bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evolution rate of hepatitis delta virus RNA isolated in Taiwan
Authors: Chao You‐Chen , Tang Hung‐Shang , Hsu Chung‐Te 
Published: March 2007

AbstractThe complete RNA sequences of hepatitis delta viruses (HDV) isolated at 3 years apart from a chronic delta hepatitis patient in Taiwan were determined. The sequence analysis showed an overall evolution rate of 3.18 × 10−3 substitutions/nucleotide/year. The evolution rates in different parts of HDV RNA varied. The hypervariable region evolved faster (4.55 × 10−3 substi‐tutions/nucleotide/year) than the hepatitis delta antigen (HDAg)‐coding region (2.60 × 10−3 substitutions/nucleotide/year) and the autocata‐lytic region (1.11 × 10−3 substitutions/nucleotide/ year). These data are compatible with the previous finding that the hypervariable region is more divergent than the HDAg‐coding region and the au‐tocatalytic regions among the HDV isolates from different geographic areas. No substitution was found in the four previously identified conserved domains of HDV RNA, further confirming their functional importance in viral replication. The evolution rate of this HDV RNA is higher than that determined from the partial RNA sequences of two Japanese HDV isolates and similar to that found in a Lebanon isolate. Further, it was found that this HDV RNA retained the same microheterogeneities at 15 nucleotide positions detected in the RNA 3 years earlier. It is concluded that HDV RNA in patients' serum is extremely heterogeneous, and that the nucleotide substitutions in certain nucleotide positions likely have conferred evolutionary advantages for HDV. Viral sequence evolution is a possible mechanism for chronic HDV infection. © 1994 Wiley‐Liss, Inc.
Racial differences in the seroprevalence of hepatitis A virus infection in Natal/KwaZulu, South Africa
Authors: Sathar M. A. , Soni P. N. , Fernandes‐Costa F. J. T. D. , Wittenberg D. F. , Simjee A. E. 
Published: March 2007

AbstractThe age‐ and race‐specific seroprevalence of hepatitis A virus (HAV) infection was determined by radioimmunoassay (RIA) in 786 subjects between the ages of 6 months to 60 years. More than 50% of African children were seropositive by the age of 5 years. In blood donors (17–60 years), 50% (93/187) of Whites, 67% (110/163) of Indians, 85% (117/137) of Coloureds, and 91% (115/127) of Africans were seropositive. There was a significant difference in the seroprevalence of HAV infection between White blood donors and blood donors from the other three racial groups [Coloureds (P < 0.0001), Africans (P < 0.0001), and Indians (P < 0.001)] and between Indians and Coloureds (P < 0.0001) and Indians and Africans (P < 0.0001). There was no significance difference in HAV infection between Coloureds and Africans (P < 0.200). Eighty‐seven per cent (32/37) of rural Africans had previous infection. In the African population HAV infection is acquired in childhood. There are significant racial differences in the seroprevalence of HAV infection. The surveillance of HAV infection may be used as a valuable yardstick to monitor the changing standards of hygiene and socioeconomic conditions of a community in transition in South Africa and to make rational public health decisions regarding a hepatitis A vaccination policy. © 1994 Wiley‐Liss, Inc.
Hepatitis C virus infections in transplant patients: Serological and virological investigations
Authors: Maple P. A. C. , McKee T. , Desselberger U. , Wreghitt T. G. 
Published: March 2007

AbstractHepatitis C virus (HCV) is transmitted by organs of HCV antibody‐positive donors to transplant recipients. This study investigated the serological and virological responses of 14 initially HCV antibody‐negative transplant patients who received organs from four HCV antibody‐positive donors (A‐D) (before donor screening for HCV infection was introduced in 1991). Second generation HCV enzyme immunoassay (Abbott HCV EIA) was used to detect anti‐HCV antibody. Re‐combinant immunoblot (RIBA‐2; Chiron Corporation) and Wellcozyme Western blot (Wwb) assays were compared as confirmatory assays of positive EIA results. Reverse transcription (RT) followed by “nested” polymerase chain reaction (PCR) was performed to detect viral RNA. HCV RNA was only found in the sera of donors B and C, however, transplantation of organs from all donors resulted in infection of all recipients.HCV RNA was found in recipient sera within 30 days after transplant and remained detectable throughout the period of sampling. An anti‐HCV antibody response was found in only 6 (of the 14) recipients and only after 300 days. Much longer periods passed before detection of HCV antibody in six recipients. For detection of HCV infection in transplant recipients it is essential that testing for HCV RNA by RT‐PCR is carried out. © 1994 Wiley‐Liss, Inc.
Sequence conservation of the major outer capsid glycoprotein of human group C rotaviruses
Authors: Grice Alexander S. , Lambden Paul R. , Caul E. Owen , Clarke Ian N. 
Published: March 2007

