bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evidence for superantigen activity of the bel 3 protein of the human foamy virus
Authors: Weissenberger Jakob , Altmann Annette , Meuer Stefan , Flügel Rolf M. 
Published: March 2007

AbstractThe human foamy virus is a complex retrovirus that codes for several regulatory bel genes in addition to the conventional gag, pol, and env genes. The bel 3 gene is located in the 3′part of the viral genome comparable to that of the superantigen of the mouse mammary tumor virus. Superantigens bound to major histocompatibility complex (MHC) class II molecules have been shown to stimulate T cells in a Vp‐specific manner. The recombinant Bel 3 protein purified to near homogeneity was assayed in vitro to determine whether or not it functions as a superantigen that stimulates human T lymphocytes expressing particular Vβ T cell receptor (TCP) chains. Therefore, an analysis including all known human Vβ elements was performed. The expression of different Vβ chains of the TCR was analyzed by reverse transcription of the Vp RNAs and subsequent amplification of the corresponding Vβ cDNA elements by polymerase chain reaction in unstimulated, phytohemaggluttinin (PHA)‐ and Bel 3‐stimulated human T lymphocytes. In addition, eight monoclonal antibodies directed against particular Vβ family members were used to determine any change in the expression of the remaining known Vβ elements upon treatment with PHA and Bel 3. The comparative Vp‐specific transcriptional analysis revealed that the in vitro expression of the Vβ18 chain was specifically and strongly expanded in Bel 3‐stimulated human T cells, a property characteristic for a superantigen. © 1994 Wiley‐Liss, Inc.
Genotype distribution of hepatitis C virus infection in Taiwan
Authors: Wu Jau‐Shin , Lee Han‐Fang , Hsiau Hui‐Ling , Lu Hsiu‐Ying , Chou Wen‐Hsiang , Lu Chih‐Feng , Chen Hour‐Young , Lee Fong‐Nien , Chen Pei‐Yuan , Tarn Kim‐Man 
Published: March 2007

AbstractTo investigate the prevalence of genotype distribution of hepatitis C virus (HCV) infection in Taiwan, genotypes were identified in 122 (36 anti‐HCV‐positive blood donors, 44 anti‐HCV‐positive aborigines, 28 hemodialysis patients, and 14 patients with chronic liver diseases) of 280 subjects, using polymerase chain reaction by Okamoto's type‐specific primer method. Type II was the dominant (66.7%) type among anti‐HCV‐positive blood donors, followed by type III and type IV with the same percentages (16.7%), while none of type I was detected. The prevalence of genotype distribution were 75.0%, 81.1%, and 64.3% for type 11,4.6%, 17.9%, and 21.4% for type III, 13.6%, 0%, and 7.1% for type IV, for the aborigines, hemodialysis, and chronic liver diseases groups, respectively. Four subjects revealed mixed infections by two different genotypes: two cases of II and III; and each one case of II and IV, and III and IV. Diverse genotype distributions in two hemodialysis groups disclose the existence of obvious regional differences even within a region. The results reveal the highest prevalence of type II as in Japan. However, there is a higher prevalence rate of type IV than in Japan. © 1994 Wiley‐Liss, inc.
Immune responses of blood donors to peptides of various lengths and those with genotypic sequence variations corresponding to the N‐terminal portion of the core protein of hepatitis C virus
Authors: Sato Atsushi , Sho Yukihiko , Nakamura Haruji , Kunitomo Tetsunosuke , Arima Terukatsu 
Published: March 2007

AbstractImmune reactivities of blood donor sera with the peptides of various lengths (24, 30, 40 and 50 mer) and those with genotypic sequence variations in the N‐terminal portion of the core protein of hepatitis C virus (HCV) were compared by enzyme‐linked immunosorbent assays. It was found that a 40‐mer oligopeptide (amino acids 2–41) was recognized more frequently than other peptides even in serum samples that did not react with the C22‐3 (core) by the recombinant immunoblot assay (RIBA‐II). On the other hand, a 30‐mer peptide (amino acids 1–30) had good correlation with viremia as confirmed by the polymerase chain reaction (PCR). In addition, four individuals showed the obvious differences in the immune responses to 30‐mer oligopep‐tides representing the 4 genotypic variations. As a result, some samples that were PCR‐positive but nonreactive by a commercial assay were found to react with short synthetic peptides in the N‐terminal portion of the core protein. © 1994 Wiley‐Liss, Inc.
Effects of hepatitis C and B viruses infection on the development of hepatocellular carcinoma
Authors: Tsai Jung‐Fa , Chang Wen‐Yu , Jeng Jen‐Eing , Ho Mei‐Shang , Lin Zu‐Yau , Tsai Juei‐Hsiung 
Published: March 2007

