, n = 21 and lvorian strains, n = 25). Seventeen (81%) of the 21 Belgian isolates belonged to subtype B and 4 (17%) were subtype A strains. Subtype A variants were predominant in the two African countries studied; 11 (61%) of 18 strains from Cameroon and 23 (92%) of 25 strains from the Ivory Coast. Of the 64 isolates, 38 (58%) and 19 (29%) belonged to subtypes A and B, respectively. No significant difference was observed for biological phenotypes (slow/low and rapid/high) of both genetic subtypes. In symptomatic individuals, however, a significantly higher number of subtype B isolates were of rapid/high phenotype, compared with subtype A (5 of 10; 50%) vs. 2 of 22; 9%), respectively; X2 = 6.7, P = 0.02). The findings suggest that overall HIV‐1 isolates belonging to genetic subtype B are not distinguishable from subtype A variants on the basis of their biological phenotypes. Syncytium‐inducing variants were less prevalent regardless of the geographic origin of the isolates. © Wiley‐Liss, Inc.
Significance of anti‐hepatitis C virus core IgM antibodies in patients with chronic hepatitis C
Authors: Pawlotsky Jean‐Michel , Darthuy Françoise , Rémiré Jocelyne , Pellet Claire , Udin Laure , Stuyver Lieven , Roudot‐Thoraval Franqoise , Duvoux Christophe , Douvin Catherine , Mallat Ariane , Mavier Jean‐Phillippe , Métreau Jean‐Michel , Duval Jean , Dhumeaux Daniel 
Published: March 2007

AbstractAntihepatitis C virus (HCV) IgM antibodies were found in patients with both acute and chronic hepatitis C. The aims of the study were to determine the significance, in terms of liver disease and virological parameters, of anti‐HCV core IgM antibodies in the serum of patients with chronic hepatitis C, and the possible relationship between the presence of these antibodies before treatment and biochemical and virological responses to interferon therapy. Sixty‐one patients with chronic hepatitis C were studied. Tests for serum anti‐HCV core IgM antibodies were carried out before treatment. The patients received 3 mega units of interferon alpha‐2a subcutaneously thrice weekly for at least 3 months (6months when alanine aminotransferase activity was normal at month 3). A biochemical response to interferon therapy was defined as normal alanine aminotransferase activity at the end of treatment (month 6: biochemical response) and 6 months later (month 12: sustained biochemical response). A sustained virological response was defined as serum HCV RNA negativity by a polymerase chain reaction‐based detection method (PCR) in patients with normal alanine aminotransferase at month 12. Anti‐HCV core IgM antibodies were detected in 28 of the 61 patients (46%). The prevalence of these antibodies was significantly higher in patients infected with HCV genotype 1 (including subtypes la and 1b) than in patients infected with other genotypes (including 2a and 3a) (57% vs. 17%; P < 0.01). No significant difference was found between IgM‐positive and IgM‐negative patients as regards the mean age, sex ratio, serum alanine aminotransferase and gamma‐glutamyl transpeptidase activities, the prevalence of cirrhosis in liver biopsy specimens, detection of HCV RNA by PCR, and quantitation by branched DNA assay. At month 6 of interferon therapy, normal alanine arninotransferase activity was significantly more frequent in lgM‐negative than in IgM‐positive patients (52% vs. 21%, respectively; P < 0.02). At month 12, normal alanine aminotransferase activity and PCR negativity were significantly more frequent in IgM‐negative than in IgM‐positive patients (18% vs. Ooh, P < 0.04). It is concluded that antiHCV core IgM antibodies in serum are significantly more frequent in patients infected by HCV type 1 than by other types. This suggests that their overall prevalence in patients with chronic hepatitis C in industrialized countries, where HCV type 1 accounts for the majority of infections, would be of the order of 50%, that antiHCV core IgM antibodies are not associated with characteristic features of liver disease, and that their presence before treatment is associated with a failure of interferon alpha therapy to clear the virus. © Wiley‐Liss, Inc.