bluuebunny/crossref_metadata_2025_split huggingface dataset:
Doyen–Wilson theorem for nested Steiner triple systems
Authors: Wang Jinhua , Shen Hao 
Published: July 2004

AbstractThe obvious necessary conditions for the existence of a nested Steiner triple system of order v containing a nested subsystem of order w are v ≥ 3w + 4 and v ≡ w ≡ 1 (mod 6). We show that these conditions are also sufficient. © 2004 Wiley Periodicals, Inc.
Persistent infection of SARS coronavirus in colonic cells in vitro
Authors: Chan Paul K.S. , To Ka‐Fai , Lo Anthony W.I. , Cheung Jo L.K. , Chu Ida , Au Florence W.L. , Tong Joanna H.M. , Tam John S. , Sung Joseph J.Y. , Ng Ho‐Keung 
Published: July 2004

AbstractSevere acute respiratory syndrome coronavirus (SARS‐CoV) can produce gastrointestinal symptoms. The intestinal tract is the only extrapulmonary site where viable viruses have been detected. This study examined seven established human intestinal cell lines, DLD‐1, HCT‐116, HT‐29, LoVo, LS‐180, SW‐480 and SW‐620, for their permissiveness to SARS‐CoV infection. The results showed that only LoVo cells were permissive to SARS‐CoV infection as evident by positive findings from indirect immunofluorescence staining for intracellular viral antigens, in situ hybridization for intracellular viral RNA, and electron microscopy for intracellular viral particles. In contrast to Vero cells, SARS‐CoV did not produce cytopathic effects on LoVo cells. However, LoVo cells were found to be highly permissive for productive infection with a high viral titre (>3 × 107 viral copies/ml) produced in culture supernatant following a few days of incubation. SARS‐CoV established a stable persistent chronic infection that could be maintained after multiple passages. Being a cell line of human origin, LoVo cells could be a useful in vitro model for studying the biology and persistent infection of SARS‐CoV. Our results on the expression of angiotensin‐converting enzyme 2 (ACE2), a recently identified cellular receptor for SARS‐CoV, in these cell lines indicated that it might not be the sole determinant for cells to be susceptible to SARS‐CoV infection. J. Med. Virol. 74:1–7, 2004. © 2004 Wiley‐Liss, Inc.
Resistance profiles observed in virological failures after 24 weeks of amprenavir/ritonavir containing regimen in protease inhibitor experienced patients
Authors: Marcelin Anne‐Geneviève , Affolabi Dissou , Lamotte Claire , Mohand Hocine Ait , Delaugerre Constance , Wirden Marc , Voujon Delphine , Bossi Philippe , Ktorza Nadine , Bricaire François , Costagliola Dominique , Katlama Christine , Peytavin Gilles , Calvez Vincent ,   the Genophar Study Group
Published: July 2004

AbstractAmprenavir (APV) is an HIV protease inhibitor (PI) used for the treatment of either naive or PI‐experienced HIV‐infected patients. Several genotypic resistance pathways in protease gene have been described to be associated to unboosted APV failure (I50V, V32I + I47V, I54L/M, or less commonly I84V, which may be accompanied by one ore more accessory mutations such as L10F, L33F, M46I/L). The aims of this study were to investigate the efficacy up to week 24 of an APV plus ritonavir containing regimen in PI experienced patients and to determine the genotypic resistance profiles emerging in patients failing to this therapy. Forty‐nine, PI experienced but APV naïve patients were treated with APV (600 mg bid) plus ritonavir (100 mg bid). By intent‐to‐treat analysis, the median decrease in viral load (VL) was −1.32 log10 (min +0.6; max −2.8) and −1.46 log10 (min +0.5; max −2.8) 12 and 24 weeks after initiating APV plus ritonavir regimen, respectively. Twelve patients harboured a VL >200 copies/ml at week 24. Among these patients, the selection of mutations previously described with the use of APV as first PI (V32I, L33F, M46I/L, I50V, 54M/L, and I84V) was observed. However, in some cases, mutations classically described after the use of other PIs (V82F and L90M) were selected but always with APV‐specific mutations. There was no relation between the resistance pathways selected with either APV or ritonavir plasma minimal concentration, but higher APV plasma minimal concentration were associated with a lower rate of resistance mutations selection. J. Med. Virol. 74:16–20, 2004. © 2004 Wiley‐Liss, Inc.
Evolution of genotypic and phenotypic resistance to Enfuvirtide in HIV‐infected patients experiencing prolonged virologic failure
Authors: Poveda Eva , Rodés Berta , Labernardière Jean‐Louis , Benito José Miguel , Toro Carlos , González‐Lahoz Juan , Faudon Jean‐Louis , Clavel François , Schapiro Jonathan , Soriano Vincent 
Published: July 2004