AbstractSeveral outbreaks of Group C rotavirus infection have occurred in the United Kingdom, in one instance infection was associated with the death of a 4‐month‐old infant in the Bristol area. The origin of human group C rotavirus is unknown although there has been some speculation that porcine species may be a possible source of human infection. Direct reverse transcription‐polymerase chain reaction sequencing of VP7 genes from two UK outbreaks (Bristol and Preston) and sequence analysis from a sporadic case of infection from Brazil (Belém) showed that each of these genes was identical in size (1,063 bp) and has revealed a surprising level (97.8–99.8%) of gene sequence conservation. Sequence comparisons with an isolate from Japan imply that the human group C rotaviruses so far characterised originate from a recent common ancestor with a worldwide distribution. © 1994 Wiley‐Liss, Inc.
Application of commercial assays to detect IgG antibodies to hepatitis C virus in urine: A pilot study from autopsy cases
Authors: Zhang Xiang , Constantine Niel T. , Li Ling , Abdel‐Hamid M. , Bansal Jaya , Smialek John E. 
Published: March 2007

AbstractHepatitis C virus (HCV), the main cause of non‐A, non‐B hepatitis in the United States and possibly in the world, is believed to be transmitted primarily through parenteral exposure. Many screening and supplemental tests are available to detect antibodies to HCV in serum. The ability to use commercial assays to detect antibodies to HCV in urine was investigated in this study. A total of 229 serum/urine matched samples were collected sequentially from forensic autopsy cases examined at the Office of the Chief Medical Examiner, State of Maryland. Testing was performed using the Ortho, Innogenetics, and Abbott second generation HCV screening tests and the INNO‐LIA HCV Ab supplemental assay. Sample volumes were increased for urine testing. Forty‐six of 229 serum samples were positive by screening and confirmed by supplemental tests. The urine samples produced positive results on 44–45 of the same 46 by screening tests and all 46 positives by the supplemental test. There were no false positive samples using urine when compared with the serum pairs. The one false negative sample using urine was still nonreactive when the urine volume was increased to 200 μl using the screening tests. Generally, five times the serum volume was required for the screening tests to be optimal for urine samples. The urine samples were stored under different conditions prior to testing to determine the influence on antibody stability in urine.
Viral specificity of hepatitis E virus antigens identified by fluorescent antibody assay using recombinant HEV proteins
Authors: Purdy Michael A. , Carson Dorrie , McCaustland Karen A. , Bradley Daniel W. , Beach Michael J. , Krawczynski Kris 
Published: March 2007

AbstractA fluorescent antibody (FA) assay for hepatitis E virus antigen (HEVAg) in infected liver tissue was used to confirm the presence of virus‐specific antigens in hepatocytes during the course of infection. With the cloning of the HEV genome it is now possible to determine which viral antigens are recognized by this FA assay. Recombinant HEV proteins covering the carboxyl half of HEV open reading frame 2 (ORF2) were used in this study to demonstrate that some of the most immunoreactive virus‐specific antigens detected by FA are contained within this region of ORF2 (nucleotides 6169–7126).
Evaluation of commercially available assays for antibodies to HIV‐1 in serum obtained from South African patients infected with HIV‐1 subtypes B, C, and D
Authors: Engelbrecht Susan , de Jager Gerrit J. , van Rensburg Estrelita J. 
Published: March 2007

AbstractBetween 1984 and 1990, virus was routinely isolated and serum collected from patients diagnosed at hospitals in the Western Cape as suffering from AIDS or AIDS‐related conditions (ARC). From these, 17 virus strains were selected at random for sequencing and molecular characterisation of the env gene. The strains were previously characterised as belonging to HIV‐1 subtypes B, C and D. The purpose of the present study was to evaluate retrospectively the serological diagnosis of HIV‐1 in these 17 South African patients. Thirteen anti‐HIV screening assays, including 7 rapid/simple test devices (RTDs), 4 enzyme‐linked immunosorbent assays (ElAs) and 2 Western immunoblot assays were evaluated. Using commercial ElAs, 16 serum samples were HIV antibody‐positive and these results were confirmed by Western immunoblot analysis. Serum from one terminal AIDS patient was found negative with all the serological tests. Some RTDs gave false negative antibody reactions on specimens from patients infected with subtype D strains. To investigate the false negative antibody reactions, the polymerase chain reaction (PCR) was used to amplify, clone and sequence proviral DNA from the immunodominant gp41 region from 7 of the HIV‐1 strains. Two patients, both subtype D strains (D214 and D482) with false negative results in the RTDs, showed a significant amino acid substitution, i.e., substitution of a histidine residue for leucine at env position 607. It was concluded that although there were false negative RTD reactions on patients with HIV‐1 subtype D strains, the commercial ElAs tested are sensitive and are able to detect patients infected with HIV‐1 subtypes B, C and D that are present in South Africa. © 1994 Wiley‐Liss, Inc.
Human rotavirus subgroups and serotypes in children with acute gastroenteritis in Saudi Arabia from 1988 to 1992
Authors: Mohammed Khalid A. , Assouli Sufian M. El , Banjar Zainy M. 
Published: March 2007