AbstractA case control study consisting of 102 patients with HCC, 102 sex‐matched and age‐matched patients with nonhepatic disease, and 204 matched healthy controls was carried out to investigate the effect of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection on the development of hepatocellular carcinoma (HCC). The prevalence of antibody to HCV (anti‐HCV) in HCC (34.3%) was higher than in nonhepatic disease (10.7%, P< 0.001) or in healthy controls (2.4%, P< 0.001). The prevalence of hepatitis B surface antigen (HBsAg) in HCC (77.4%) was higher than in nonhepatic disease (16.6%, P< 0.001) or in healthy controls (19.6%, P< 0.001). Anti‐HCV positivity in nonhepatic disease was higher than in healthy controls (P<0.01). Using patients with nonhepatic disease as controls, stepwise logistic regression analysis indicated that both anti‐HCV (odds ratio, 3.4; 95% confidence interval, 2.1‐5.6) and HBsAg (odds ratio, 5.6; 95% confidence interval, 3.6–8.5) are independent risk factors for HCC. Using healthy controls, the development of HCC was also strongly associated with anti‐HCV (odds ratio, 8.0; 95% confidence interval, 4.3–14.6) and HBsAg (odds ratio, 5.5; 95% confidence interval, 3.7–8.2). Calculation of incremental odds ratio indicated that there is no interaction between HBV and HCV. In conclusion, HBV and HCV are risk factors of HCC. They act independently and without interaction. © 1994 Wiley‐Liss, Inc.
Differences in the entire nucleotide sequence between hepatitis B virus genomes from carriers positive for antibody to hepatitis B e antigen with and without active disease
Authors: Horikita Minoru , Itoh Susumu , Yamamoto Kayoko , Shibayama Takao , Tsuda Fumio , Okamoto Hiroaki 
Published: March 2007

AbstractThe entire nucleotide sequence was determined for eight hepatitis B virus (HBV) genomes from three symptom‐free carriers, two patients with chronic persistent hepatitis and one patient with chronic active hepatitis, who were positive for antibody to hepatitis B e antigen (HBeAg). The two patients with chronic persistent hepatitis were tested again after they developed chronic active or fulminant hepatitis, making a total of eight samples. Six had a point mutation in the preC region prohibiting the encoding of HBeAg precursor, while the remaining two had a deletion of 8 or 21 nucleotides within the X gene upstream of the preC transcription initiation sites which would affect the X gene and the putative preC/C promoter. Most genomes from the three symptom‐free carriers and the two patients with chronic persistent hepatitis, with HBV DNA levels of 102–103/ml, had deletion, frameshift mutation, initiation failure or a premature stop codon, rendering them replication‐incompetent. In contrast, such mutations were rarely seen in HBV genomes from the two patients with chronic persistent hepatitis after they had developed active or fulminant hepatitis and from the patient with chronic active hepatitis, all of whom had vigorous HBV replication with serum HBV DNA from 106 to 109/ml. Unique mutations for amino acid changes were more frequent in HBV genomes with a higher replicative activity. These results indicate two kinds of HBV genomes with an HBeAg‐minus phenotype, one with defects seriously affecting viral replication and the other without such defects, which would account for different clinical profiles in carriers with antibody to HBeAg. © 1994 Wiley‐Liss, Inc.
Detection of hepatitis B virus DNA in the serum of Canadian hepatitis B surface antigen negative, anti‐HBc positive individuals, using the polymerase chain reaction
Authors: Scully Linda J. , Sung Howard , Pennie Ross , Gill Peter 
Published: March 2007

