bluuebunny/crossref_metadata_2025_split huggingface dataset:
Serological and molecular screening for viruses in blood donors from Ntcheu, Malawi: High prevalence of HIV‐1 subtype C and of markers of hepatitis B and C viruses
Authors: Candotti D. , Mundy C. , Kadewele G. , Nkhoma W. , Bates I. , Allain J.‐P. 
Published: October 2004

AbstractThe prevalence of antibodies to human immunodeficiency virus type 1 (HIV‐1), hepatitis C virus (HCV), human T lymphotropic virus I (HTLV‐I), and hepatitis B (HBV) surface antigen (HBsAg) was determined in blood donors from Ntcheu, Malawi. Each donation was also screened for HIV‐1 RNA and HCV RNA. Among 159 blood donations, the prevalence of HIV‐1 infection was 10.7%, 8.1% for HBV carriage, 6.8% for anti‐HCV, and 2.5% for anti‐HTLV‐I. HIV‐1/HTLV‐I and HIV‐1/HCV dual infections were observed in 1.2% of the donations. Consequently, 13% of blood donors from Ntcheu should be deferred for retroviral infections and 15% for hepatitis viral infections. Sequence analyses of the HIV‐1 strains revealed a relatively homogeneous circulation of subtype C viruses in Malawi. These findings confirm the high endemicity of blood‐borne viruses in Malawi and the need for a sensitive viral screening of blood donations to improve blood safety. J. Med. Virol. 65:1–5, 2001. © 2001 Wiley‐Liss, Inc.
Persistent hyperendemicity of hepatitis C virus infection in Taiwan: The important role of iatrogenic risk factors
Authors: Sun Chien‐An , Chen Hui‐Chi , Lu Sheng‐Nan , Chen Chien‐Jen , Lu Chih‐Feng , You San‐Lin , Lin Szu‐Heng 
Published: October 2004

AbstractThe purpose of this study was to investigate determinants of endemic hepatitis C virus (HCV) infection within communities in Taiwan. A two‐phase study, including a seroprevalence survey and a prevalent case‐control study at the first phase, which has been published previously, and a follow‐up seroconversion determination and an incident case‐control study during the second phase, was carried out to evaluate correlates of persistent endemic HCV infection. At the first phase, a total of 12,021 men and 1,819 women who were 30–64 years old and living in seven townships in Taiwan were tested for the seroprevalence of antibodies to HCV (anti‐HCV). In addition, a prevalent case‐control study involving 272 HCV‐positive cases and 282 seronegative controls identified from the anti‐HCV testing was conducted to investigate risk factors associated with HCV prevalence. During the second phase, a total of 2,728 men and 834 women who were seronegative at recruitment participated in the 1‐year prospective study on anti‐HCV seroconversion. Subsequently, an incident case‐control study based on 39 seroconverters and 81 persistently seronegative controls were carried out to elucidate determinants of HCV seroconvertion. Antibodies to HCV were tested by the second‐generation enzyme immunoassay. Information on risk factors of HCV infection was collected from subject interviews. The prevalence of anti‐HCV consistently increased with age (range 2.9–5.4%), whereas no apparent age trend was observed for anti‐HCV seroconversion rate (range 0.9–1.7%). A striking geographical variation in seroprevalence and seroconversion rates of anti‐HCV was observed in the study townships. Furthermore, a significant geographical correlation between HCV seroprevalence and seroconversion rates was noted (r = 0.962, P = 0.001). From the results of both prevalent and incident case‐control comparisons, medical injections were found to be the main mode to sustain the persistent endemic state of HCV infection within a community (odds ratios for prevalent and incident case‐control studies were 2.5 (95% CI = 1.7–3.6) and 3.1 (95% CI = 1.4–7.1), respectively. The data indicate that the basis for HCV transmission has already been existed in study areas and the iatrogenic risk factor tended to be the major determinant for sustaining persistent endemicity within a community. J. Med. Virol. 65:30–34, 2001. © 2001 Wiley‐Liss, Inc.
Fatal adenovirus type 7b infection in a child with Smith‐Lemli‐Opitz syndrome
Authors: Beby‐Defaux A. , Maille L. , Chabot S. , Nassimi A. , Oriot D. , Agius G. 
Published: October 2004