AbstractFour heavily antiretroviral‐experienced HIV‐infected patients had significant plasma HIV‐RNA reductions (>1 log) after beginning an Enfuvirtide (ENF)‐based rescue regimen. However, all had viral rebound shortly thereafter, sustaining high levels of plasma viremia over 80 weeks. These patients developed rapidly genotypic and phenotypic resistance to ENF. Mutations within the HR1 env region were selected (N43D in three and G36V/D in one), resulting in high‐level phenotypic resistance to ENF. Interestingly, two patients had a sustained CD4+ T‐cell increase and two maintained stable CD4+ T‐cell counts despite virologic failure under ENF. The possible mechanisms involved in this response were examined. Changes in virus tropism from R5 to R5/X4 were observed in two patients, in parallel with increases in ENF phenotypic resistance. Low levels of T‐cell activation, T‐cell turnover, and cytotoxic T lymphocyte (CTL) activity were found in all four patients. An overall increase in the proportion of viruses released from cells of the macrophage lineage was observed. In summary, single mutations at the HR1 env region result in significant loss of susceptibility to ENF. Despite virologic failure, these patients may maintain elevated CD4+ counts through a reduction in their overall immune activation. J. Med. Virol. 74:21–28, 2004. © 2004 Wiley‐Liss, Inc.
Consumption of uncooked deer meat as a risk factor for hepatitis E virus infection: An age‐ and sex‐matched case‐control study
Authors: Tei Shuchin , Kitajima Naoto , Ohara Shunji , Inoue Yoshifumi , Miki Masaharu , Yamatani Toshiyuki , Yamabe Hiroshi , Mishiro Shunji , Kinoshita Yoshikazu 
Published: July 2004

AbstractIt was reported previously food‐borne transmission of hepatitis E virus (HEV) to humans from deer meat. The present study attempted to clarify whether eating uncooked deer meat is a major epidemiological risk factor for HEV infection in Kasai, a city in western Japan. In total, 45 volunteer subjects with experience of eating raw deer meat were enrolled. An equivalent number of people from the same area who had never eaten raw deer meat served as controls. The subjects and controls had comparable age and sex distributions. Serum anti‐HEV IgG and anti‐hepatitis A virus (HAV) IgG levels were measured in all 90 volunteers. There was no significant difference in age, overseas travel history, or rate of anti‐HAV antibody positivity between the subjects and controls. Eight (17.7%) of the subjects but only one (2.2%) of the controls had measurable serum anti‐HEV IgG levels (P = 0.014). Anti‐HAV prevalence did not differ between the anti‐HEV‐positive and negative groups. The results suggest that eating uncooked deer meat is an epidemiological risk factor for HEV infection in the studied area. In countries such as Japan where deer meat is sometimes eaten raw, attention must be paid to this route of HEV infection. J. Med. Virol. 74:67–70, 2004. © 2004 Wiley‐Liss, Inc.
Assessment of CMV load in solid organ transplant recipients by pp65 antigenemia and real‐time quantitative DNA PCR assay: Correlation with pp67 RNA detection
Authors: Mengoli Carlo , Cusinato Riccardo , Biasolo Maria A. , Cesaro Simone , Parolin Cristina , Palù Giorgio 
Published: July 2004

AbstractAfter bone marrow (BM) or solid‐organ (SO) transplantation viremic Cytomegalovirus (CMV) infection is observed frequently. Quantitative assay of CMV in blood helps the management of this clinical condition. In the present report, 83 samples from 39 solid organ recipients, three CMV assays were compared simultaneously for the first time: the Nuclisens CMV pp67 assay (nucleic acid sequence‐based amplification, NASBA), an “in‐house” quantitative real‐time PCR assay (TaqMan) for CMV DNA, and pp65 antigenemia. The relation between CMV DNA and pp65 antigenemia, the quantitative assays, was evaluated on a larger group including 251 blood samples from 118 solid organ recipients. Real‐time PCR provided the best results; ≥130 CMV DNA copies/2 × 105 peripheral blood leukocytes (PBLs) predicted ≥1 pp65 antigen positive (Ag+) cell/2 × 105 PBLs. By taking pp65 antigenemia as the “gold standard,” the sensitivity of CMV DNA quantitation and of the pp67 RNA assay were 0.95 and 0.20, respectively, while the corresponding specificity values were 0.50 and 0.93. When real‐time PCR was considered as the “gold standard,” the sensitivity and specificity of the pp65 antigenemia were 0.65 and 0.91, respectively. Among the three tests examined, the sensitivity of the pp67 RNA assay was the lowest. On the other hand, the pp67 RNA assay was highly specific and effective in pinpointing high viremia patients. The present report, by providing predictive values for all three diagnostic profiles, DNA load, antigenemia, and pp67RNA, is a contribution for validation of real‐time PCR as a new standard for quantitative assessment of CMV viremia in clinical settings. J. Med. Virol. 74:78–84, 2004. © 2004 Wiley‐Liss, Inc.
Molecular markers of clonality and identity in epstein–barr virus‐associated B‐cell lymphoproliferative disease
Authors: Walling Dennis M. , Andritsos Leslie A. , Etienne Wiguins , Payne Deborah A. , Aronson Judith F. , Flaitz Catherine M. , Nichols C. Mark 
Published: July 2004