AbstractRotavirus infection was detected in 524 (42.2%) of the 1,242 stool specimens collected from infants and young children with acute gastroenteritis admitted to a major pediatric hospital in Jeddah, Saudi Arabia, between March 1988 and December 1992. Enzyme‐linked immunosorbent assay (ELISA) and monoclonal antibodies specific for subgroup I and II were used to examine 80 rotavirus positive specimens. Subgroup I was detected in 21 (26.3%) and subgroup II in 49 (61.3%) specimens. Six specimens reacted with both subgroup I and II monoclonal antibodies and four specimens were untypeable. Serotyp‐ing of 355 rotavirus positive specimens using monoclonal antibodies specific for the human rotavirus serotypes 1 to 4 revealed a distribution profile of serotype 1, 53.5%; serotype 2, 6.8%; serotype 3, 5.9%; and serotype 4, 22.8%, along with mixed and untypeable specimens (11%). When the correlation between subgroup and serotype specificities was examined in 62 specimens, all subgroup I specimens were found to be serotype 2 or untypeable and all subgroup II specimens belonged predominantly to serotypes 1 (54.7%) and 4 (9.4%). Serotype 1, followed by, to a lesser extent, serotype 4, exhibited a temporal predominance in the 5‐year investigation. A significant clustering of the various serotypes during the cooler months was evident almost throughout the study, particularly in 1989 and 1990. © 1994 Wiley‐Liss, Inc.
Hepatitis C virus and its genotypes in patients suffering from chronic hepatitis C with or without a cryoglobulinemia‐related syndrome
Authors: Willems M. , Sheng L. , Roskams T. , Ramdani B. , Doutrelepont J. M. , Nevens F. , Durez P. , Treille S. , Adler M. , Desmet V. , Fevery J. , Yap S. H. 
Published: March 2007

AbstractRecently, evidence has been presented for a possible association between hepatitis C virus (HCV) infection and essential mixed cryoglobulinemia (EMC). Eleven consecutive patients with EMC and two with cryoglobulinemia type I were examined for the presence of markers of HCV infection. Eleven of 13 patients (10 with EMC and 1 with type I cryoglobulinemia) had anti‐HCV antibodies (as determined by a second generation anti‐HCV assay) and HCV‐RNA in plasma or serum. HCV‐RNA was also detected in liver biopsies of five patients.Genotyping showed that HCV genotype 1 was found in 10 of 11 patients with HCV‐RNA (9 genotype 1b and 1 genotype 1a) and only one patient had HCV genotype 2. However, a similar high prevalence of genotype 1b (100%) was found in a group of 14 consecutive patients with chronic hepatitis C, who had no clinical evidence of cryoglobulinemia. Concomitant infection was present in three patients with genotypes 2, 3 and 4, respectively.These findings stress the high prevalence of HCV infection in patients with EMC and further study shows that a difference in genotype prevalence was not found between HCV‐related EMC and chronic hepatitis C without clinical manifestations of EMC. © 1994 Wiley‐Liss, Inc.
Genotyping of hepatitis C virus isolates by a modified polymerase chain reaction assay using type specific primers: Epidemiological applications
Authors: Widell Anders , Shev Steven , Månsson Siv , Zhang Yong‐Yuan , Foberg Ulla , Norkrans Gunnar , Frydén Aril , Weiland Ola , Kurkus Jan , Nordenfelt Erik 
Published: March 2007