AbstractContinuing hepatitis B virus (HBV) infection is normally associated with the presence of hepatitis B surface antigen (HBsAg) in the serum. In spite of sensitive screening assays for HBsAg, rare cases of post‐transfusion HBV infection are still observed. Antibody to hepatitis B core antigen (anti‐HBc) often indicates remote HBV infection but DNA hybridisation and more sensitive polymerase chain reaction (PCR) assays have demonstrated that some HBsAg negative individuals, positive for anti‐HBc, have continuing HBV replication. To determine the incidence of ongoing HBV infection in a Canadian HBsAg negative, anti‐HBc positive population we studied three groups with this combination of HBV markers: Group A, 36 patients referred for investigation of raised serum aminotransferases; Group B, 21 Canadian Red Cross blood donors; Group C, seven vaccinees in an Ottawa Health Care Student hepatitis B vaccination programme. The PCR was carried out using a nested PCR reaction with primers specific for the pre‐core region of HBV.Seven of 36 (19%) patients in Group A had detectable HBV DNA whereas none of Group B or C were positive. This data indicates that in some HBsAg negative patients with ongoing hepatic inflammation, continuing HBV replication may persist. This was not observed in any healthy blood donors or health care students investigated. Larger studies are required, but this data would suggest that, in Canada, the addition of anti‐HBc testing for all blood donors for detection of low level HBV replication would not be indicated. © 1994 Wiley‐Liss, Inc.
Polymerase chain reaction and sequencing for typing rhinovirus RNA
Authors: Mori Julie , Clewley Jonathan P. 
Published: March 2007

AbstractPrimers were designed and tested for their ability to distinguish rhinoviruses from enterovi‐ruses. A primer set derived from the 5′‐UTR/VP coding region junction was able to amplify all the rhinovirus serotypes tested. Enteroviruses were either not amplified by these primer pairs or produced a band of larger size that could easily be discriminated from the rhinovirus‐specific product. In contrast, primers embedded in the 5′‐UTR region alone were able to amplify both rhinovirus and enterovirus RNA. It is shown that rhino‐viruses could be specifically typed by sequencing the amplicon derived from this 5′‐UTR set. The sequences of the 5′‐UTR region often previously unsequenced rhinoviruses were derived. The sequences obtained cluster into two groups: 18,41, 15, 30, 63, 31,56, and 44; and 17, 69, and 70. Ampliconsfrom serotypes 17, 69, and 70 also group by sequence with the equivalent region of HRV14 from the genetic database, while the others group with 2 and 89. © 1994 Wiley‐Liss, inc.
Long‐term follow‐up of hepatitis B virus carrier infants
Authors: Chan Cho‐Yu , Lee Shou‐Dong , Yu May‐Ing , Wang Yuan‐Jen , Tsai Yang‐Te , Lo Kwang‐Juei 
Published: March 2007

AbstractOne hundred twenty‐two hepatitis B surface antigen (HBsAg) carrier infants were followed‐up for 8–10 years. One hundred eleven had antibody to hepatitis B core antigen (anti‐HBc; 83 had been vaccinated) and the remaining 11 were without anti‐HBc (7 had been vaccinated). During the follow‐up period, 29 (26.1%) carrier infants with anti‐HBc had one or more episodes of ala‐nine aminotransferase (ALT) elevation and up to 32.8% (21/64) of the carriers in this group lost their hepatitis B e antigen (HBeAg) before the age of 10. In addition, 2 (1.8%) carriers lost their HBsAg at the age of 3 and 8, respectively. No significant symptom or sign was noted during HBeAg seroconversion. In contrast, all the carrier infants without anti‐HBc were still positive for both HBeAg and hepatitis B virus (HBV) DMA and none displayed abnormal ALT levels or any symptom related to liver disease. One became anti‐HBc positive at the age of 9, and 5 other carriers had inconsistent borderline or weakly positive titers of anti‐HBc. The episodes of ALT elevation and the prevalence of HBeAg seroconversion were not significantly different between immunized carrier infants. In conclusion, HBeAg seroconversion may occur in about one third of the anti‐HBc‐positive carrier infants during the first decade. On the other hand, the anti‐HBc‐negative HBsAg carrier infants' immune incompetence to the HBV antigens could persist for more than 10 years. Hepatitis B immunization did not have significant effect on the clinical course in carriers. © 1994 Wiley‐Liss, Inc.
Complete nucleotide sequence of a strain of coxsackie B4 virus of human origin that induces diabetes in mice and its comparison with nondiabetogenic coxsackie B4 JBV strain
Authors: Kang Yup , Chatterjee Nando K. , Nodwell Michael J. , Yoon Ji‐Won 
Published: March 2007