AbstractEpstein–Barr virus (EBV)‐associated B‐cell lymphoproliferative disease may be polyclonal, oligoclonal, or monoclonal. The degree of tumor clonality reflects the disease pathogenesis and may have implications for disease diagnosis, prognosis, and treatment. In this study, specimens of EBV‐associated B‐cell lymphoproliferative disease obtained from immunocompromised hosts were analyzed for molecular markers of cellular and virologic clonality and virologic identity. Each tumor specimen was assessed for immunoglobulin gene JH region rearrangement, the structure of the EBV genome termini, and the EBV genotype(s) present using a new EBV genotyping assay based upon LMP‐1 gene sequence variation. The results of the JH rearrangement and EBV termini assays were generally concordant in their assessment of tumor specimen clonality, and both assays contributed to establishing clonal identity between different tumor specimens. The EBV genotyping assay did not significantly contribute to the assessment of tumor clonality but did established clear virologic identity between different tumor specimens obtained from the same individual. In one individual, these three assays together characterized a multi‐focal, monoclonal tumor that may have arisen through clonal selection after sequential infections with two different EBV genotypes. In summary, the JH rearrangement and EBV termini assays each provided different but complementary information on tumor clonality, while the EBV genotyping assay proved most useful for establishing virologic identity among tumors. Utilization of these three assays together may provide new insight into the pathogenesis of EBV‐associated B‐cell lymphoproliferative disease. J. Med. Virol. 74:94–101, 2004. © 2004 Wiley‐Liss, Inc.
Prevalence and distribution of HSV‐1, VZV, and HHV‐6 in human cranial nerve nuclei III, IV, VI, VII, and XII
Authors: Theil Diethilde , Horn Anja KE , Derfuss Tobias , Strupp Michael , Arbusow Viktor , Brandt Thomas 
Published: July 2004

AbstractThe etiology of idiopathic cranial nerve palsies often remains unresolved. It has been hypothesised that viral reactivation of herpesviruses in the corresponding nuclei in the brainstem is the cause. We investigated the distribution of herpes simplex virus type 1 (HSV‐1) and varicella zoster virus (VZV) in nuclei that are associated with peripheral sensory ganglia [oculomotor (nIII), facial (nVII) nuclei] and in nuclei that are not associated with peripheral sensory ganglia [trochlear (nIV), abducens (nVI), and hypoglossal (nXII) nuclei] of five human brainstems. Samples of the cranial nerve nuclei and adjacent control tissue were taken from histological sections after precise identification of every single nucleus and control tissue. DNA and RNA amplification methods were used to determine the prevalence and distribution of HSV‐1 and VZV. The distribution of human herpes virus type 6 (HHV‐6) was also determined and served as a control, since HHV‐6 infection has never been associated with idiopathic cranial nerve palsies. HSV‐1 was distributed at random in all cranial nerve nuclei and control tissue, whereas VZV DNA was not detected in any of the samples examined. Surprisingly, HHV‐6 was present in almost all samples where HSV‐1 was also present, however, the latency associated transcript (LAT) of HSV‐1 was not found in any of the samples positive for HSV‐1 DNA. The absence of LAT in the samples positive for HSV‐1 and the distribution of HSV‐1 and HHV‐6 do not support the hypothesis that idiopathic cranial nerve palsies result from viral reactivation in the brainstem nuclei. J. Med. Virol. 74:102–106, 2004. © 2004 Wiley‐Liss, Inc.
New point of care test is highly specific but less sensitive for influenza virus A and B in children and adults
Authors: Rawlinson William D. , Waliuzzaman Zubair M. , Fennell Michael , Appleman James R. , Shimasaki Craig D. , Carter Ian W. 
Published: July 2004