AbstractA polymerase chain reaction (PCR)‐based assay using primers against the hepatitis C core gene has been described [Okamoto et al. (1992a): Journal of General Virology 73:673–679]. Within the two major HCV genotypes 1 and 2, the Okamoto system identifies two subtypes each (1a,1 b and 2a, 2b, respectively). Typing is achieved by a primary PCR with consensus primers followed by a nested PCR with type specific primers. The original assay was modified by addition of a parallel second PCR identifying the recently described major genotype 3. The assay also identifies in duplicate subtype 1 b (type II by Okamoto), suggested to respond poorly to interferon. Reaction conditions were reviewed and melting temperatures of all typing primers equalised to increase stringency.The modified system functioned well and typing results were supported by partial core sequencing. The following distribution of genotypes was found in 53 hepatitis C virus (HCV) infected Swedish blood donors: genotype 1a (57%), 3 (19%), 1b (13%), and 2b (11%). In six recipients of HCV infected blood identified in a retrospective study, the recipient HCV genotype was identical to donor HCV genotype. Furthermore, in HCV positive couples identical genotype was observed when only one partner had an external risk factor; whereas genotypes were often diverse if both sex partners had parenteral risk factors. Finally, a cluster of hepatitis C cases in a haemodialysis unit was evaluated retrospectively. Eight patients had genotype 1b, two had mixed 1a and 1b, and one had type 1a.The modified HCV genotyping assay was of value in examining different epidemiological situations and can be expanded presumably to include future genotypes. © 1994 Wiley‐Liss, inc.
Use of the colonic carcinoma cell line CaCo‐2 for in vivo amplification and detection of enteric viruses
Authors: Pintó Rosa M. , Diez José M. , Bosch Albert 
Published: March 2007

AbstractThe use of the continuous cell line CaCo‐2 as an in vivo amplification system for the detection of fastidious human enteric viruses is reported. CaCo‐2 cells showed an increased sensitivity to laboratory strains of group A rotavirus 3, reovi‐rus3, astrovirus 1, poliovirus 1, coxsackievirus A 24, enterovirus 70, and adenovirus 5, 40 and 41, when compared to a routine host cell line for each virus. Nucleic acids from wild‐type infectious rotavirus, astrovirus, and adenovirus 40 in stool samples of patients with acute gastroenteritis could be amplified after infection of CaCo‐2 cells with trypsin‐pretreated virus inoc‐ula. Virus diagnosis was carried out subsequently by dot‐blot hybridisation with specific cDNA probes. An amplification factor between 10 and 1,000x was obtained by infection of CaCo‐2 cells, thus enabling specific detection of low numbers of a wide range of enteric viruses, and the differentiation between infectious and noninfectious particles. © 1994 Wiley‐Liss, inc.
Mixed cryoglobulinemia type II in chronic hepatitis B associated with HBe‐minus HBV mutant: Cellular immune reactions and response to interferon treatment
Authors: Löhr Hanns , Goergen Bernd , Weber Wolfgang , Godderz Werner , zum Büschenfelde Karl‐Hermann Meyer , Gerken Guido 
Published: March 2007

AbstractThe case of a young female patient with chronic active hepatitis B, vasculitic purpura, edema, and circulating immune complexes due to mixed Cryoglobulinemia is described. Serum transami‐nases were elevated. Serological assays showed hepatitis B surface antigen (HBsAg), antibody to hepatitis B e antigen (anti‐HBe), and antibody to hepatitis B core antigen (anti‐HBc) antibodies but no antibody to hepatitis C virus (anti‐HCV) or antibody to hepatitis delta virus (anti‐HDV) antibodies. Using hepatitis B virus‐polymerase chain reaction (HBV‐PCR) and direct sequencing a precore/core (preC/C) mutant unable to synthesize HBeAg was detected in serum. HBV antigens were demonstrated in the circulating immune complexes. Following 1 month of treatment with interferon‐a 2b 3 miu three times weekly, alanine aminotransferases returned to normal levels while cryoglobulins and immune complexes disappeared from serum. In addition, 2 months after the onset of treatment serum HBV‐DNA was no longer detectable by PCR.Prior to treatment the analysis of cellular immune reactions of peripheral blood mononu‐clear cells showed a major proliferative response to HBcAg, preS1Ag and HBxAg and a minor response to HBeAg and HBsAg. One month after conclusion of treatment a decline in T‐cell reactivity against all HBV antigens was observed. During clinical response to the therapy, however, a strong proliferative response of T cells to HBcAg and HBeAg was demonstrated.In conclusion, immune complex disease may complicate chronic hepatitis B in patients expressing HBe‐minus HBV mutants. Treatment with interferon‐a was found to be effective in mixed Cryoglobulinemia even in the presence of HBe‐minus HBV mutants. Antiviral effects of interferon‐a induce a decrease in specific T‐cell recognition of HBV antigens. Clinical response and virus elimination were, however, accompanied by a reconstitution of cellular immune responses to HBV core antigens, i.e., HBcAg and HBeAg. The response to certain T cell epitopes on these antigens may be of pathogenetic relevance for virus elimination. © 1994 Wiley‐Liss, Inc.
Nucleotide sequence of the core region of hepatitis C virus in Pakistan and Bangladesh and the geographic characterisation of hepatitis C virus in South Asia
Authors: Ohno Tomoyoshi , Mizokami Masashi , Tibbs Christopher J. , Nouri‐Aria Kayhan T. , Wu Rong‐Rong , Ohba Ken‐Ichi , Orito Etsuro , Suzuki Kaoru , Mizoguchi Naoto , Nakano Tatsunori , Khan Mobin , Yano Michitani , Kiyosawa Kendo , Williams Roger 
Published: March 2007