AbstractAdenovirus type 7 causes worldwide respiratory tract infections, mainly in children. Severe systemic infections can occur, especially in immunocompromised patients and in patients with underlying chronic diseases. This report describes the first case of a fatal disseminated adenovirus type 7 infection in a child with Smith‐Lemli‐Opitz syndrome, a rare autosomal recessive disorder due to a primary enzymatic defect in cholesterol metabolism. Nasopharyngeal secretions and autopsy specimens including liver, lung, pleural fluid, and rectum were collected for viral culture. Adenovirus serotype 7 strains were obtained from all anatomic sites, except the liver. All these clinical isolates were analyzed using restriction endonuclease digestion of the genome, identifying them as genome type 7b, a virulent type. In this case, the fatal evolution could have been accelerated by the presence of an immunodeficiency although immunodeficiency is not included in the definition of Smith‐Lemli‐Opitz syndrome. The frequent recurrent banal infections in Smith‐Lemli‐Opitz syndrome could be prevented by a cholesterol supplementation regimen. Finally, this report emphasizes the need for efficient therapy for disseminated adenovirus infections, especially for virulent genome types. J. Med. Virol. 65:66–69, 2001. © 2001 Wiley‐Liss, Inc.
Area under the viraemia curve versus absolute viral load: Utility for predicting symptomatic cytomegalovirus infections in kidney transplant patients
Authors: Schäfer Peter , Tenschert Werner , Cremaschi Liana , Schröter Matthias , Zöllner Bernhard , Laufs Rainer 
Published: October 2004

AbstractA novel approach to predicting symptomatic cytomegalovirus (CMV) infections combines the level and the duration of viraemia in a single parameter. Sixty‐four kidney transplant recipients were monitored by quantitative shell vial culture, pp65 antigenaemia, and polymerase chain reaction (PCR) of leucocytes. The area under the curve (AUC) of each parameter was determined from the onset of viraemia to the beginning of antiviral treatment. The AUC values were significantly higher in symptomatic than in asymptomatic patients. For antigenaemia and PCR, optimal AUC thresholds for predicting symptomatic CMV infections were determined. They were superior to standard cutoff levels of absolute viral load in sensitivity, specificity, and positive and negative predictive value. In 8 of the 23 patients who became symptomatic, impending clinical features were indicated earlier by the AUC thresholds than by standard viral load. In conclusion, the concept of the AUC should facilitate identification of patients at risk of symptomatic CMV infection. J. Med. Virol. 65:85–89, 2001. © 2001 Wiley‐Liss, Inc.
Kaposi's sarcoma‐associated herpesvirus serology in Europe and Uuganda: Multicentre study with multiple and novel assays
Authors: Schatz Octavian , Monini Paolo , Bugarini Roberto , Neipel Frank , Schulz Thomas F. , Andreoni Massimo , Erb Peter , Eggers Maren , Haas Jürgen , Buttò Stefano , Lukwiya Matthew , Bogner Johannes R. , Yaguboglu Svenja , Sheldon Julie , Sarmati Loredana , Goebel Frank Detlef , Hintermaier Renate , Enders Gisela , Regamey Nicolas , Wernli Marion , Stürzl Michael , Rezza Giovanni , Ensoli Barbara 
Published: October 2004