AbstractThe E2 strain of coxsackie B4 virus (CB4), which is of human origin, can induce a diabetes‐like syndrome in mice. The cDNA of the genome of the E2 strain was cloned and sequenced. The E2 viral genome was found to comprise 7,396 bases, which appear to encode a polyprotein of 2,183 amino acids with an overall similarity of 94.91% to nondiabetogenic CB4 prototype JBV strain. The E2 genome is organized like other enteroviruses. It has a 5′ noncoding region of 744 nucleotides, a single long open translational reading frame starting at nucleotide 745 and extending to nucleotide 7293, a 3′ noncoding region of 100 nucleotides, and a poly (A) tract. Ge‐nomic sequence comparison of the E2 and JBV strains showed 1,369 nucleotide substitutions in the genome of the E2 strain, most of which are single and silent. There were 111 resultant amino acid changes arising from some of these substitutions, including 82 amino acid changes in the noncapsid proteins, and 29 amino acid changes in the capsid proteins VP1, VP2, VP3, and VP4, which showed 11, 13, 4, and 1 substitution(s), respectively. Noncapsid protein P2‐C showed eight amino acid substitutions. On the basis of the sequence comparison of E2 and JBV strains of CB4, we suggest that some of the amino acid changes in the capsid and noncapsid proteins of the E2 strain may be involved in the determination of its diabetogenicity. © 1994 Wiley‐Liss, Inc.
Hepatitis E seroprevalence in selected individuals in South Africa
Authors: Grabow W. O. K. , Favorov M. O. , Khudyakova N. S. , Taylor M. B. , Fields H. A. 
Published: March 2007

AbstractAntibodies to the hepatitis E virus (HEV) were detected by an enzyme immunoassay using synthetic HEV peptides. Positive anti‐HEV results were confirmed by a neutralization assay and Western blot analysis. Anti‐HEV was detected in 10 of 555 canoeists (1.8%) with regular exposure to sewage‐polluted water and in 6 of 227 (2.6%) medical students with minimal exposure. The overall prevalence of 16 per 782 individuals (2.05%) suggests that HEV may be endemic in South Africa. This is confirmed by indications of infection earlier than the third decade of life, and by individuals with anti‐HEV who had rarely or never been out of the country. The prevalence data suggest that regular exposure to sewage‐polluted water was not a particular risk factor. None of the individuals with anti‐HEV had a history of clinical hepatitis E, suggesting sporadic low level subclinical cases of infection. This is in agreement with the absence of reports on clinical cases or outbreaks of hepatitis E in South Africa. © 1994 Wiley‐Liss, Inc.
Monitoring of renal allograft recipients by quantisation of human cytomegalovirus genomes in peripheral blood leukocytes
Authors: Kühn J. E. , Wendland T. , Schäfer P. , Möhring K. , Wieland U. , Elgas M. , Eggers H. J. 
Published: March 2007

AbstractThe ratio of human cytomegalovirus (HCMV) genomes per cellular genomes in serial peripheral blood leukocyte (PEL) extracts of renal allograft recipients was quantitated by competitive nested polymerase chain reaction (PCR). Patients were also monitored for the development of acute HCMV infection by detection of HCMV pp65 antigenemia, HCMV IgM antibodies, and viruria. Compared to qualitative nested HCMV PCR, the frequency of positive PCR results in renal allograft recipients without further evidence of acute HCMV infection was significantly reduced by quantitative HCMV PCR. HCMV DMA levels ≥1,000 copies HCMV/106 copies β‐globin were found to be highly indicative for the development of a clinically symptomatic HCMV infection following renal allograft transplantation. In patients treated with ganciclovir, quantitation of HCMV target sequences allowed the assessment of the efficacy of antiviral therapy. © 1994 Wiley‐Liss, Inc.
Immunogenicity and safety in adults of hepatitis A virus vaccine administered as a single dose with a booster 6 months later
Authors: Briem H. , Safary A. 
Published: March 2007

AbstractAn inactivated vaccine against hepatitis A was administered as a single 1,440 enzyme‐linked immunosorbent assay (ELISA) units dose at month 0 with a booster at month 6 to 200 subjects divided into two age groups: group 1, 20–39 years (n = 134) and group II, 40–62 years (n = 66). At day 15, the seropositivity rates were 90% and 77% in groups I and II, respectively. At month 1 the seropositivity rate was 97% in both groups. At month 6 the seropositivity rates were 94% and 88% in groups I and II, respectively. One month after the booster, at month 7, 100% in both groups had become seropositive. The vaccine was well tolerated and did not cause any severe reactions. The results indicate that a single high vaccine dose offers protection against hepatitis A virus (HAV) for at least 6 months in the majority of cases where rapid vaccination is required even in travellers of older age. A booster dose will ensure long‐term protection. © 1994 Wiley‐Liss, Inc.
Inactivated hepatitis A vaccine: Reactogenicity, immunogenicity, and long‐term antibody persistence
Authors: van Damme P. , Thoelen S. , Cramm M. , de Groote K. , Safary A. , Meheus A. 
Published: March 2007