AbstractA large number of complete and partial hepatitis C virus (HCV) sequences have been reported and classified into several genotypes, although none have been reported from South Asia. We have determined and evaluated partial sequences in the core region of HCV obtained from patients with chronic hepatitis in Pakistan and Bangladesh. Nucleotide sequences from these viruses show significant homology with the Japanese HCV‐TR isolate (91.7%–97.9%) and low homology with other Japanese, American, and UK isolates including HCV‐1, HC‐J4, HC‐J6, HC‐J8, and E‐b1 (79.3%–86.2%). The homologies of their deduced amino acids sequence with HCV‐1, HC‐J4, HC‐J6, HC‐J8, E‐b1, and HCV‐TR were 84.3%–89.8%, 85.0–87.9%, 84.1%–86.9%, 84.3%–87.0%, 90.2%–93.1%, and 89.8%–93.5%, respectively. These results suggest that our clones might be classified into the same genotype as HCV‐TR. Further analysis using molecular evolutionary methods strongly supported the classification of these sequences with the HCV‐TR genotype. Moreover, we could not detect any isolates which were closely related to our clones or HCV‐TR in countries outside the South Asian area. These data further support the association of HCV genotypes with distinct geographic regions. © 1994 Wiley‐Liss, Inc.
Elimination of hepatitis delta virus infection after loss of hepatitis B surface antigen in patients with chronic delta hepatitis
Authors: Battegay Manuel , Simpson Lisa H. , Hoofnagle Jay H. , Sallie Richard , di Bisceglie Adrian M. 
Published: March 2007

AbstractThe aim of this study was to evaluate whether patients with chronic hepatitis delta virus (HDV) infection treated with alpha interferon and subsequent loss of hepatitis B surface antigen (HBsAg) eliminate HDV. HDV RNA was detected in 26 of 28 patients with chronic delta hepatitis using the polymerase chain reaction. Seventeen patients in whom HDV RNA was detected were treated with alpha interferon; in 65%, HDV RNA remained detectable during treatment or reappeared after stopping therapy whereas in three patients HDV RNA remained absent (17.5%). HDV RNA became and remained undetectable in serum and liver of two of these three patients who lost HBsAg from serum and in one patient who was intermittently HBsAg negative during therapy. After loss of HBsAg, hepatitis B virus (HBV) DNA was still detectable in the liver, but not HBV RNA, indicating absent or very low HBV replication. Three patients were lost to follow up (17.5%). Two nontreated patients with chronic HDV infection also lost HBsAg during follow up; HDV RNA also became undetectable in their serum. Thus, HDV replication does not persist after the loss of HBsAg. Clearance of HBsAg may be a useful guide to when therapy can be stopped. © 1994 Wiley‐Liss, Inc.
Viral load as a determinant for transmission of human papillomavirus type 16 from mother to child
Authors: Kaye Jeremy N. , Cason John , Pakarian Farzin B. , Jewers Richard J. , Kell Barbara , Bible Jon , Raju Kankipati S. , Best Jennifer M. 
Published: March 2007

AbstractWhilst genital papillomaviruses are commonly believed to be sexually transmitted, transmission of human papillomavirus type 16 (HPV‐16) from mother to child at delivery has been described previously [Pakarian et al. (in press) British Journal of Obstetrics and Gynaecology]. In order to determine whether viral load in cervical/vaginal cells was an important determinant of transmission 15 pregnant women with HPV‐16 infections were studied. Eight of these women had infants who were positive for HPV‐16 DNA at genital and/or buccal sites. Viral load was estimated by laser densitometry of polymerase chain reaction (PCR) products. The eight mothers—four with a previous history of abnormal smears and two with previous genital warts— who transmitted infection to their infants had significantly higher viral loads (P < 0.05) than those who did not. It is concluded that viral load is an important, but not the sole, determinant for the transmission of HPV‐16 from mother to infant. © 1994 Wiley‐Liss, Inc.