AbstractA multicentre study was undertaken to define novel assays with increased inter‐assay concordance, sensitivity, specificity and predictive value for serological diagnosis of human herpesvirus type 8 (HHV‐8) infection. A total of 562 sera from European and Ugandan human immunodeficiency virus (HIV)‐infected or uninfected individuals with or without Kaposi's sarcoma (KS) and blood donors were examined under code by 18 different assays in seven European laboratories. Sera from KS patients and all non‐KS sera found positive by at least 70%, 80%, or 90% of the assays were considered “true positive.” The validity of the assays was then evaluated by univariate logistic regression analysis. Two immunofluorescence assays (IFA) for detection of antibodies against HHV‐8 lytic (Rlyt) or latent (LLANA) antigens and two enzyme‐linked‐immunosorbent assays (ELISA) (M2, EK8.1) for detection of antibodies against HHV‐8 structural proteins were found to be highly concordant, specific, and sensitive, with odds ratios that indicated a high predictive value. When used together, the two IFA (Rlyt‐LLANA) showed the best combination of sensitivity (89.1%) and specificity (94.9%). The performance of these assays indicate that they may be used for the clinical management of individuals at risk of developing HHV‐8 associated tumours such as allograft recipients. J. Med. Virol. 65:123–132, 2001. © 2001 Wiley‐Liss, Inc.
Detection of influenza a subtypes in community‐based surveillance
Authors: Boon A.C.M. , French A.M.F. , Fleming D.M. , Zambon M.C. 
Published: October 2004

AbstractA rapid microtitre cell enzyme immuno assay (cell‐EIA) was developed for the detection of influenza A subtypes in nasopharyngeal(NPS) swabs taken for surveillance. During the 1997/1998 influenza season in the United Kingdom, cell‐EIA was compared to cell culture for the detection and typing of influenza A viruses in NPS obtained by sentinel general practitioners in community surveillance. The cell EIA can also be used to detect different influenza A subtypes (H3N2, H1N1, H5N3, H5N1, H7N7, and H9N2) and was used as a rapid detection assay for the screening of individuals returning from Hong Kong with influenza‐like illness suspected to be due to H5N1 in 1997/98, providing a rapid, efficient, inexpensive method for the screening of influenza A cases during an outbreak or pandemic situation. The cell‐EIA results reflected the results obtained by traditional virus culture within the age distribution of samples, clinical symptoms, and time between date of illness onset and sampling of cases, indicating its usefulness in surveillance of human and non‐human influenza viruses. During two outbreaks of influenza in schools, Directigen© Flu‐A, a near patient test, the cell‐EIA, and tissue culture were compared. The cell‐EIA gave higher sensitivity and specificity (74% and 90%) than Directigen© Flu‐A (65% and 84.6%) in comparison with cell culture. J. Med. Virol. 65:163–170, 2001. © 2001 Wiley‐Liss, Inc.
Presumed common source outbreaks of hepatitis A in an endemic area confirmed by limited sequencing within the VP1 region
Authors: Arauz‐Ruiz Patricia , Sundqvist Lena , García Zaida , Taylor Lizeth , Visoná Kirsten , Norder Helene , Magnius Lars O. 
Published: October 2004

AbstractHepatitis A virus isolates from anti‐HAV IgM positive sera of 70 hepatitis cases in two outbreaks and 216 other cases in Central America, 136 sporadic cases and 53 cases from an hyper‐endemic region in Costa Rica, were compared by phylogenetic analyses within the VP1 region. The outbreaks in all 531 cases, in 1992 and 1999, respectively, were presumed water borne. In the first outbreak, HAV RNA could be detected in 70% of the cases sampled during 6 weeks after onset of jaundice. In the hyper‐endemic region of San Ramón in Costa Rica, 1,932 cases were registered between 1972 and 1985. All isolates belonged to subtype 1A. Background isolates from Costa Rica and El Salvador tended to form separate subclusters in the phylogenetic tree construction and were mostly unrelated to subtype 1A strains from other parts of the world. Based on their amino acid sequences, four HAV strains, all related to CR326 sampled in Costa Rica in 1960, were found to have circulated in the area during the last three decades. However, on the basis of nucleotide variability the isolates from the outbreaks could be distinguished from the strains from sporadic cases and sequence analysis could confirm the epidemiological homogeneity of both outbreaks. In the hyper‐endemic region, 16 different sequences were encountered forming one single subcluster. Thus, limited sequencing within the VP1 region proved useful to identify outbreaks of hepatitis A in a highly endemic area, where most strains were local and only one subtype was prevalent. J. Med. Virol. 65:449–456, 2001. © 2001 Wiley‐Liss, Inc.
Sequence analysis of hepatitis B virus genomes from an infant with acute severe hepatitis and a hepatitis B e antigen‐positive carrier mother
Authors: Komatsu Haruki , Inui Ayano , Morinishi Youichi , Sogo Tsuyoshi , Fujisawa Tomoo 
Published: October 2004