AbstractThe importance of rapid diagnosis of influenza has increased with the availability of neuraminidase inhibitors, which need to be commenced within 48 hr of symptom onset. Furthermore, the recent development of influenza‐like clinical syndromes with novel aetiologies (severe acute respiratory syndrome, SARS) has increased the need for rapid and accurate near‐patient diagnosis. A new, modified point of care (POC) diagnostic test (ZstatFlu) was assessed on 469 nasopharyngeal aspirates (NPAs) and 260 nose/throat swabs (TS) taken from children and adults. The test was specific (77–98%) for all specimen types for influenza virus A and B, depending upon incubation conditions. However, it was less sensitive, detecting 65–77% of specimens confirmed as positive on culture, direct immunofluorescence or PCR testing. A positive test is useful, for both directing initiation of therapy in the clinician's office, and making a positive diagnosis of influenza in patients with influenza‐like clinical syndromes. J. Med. Virol. 74:127–131, 2004. © 2004 Wiley‐Liss, Inc.
Genetic diversity of influenza B virus: The frequent reassortment and cocirculation of the genetically distinct reassortant viruses in a community
Authors: Matsuzaki Yoko , Sugawara Kanetsu , Takashita Emi , Muraki Yasushi , Hongo Seiji , Katsushima Noriko , Mizuta Katsumi , Nishimura Hidekazu 
Published: July 2004

AbstractTo characterize the genetic diversity of influenza B viruses isolated during one influenza season, the antigenic and genetic relationships among 20 strains of influenza B virus isolated in February and March 2001 at one pediatric clinic in Yamagata City, Japan, were investigated. The HA gene and seven other gene segments were phylogenetically divided into three distinct sublineages (Harbin/7/94‐, Tokyo/6/98‐, and Shiga/T30/98‐related lineage) of the Yamagata/16/88‐like lineage. The NS genes of the viruses belonging to the Harbin/7/94‐related lineage have additional three nucleotides at positions 439–447, and were phylogenetically distinguishable from those of the currently circulating Yamagata/16/88‐ and Victoria/2/87‐like lineages, but were closely related to that of the Yamagata/16/88‐like lineage isolated before 1994. Moreover, four strains of influenza B virus isolated in the same community between 2002 and 2003 were further examined. Phylogenetic analysis revealed that a virus of Victoria/2/87‐like lineage isolated in 2003 had acquired the NA, NS, M, and PA gene segments from a Shiga/T30/98‐like virus, and two strains of Harbin/7/94‐related lineage had acquired the various gene segments from Shiga/T30/98‐like virus through a reassortment event. These results indicate that genetically distinct multiple viruses can combine to cause an influenza B epidemic in a community and that the frequent reassortment among these viruses plays a role in generating the genetic diversity of influenza B viruses. J. Med. Virol. 74:132–140, 2004. © 2004 Wiley‐Liss, Inc.
Antigenic characterisation of influenza B virus with A new microneutralisation assay: Comparison to haemagglutination and sequence analysis
Authors: Ansaldi Filippo , Bacilieri Sabrina , Amicizia Daniela , Valle Laura , Banfi Federica , Durando Paolo , Sticchi Laura , Gasparini Roberto , Icardi Giancarlo , Crovari Pietro 
Published: July 2004

AbstractAlthough the haemagglutination inhibition assay is considered the “gold standard” for antigenic characterisation of influenza viruses, some limitations of this technique are well known. A new microneutralisation assay, as a tool for antigenic characterisation of influenza B viruses, has been standardised and its performance evaluated in comparison with the haemagglutination inhibition test in the light of molecular characterisation of the haemagglutinin. Twelve B viruses belonging to the two lineages and the four sub‐lineages discriminated by phylogenetic analysis of HA were tested. The microneutralisation assay clearly distinguishes viruses belonging to different lineages and, in addition, discriminates strains belonging to different sub‐lineages that are poorly or not discriminated using the haemagglutination inhibition test. This new microneutralisation assay could provide a useful tool for antigenic characterisation of circulating influenza viruses and contribute, together with the haemagglutination inhibition test and sequence analysis of the haemagglutinin and neuraminidase, in the choice of the strain for use in vaccine composition. J. Med. Virol. 74:141–146, 2004. © 2004 Wiley‐Liss, Inc.
Circulating cytokines and chemokines in acute symptomatic parvovirus B19 infection: Negative association between levels of pro‐inflammatory cytokines and development of B19‐associated arthritis
Authors: Kerr Jonathan R. , Cunniffe Victoria S. , Kelleher Peter , Coats Andrew J.S. , Mattey Derek L. 
Published: July 2004