AbstractThis trial evaluated the reactogenicity, kinetics of antibody induction, and long‐term immunogenicity of a 720 enzyme‐linked immunosorbent assay units (EL. U.) antigen dose of an inactivated hepatitis A vaccine (Havrix(tm), SmithKline Beecham Biologicals, Rixensart, Belgium). One hundred six healthy adult volunteers were enrolled to receive vaccine intramuscularly according to a 0, 1, and 6‐month schedule. The vaccine was well tolerated. The most frequently reported local symptom was soreness, observed following 37.1% of all doses. Headache was the most frequently reported general symptom observed following 12.9% of documented vaccine doses. The administration of one vaccine dose induced seropositivity (anti‐hepatitis A virus [HAV] ≥ 20 mlU/ml) in 91% of all vaccinees 1 month later. The second vaccine dose resulted in seropositivity of the remaining vaccinees at month 2. All subjects remained seropositive for HAV antibodies at month 6, at which time the booster vaccine dose was given. At month 7, all vaccinees had anti‐HAV titres > 200 mlU/ml.Serological results obtained at months 12, 18, 24, and 36 showed that antibodies against HAV induced by the vaccine booster dose persist for at least 30 months following its administration. All 49 subjects followed up until month 36 had antibody titres ≥ 20 mlU/ml. The geometric mean titre (GMT) decreased by 60% from month 7 to month 12; between month 12 and 36, the GMT decreased by approximately 14% per period of 12 months. According to the vaccine‐induced antibody kinetics and the magnitude of antibody level decrease overtime, the predicted duration of antibody persistence is estimated to be at least 20 years. © 1994 Wiley‐Liss, Inc.
A rapid and sensitive method of identification of HTLV‐II subtypes
Authors: Dube Syamalima , Spicer Timothy , Bryz‐Gornia Virginia , Jones Barbara , Dean Therese , Love Jayne , Dube Dipak K. , Poiesz Bernard J. , Ferrer Jorge , Esteban Nestor , Harrington William , Glaser Jordan , Williams Allan , Dosik Harvy , Siegal Frederick 
Published: March 2007

AbstractThere are 2 subtypes of human T‐cell lymphoma/ leukemia virus type II (HTLV‐II), A and B. HTLV‐II is increasingly associated with rare forms of lymphocytic neoplasia and a neurodegenerative disorder, characterized by hyperspasticity and ataxia. We have used PCR to amplify, clone and sequence 140 bp of the pol gene from many isolates of HTLV‐IIA and HTLV‐IIB from around the world. Analysis of these and other published sequences established that all HTLV‐IIA sequences contained a unique Hinf I site and all HTLV‐IIB sequences a unique Mse I site. A rapid and specific oligomer restriction (OR) assay was developed utilizing the primer pair SK110/SK111 and subsequent digestion with these enzymes. Concordance between sequenced and OR‐based subtyping of DNA amplified by PCR was absolute among 22 HTLV‐II isolates tested.Further OR or sequence analyses on an additional 30 other isolates indicated that the majority of North American non‐indian HTLV‐II isolates were subtype A, while all Paleo‐Amerindian samples, including those from the Seminole of Florida; the Guaymi from Panama; and the Toba, Chorote, Wichi, and Chulupe of Argentina, belonged to subtype B. The SK110/SK111 PCR‐OR format should facilitate molecular epidemiology studies of HTLV‐II infection and allow for subtype stratification in assessing the sensitivity and specificity of HTLV detection formats and HTLV‐II disease association. © 1995 Wiley‐Liss, inc.
Clinical recurrence of hepatitis A following liver transplantation for acute liver failure
Authors: Gane Edward , Sallie Richard , Saleh Mohammed , Portmann Bernard , Williams Roger 
Published: March 2007

AbstractThis paper documents clinically significant recurrence of hepatitis A virus (HAV) infection in a 63‐year‐old man transplanted for HAV‐related acute liver failure. HAV RNA was documented in the explant and, following early clearance from the blood and graft, was again detected in postoperative biopsies at the time of an acute hepatic illness. Although the clinical and biochemical abnormalities resolved completely, the patient had a second episode of graft dysfunction 6 months later and investigations revealed hepatitis C virus (HCV)‐related chronic active hepatitis consistent with acquired HCV infection at the time of transplantation. The possible interaction with hepatitis A may have delayed the appearance of hepatitis C. Administration of HAV immunoglobulin at the time of transplantation should be considered in all cases of HAV‐related fulminant hepatic failure. © 1995 Wiley‐Liss, Inc.