AbstractIt is well known that fulminant hepatitis B can occur in infants born to hepatitis B e antigen (HBeAg)‐negative hepatitis B virus (HBV) carrier mothers, whereas fulminant hepatitis and severe hepatitis are uncommon in infants born to HBeAg‐positive mothers. We have encountered an infant with severe acute hepatitis B born to a HBeAg‐positive mother. The aim of this study was to determine whether HBV variants contribute to the pathogenesis of fulminant hepatitis and severe hepatitis in an infant born to an HBeAg‐positive mother. The nucleotide sequence of HBV genomes from the infant and his HBeAg‐positive carrier mother was analyzed. All HBV isolated from the infant and his mother were subtype adr. The sequences of the cloned HBV genomes, each including a part of the X and precore/core regions, isolated from the infant were almost identical (homology of 99.1–99.9%) to those from his mother. There was no mutation in any of the 17 clones examined at nucleotides 1762 and 1764 in the core promoter, which is reported to be associated with fulminant hepatitis. A point mutation at nucleotide 1758 in the second AT‐rich region of the basic core promoter was present in all clones. None of the clones had a point mutation at nucleotide 1896 of the precore region. In this study, no specific HBV variants contributing to the development of neonatal severe hepatitis were found. There is a possibility that host factors rather than viral factors play an important role in some cases of severe neonatal hepatitis B. J. Med. Virol. 65:457–462, 2001. © 2001 Wiley‐Liss, Inc.
Molecular analysis of hepatitis B virus genomes isolated from black African patients with fulminant hepatitis B
Authors: Owiredu William K.B.A. , Kramvis Anna , Kew Michael C. 
Published: October 2004

AbstractTo investigate further the possible role of mutant hepatitis B viruses in the pathogenesis of fulminant hepatitis B, the genomic sequence of hepatitis B virus isolates from 9 South African blacks with this disease, including 5 entire genomes, was analysed. Seven of the isolates were genotype A. The mutation most often reported in patients with fulminant hepatitis B, the G1896A precore stop‐codon substitution, was, as expected, not present in the genotype A isolates with the exception of one in which it was accompanied by a compensatory C1858T substitution. G1896A was, however, present in the one genotype D isolate. No other precore‐defective mutants were detected. The other mutation commonly found in patients with fulminant hepatitis B, the paired A1762T, G1764A substitution in the basic core promoter, was present in only one patient and G1764A in one other. The pre‐surface initiation‐codon mutation documented in a number of patients with fulminant hepatitis B was not found in our isolates. An 18–amino acid deletion present in the pre‐surface region of one isolate has not previously been described in fulminant hepatitis B. Variations within the surface region were mainly genotype specific and not previously described. A relatively large number of mutations were present in the middle region of the core gene in those isolates without G1896A or A1762T, G1764A mutations, although the pattern was not consistent with those in published studies. Thus, as in other published series in which the entire genome of hepatitis B virus responsible for fulminant hepatitis was sequenced, we detected many mutations in different genes, but none was common to all the reported isolates. J. Med. Virol. 65:485–492, 2001. © 2001 Wiley‐Liss, Inc.
Hepatitis C viral genotype influences the clinical outcome of patients with acute posttransfusion hepatitis C
Authors: Hwang Shinn‐Jang , Lee Shou‐Dong , Lu Rei‐Hwa , Chu Chen‐Wei , Wu Jaw‐Ching , Lai Shiau‐Ting , Chang Full‐Young 
Published: October 2004