AbstractThe aim of the study was to characterise the profile and clinical correlates (arthritis, rash, and fatigue) of cytokines, chemokines, and other mediators in symptomatic acute parvovirus B19 infection. Serum was examined from cases of acute B19 infection (as defined by serum anti‐B19 IgM positivity) (n = 84), and in normal persons (n = 43) for B19 markers (serum B19 antibodies and DNA), rheumatoid factor (RF), and antinuclear antibody (ANA). A panel of cytokines/chemokines was measured in duplicate using the Bioplex Protein Array system (BioRad Hemel Hempstead, UK). These included interleukin‐1β (IL‐1β), IL‐4, IL‐5, IL‐6, IL‐8, IL‐13, tumor necrosis factor‐α (TNF‐α), interferon‐γ (IFN‐γ), macrophage chemoattractant protein‐1 (MCP‐1), granulocyte‐monocyte colony stimulating factor (GM‐CSF), transforming growth factor‐β1 (TGF‐β1), endothelin‐1 (ET‐1), and neopterin. Acute symptomatic infection was characterised by specific IgG positivity (83%), serum B19 DNA positivity (96%), and raised levels of IL‐4, IL‐6, IL‐8, TNF‐α, IFN‐γ, MCP‐1, GM‐CSF, TGF‐β1, and ET‐1. Patients with acute B19‐associated arthritis were found to have lower levels of IL‐6, TNF‐α, and GM‐CSF than patients without arthritis, while those with rash had lower levels of TGF‐β1. It is concluded that cytokine levels following acute symptomatic infection with parvovirus B19 indicate a state of immune activation. The profile of circulating mediators may provide insights into the possible pathogenesis of particular clinical manifestations of this infection. J. Med. Virol. 74:147–155, 2004. © 2004 Wiley‐Liss, Inc.
Genetic diversity of respiratory syncytial virus isolated during an epidemic period from children of northeastern Brazil
Authors: Moura Fernanda Edna Araújo , Blanc Andrea , Frabasile Sandra , Delfraro Adriana , de Sierra María José , Tome Lorena , Gonçalves Ramos Eduardo Antônio , Siqueira Marilda Mendonça , Arbiza Juan 
Published: July 2004

AbstractOutbreaks of human respiratory syncytial virus (HRSV) are the leading cause of serious acute lower respiratory viral disease in many countries in different continents. Data on clinical and epidemiological aspects of HRSV infections in this country have been reported, but there is lack of data regarding the molecular epidemiology of this virus in Salvador. The genetic variability of HRSV isolated during an outbreak in Salvador, Brazil (1999) has been analysed. Partial sequences of the G protein gene of 13 isolates from antigenic group A and 4 isolates from antigenic group B of HRSV were determined. Nucleotide sequences of C‐terminal G gene were compared to sequences of HRSV isolates from countries of South America and from the rest of the world available at the GenBank. Brazilian group A and B isolates were clustered into previously characterised genotypes: GA5, GA2, GA7, and GB3, SAB3, respectively. This is the first study of GA7 and SAB3 genotypes circulation in South American countries. It is interesting to point out that viruses isolated in Salvador appear to be closer related with those from Montevideo‐Uruguay and Buenos Aires, Argentina strains, suggesting circulation of similar strains among different South American countries in different seasons. Moreover, viruses closely related genetically circulated in the same year in Salvador and distant places such as Mozambique, supporting the previous suggestion on the complexity of HRSV strain circulation patterns, and the high capability of HRSV spreading world‐wide. J. Med. Virol. 74:156–160, 2004. © 2004 Wiley‐Liss, Inc.
Nosocomial outbreak of respiratory syncytial virus subgroup B variants with the 60 nucleotides‐duplicated G protein gene
Authors: Nagai Kazushige , Kamasaki Hotaka , Kuroiwa Yuki , Okita Lisa , Tsutsumi Hiroyuki 
Published: July 2004

AbstractIn January 2001, 20 children among 40 residents under 2 years old at a nursery home in Sapporo, Japan had respiratory symptoms and were confirmed as having respiratory syncytial virus (RSV) infection by a conventional diagnostic kit. Nasopharyngeal aspirates were collected from four RSV‐positive patients and total RNA was extracted directly from the specimens for the analysis of RSV grouping and genotyping. All four RSV strains had the same G protein gene sequence of subgroup B and were assigned to identical strains. Interestingly, the G protein gene had a duplication of 60 nucleotides at the C‐terminal third of the G protein gene in which three nucleotides differed each other. The predicted polypeptide is lengthened by 20 amino acids. The clinical picture of these cases was not different from those of patients with other RSV strains. These novel mutations were thought to be introduced in vivo. J. Med. Virol. 74:161–165, 2004. © 2004 Wiley‐Liss, Inc.