AbstractMost patients with an acute infection of hepatitis C virus (HCV) will develop chronic hepatitis, and only about 15–20% of the cases will resolve spontaneously. The mechanism for the different outcomes in patients with acute HCV infection remains unclear. HCV genotype has been recognized as an important factor affecting the clinical course and outcome of chronic hepatitis C patients. In order to evaluate the role of HCV genotype in the clinical course and outcome of acute posttransfusion hepatitis C, 67 patients with acute posttransfusion hepatitis C from a prospective study of posttransfusion non‐A, non‐B hepatitis were enrolled. Thirty‐nine patients (58.2%) were HCV genotype 1b. Among the 67 patients with acute posttransfusion hepatitis C, 53 (79.1%) progressed to chronic hepatitis. Significantly more patients with genotype 1b than non‐1b genotypes developed chronic hepatitis (89.7% vs. 64.3%; P = 0.019). There was no significant difference in gender, mean age, amount of transfused blood, hepatitis symptoms, jaundice, incubation period, peak serum alanine transaminase, or serum HCV RNA titer between patients with HCV genotype 1b and non‐1b infections. Patients who developed chronic hepatitis had a significantly greater incidence of genotype 1b infection (66.0% vs. 28.6%; P = 0.013) and a longer incubation period (7.3 weeks vs. 5.4 weeks; P = 0.052) than patients whose infection was resolved. Patients with a genotype 1b infection that resolved itself spontaneously all had an incubation period of less than 6 weeks. Multivariate logistic regression analysis revealed that genotype 1b and an incubation period ≥ 6 weeks were significant predictive factors for the development of chronic hepatitis. Therefore, the HCV genotype can influence the outcome of patients with acute HCV infection. J. Med. Virol. 65:505–509, 2001. © 2001 Wiley‐Liss, Inc.
Ethnicity and cytokine production gauge response of patients with hepatitis C to interferon‐α therapy
Authors: Kimball Pam , Elswick R.K. , Shiffman Mitchell 
Published: October 2004

AbstractInterferon is the primary treatment for hepatitis C virus (HCV). However, the long‐term success rate is low particularly for African Americans relative to Caucasians and may be due to differential immune abilities. This study compared cytokine production from PHA‐stimulated peripheral blood from 25 healthy and 40 HCV‐infected African Americans and Caucasians. HCV patients were designated as IFN responders or nonresponders based on outcome after therapy. Ethnicity and genotype were associated with IFN response. IFN responders were 100% Caucasian, whereas nonresponders were 67% Caucasian and 33% African American (P = 0.01). Genotype 1 was present in 100% nonresponders and 50% responders (P < 0.05). Age, sex, liver histology, ALT, and viral titers were equivalent (ns). Cytokine production from healthy individuals showed ethnic variation in cytokine levels. Healthy African Americans produced greater amounts of IL‐2 (P = 0.06), TNF‐α (P = 0.06) and less IL‐10 (P = 0.05) than healthy Caucasians. In contrast, IFN‐γ and TGF‐β levels were equivalent. Pretherapy cytokine production among HCV patients showed a similar pattern of ethnic variation. African American nonresponders produced more IL‐2 (P = 0.06) and TNF‐α (P = 0.02) than Caucasian nonresponders. Cytokine levels among Caucasian and African American nonresponders were equivalent (P = ns) to ethnically matched healthy individuals whereas Caucasian responders produced subnormal levels of IL‐10 (P < 0.05) and TGF‐β (P < 0.05). Since all African Americans failed IFN therapy, cytokine production could not be compared with therapeutic outcome. However, comparison of cytokine production among Caucasians showed that responders produced less IL‐10 (P < 0.001) and more TGF‐β (P = 0.06) than nonresponders and predicted Caucasian nonresponders with 83% sensitivity and 96% specificity. HCV genotype was not relevant to cytokine production (P = ns). Distribution of cytokine genetic polymorphisms (TNF‐α, TNF‐β, IL‐10, TGF‐β) was equivalent in all ethnic groups and did not predict clinical nonresponders. In summary, it appears that ethnicity may contribute to variable immune responses and therapeutic outcome. The cytokine profile among African Americans suggests a more robust immune response, hich may complicate therapy with IFN. In contrast, the subnormal cytokine production among Caucasian responders may be more permissive to IFN therapy. Pretherapy cytokine production may allow prediction of drug resistance among Caucasians. J. Med. Virol. 65:510–516, 2001. © 2001 Wiley‐Liss, Inc.
New genome type of adenovirus serotype 19 causing nosocomial infections of epidemic keratoconjunctivitis in Japan
Authors: Tanaka‐Yokogui Keico , Itoh Norihiko , Usui Norio , Takeuchi Satoshi , Uchio Eiichi , Aoki Koki , Usui Masahiko , Ohno Shigeaki 
Published: October 2004

AbstractTwelve strains of adenovirus serotype 19, isolated from cases of epidemic keratoconjunctivitis in Japan in 1992, 1993, 1997, and 1998, were analyzed by DNA restriction analysis, using restriction endonucleases BamHI, BglI, BglII, EcoRI, HindIII, KpnI, PstI, SacI, SalI, SmaI, and XhoI. Among these 11 restriction endonucleases, EcoRI, PstI, SacI, and SmaI were discriminative enzymes, showing restriction patterns different from those reported previously for the prototype and the variant 19a. This new genome type was isolated in 1997 and 1998, when an increase of epidemic keratoconjunctivitis cases caused by adenovirus serotype 19 was observed for both sporadic and nosocomial infections. Strains from 1992 and 1993 showed restriction patterns similar to those of the worldwide reported variant 19a for all enzymes used. The changes detected in strains from 1997 and 1998 could be the reason for the recent epidemic. J. Med. Virol. 65:530–533, 2001. © 2001 Wiley‐Liss, Inc.
Quantification of Epstein‐Barr virus load in peripheral blood of human immunodeficiency virus‐infected patients using real‐time PCR
Authors: Dehee Axelle , Asselot Catherine , Piolot Tristan , Jacomet Christine , Rozenbaum Willy , Vidaud Michel , Garbarg‐Chenon Antoine , Nicolas Jean‐Claude 
Published: October 2004

AbstractEpstein‐Barr virus (EBV) reactivation is more likely to occur in immunocompromised patients with subsequent higher susceptibility to EBV‐associated lymphoproliferations. In contrast to transplant recipients, limited data are available concerning the EBV load in HIV‐infected patients, with or without AIDS‐related non‐Hodgkin's lymphomas. We developed a TaqMan real‐time PCR assay, allowing both the EBV genome and a cellular gene to be quantified in order to obtain a reliable normalized measurement of the EBV load in peripheral blood mononuclear cells (PBMCs). With a wide 6‐log10 quantification range and inter‐assay variations of less than 24%, this quantitative PCR was sufficiently accurate and reproducible for routine follow‐up. The EBV load was determined in PBMCs from 113 HIV‐infected patients, 11 patients with primary HIV infection and 24 HIV‐seronegative healthy controls. The rates of EBV detection were similar in the three groups. However, EBV loads were higher in the HIV‐infected group (P < 0.00001) except for the patients with primary HIV infection. Unexpectedly, EBV loads were not correlated with the clinical stages of HIV infection or HIV replication, and did not depend on the degree of immunodepression, as judged by CD4+ counts. This study contributes towards the definition of the baseline EBV load during HIV infection and stresses the broad inter‐individual variability of the EBV load in HIV‐infected patients. Real‐time PCR provides a useful tool that can be used in further longitudinal studies to assess the relevance of the EBV load to identify HIV‐infected patients with a high risk of EBV‐associated lymphoproliferations. J. Med. Virol. 65:543–552, 2001. © 2001 Wiley‐Liss, Inc.