bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monitoring the response to antiretroviral therapy in HIV‐1 group O infected patients using two new RT‐PCR assays
Authors: de Mendoza Carmen , Lu Wei , Machuca Ana , Sainz María , Castilla Jesús , Soriano Vincent 
Published: August 2002

AbstractFailure to recognise infection caused by human immunodeficiency virus type 1 (HIV‐1) group O variants has been described using both serological and genetic procedures. Moreover, monitoring the response to antiretroviral therapy is a difficult task in patients infected with HIV‐1 group O since commercial tests are not available so far for the quantitation of this virus. In this study, the virological response to antiretroviral therapy were assessed in five HIV‐1 group O‐infected patients living in Spain by using two new and different RT‐PCR methods (MUPROVAMA and LCx). Twenty‐four plasma samples belonging to these five patients were selected. As reference, p24 antigenaemia levels and CD4+ cell counts were used. All samples yielded positive viral load values using MUPROVAMA (range: 138 to 595,500 HIV‐RNA copies/ml) and 23 of 24 using LCx (range: < 178 to 98,356 HIV‐RNA copies/ml). Overall, the results obtained using both assays showed a good correlation among themselves, and in respect to p24 antigenaemia and CD4+ cell counts. However, the values provided by LCx were significantly lower (0.33 logs on average) than those provided by MUPROVAMA. In conclusion, both the highly sensitive MUPROVAMA and LCx Quantitative assays might represent an useful tool for guiding the decision on when start treatment and for monitoring the response to antiretroviral therapy in HIV‐1 group O‐infected patients. J. Med. Virol. 64:217–222, 2001. © 2001 Wiley‐Liss, Inc.
Human immunodeficiency virus‐1 specific and natural cellular immunity in HIV seronegative subjects with multiple sexual exposures to virus
Authors: Nicastri Emanuele , Ercoli Lucia , Sarmati Loredana , d'Ettorre Gabriella , Iudicone Paola , Massetti Paola , Vullo Vincenzo , Andreoni Massimo 
Published: August 2002

AbstractThe probability of HIV infection by sexual contact, although it varies greatly, appears to be lower than that of infection by other routes of exposure. The aim of this study was to evaluate immunological determinants involved in protection against HIV infection in subjects with multiple and repeated sexual exposures to the virus. Twenty‐two subjects were studied for CD8+ cell anti‐HIV suppression activity and serum neutralizing activity against the HIV strain of their own partners, β‐chemokine production, and natural killer cell activity. CD8+ cell anti‐HIV activity and neutralizing activity of sera were found in 13 (76%) and 12 (70.5%) out of 17 HIV‐1 negative subjects, respectively. Six individuals had a relevant immune response against HIV: three subjects with a high CD8+ cell antiviral suppression activity and three individuals with sera neutralizing activity titer >1:10. These last three subjects had the highest β‐chemokine levels, a very prolonged period of multiple sexual intercourse (>6 years) and a seropositive partner with a high viral load. A partial reduction of neutralizing activity titer was observed when pre‐incubating the sera with anti‐β‐chemokine neutralizing antibodies. A spontaneous natural killer cell activity was suppressed in the majority of HIV‐1 negative subjects with sexual exposure in comparison with normal individuals. The protection from sexual HIV transmission appears to be the result of a network of different humoral and cellular factors. J. Med. Virol. 64:232–237, 2001. © 2001 Wiley‐Liss, Inc.
Quantitative analysis of specific Th1/Th2 helper cell responses and IgG subtype antibodies in interferon‐α‐treated patients with chronic hepatitis C
Authors: Hempel Gerd , Galle Peter R. , Löhr Hanns F. 
Published: August 2002

AbstractThis study aimed to characterise the immune mechanisms relevant to viral clearance in interferon (IFN)‐α‐treated chronic hepatitis C virus (HCV) infection. Proliferative responses of peripheral blood mononuclear cells from sustained complete IFN‐α therapy responders (n = 8), nonresponders (n = 13), untreated patients (n = 10), and healthy controls (n = 5) were measured retrospectively upon stimulation with recombinant HCV‐antigens (core, helicase, NS3, NS4, and NS5) and the secretion of IFN‐γ and interleukins (IL‐4, IL‐5, IL‐10, and IL‐12) were tested by ELISA. Furthermore, IFN‐γ as well as IL‐10 secreting CD4+ T cells were quantitated by intracellular cytokine staining. Anti‐HCV core and NS3‐specific IgG subclass antibodies were quantitated in the corresponding patient sera. Sustained therapy responders had more frequent and stronger NS3 and helicase‐specific cellular immune responses than nonresponders, untreated HCV patients and healthy controls. Independent from therapy outcome HCV‐stimulated T cells in IFN‐α treated patients secreted preferentially IFN‐γ The Th2 cytokines IL‐4 and IL‐10 were even decreased in nonresponders, while the IL‐12 secretion was not influenced. With respect to the humoral immune response sustained complete responders showed significantly reduced IFN‐γ independent anti‐HCV‐core and ‐NS3 IgG1 antibody synthesis. In conclusion, vigorous NS3‐specific T‐helper cell responses were associated with viral clearance in IFN‐α recipients; however, the cytokine and antibody analysis argues against a Th1/Th2 imbalance as a major factor that influence the therapy outcome. J. Med. Virol. 64:340–349, 2001. © 2001 Wiley‐Liss, Inc.
Analysis of the relationship between immunogenicity and immunity for viral subunit vaccines
Authors: Wilson J.N. , Nokes D.J. , Dimmock N.J. 
Published: August 2002

AbstractThe prevention of viral infection by vaccination relies on stimulating an appropriate immune response in order to reduce the probability with which a virus can establish an infection. Post‐vaccination antibody responses have therefore been associated with reducing the probability with which an individual can be infected (i.e., the vaccine's “impact”). Quantifying this relationship is essential in evaluating new vaccines, especially since comparisons between vaccines, and vaccine licensure, may be dependent on antibody responses alone. In this paper two principal questions are identified which need to be addressed in the evaluation of subunit vaccines: i) how do specific antibody levels relate to complete protection from infection or disease and ii) how do antigenic subunits interact in developing protection when combined together in a single vaccine. The aim is to identify explicitly certain assumptions that are frequently made implicitly in the discussion of vaccine action. First, antibody levels are related to levels of protection through a novel statistical analysis of incidence data from a published hepatitis B vaccine trial. The antibody response observed after influenza A virus infection is discussed in relation to the selection of neutralisation escape variants. Finally, by way of example, a theoretical situation is examined and three simple models of subunit vaccine action are constructed in order to describe how antibody levels may be related to population level phenomena such as the elimination of an infection by mass vaccination. J. Med. Virol. 64:560–568, 2001. © 2001 Wiley‐Liss, Inc.
Low cell dosage of lymphoblastoid human cell lines EBV+ is associated to chronic hepatitis in a minority of inoculated nu/nu mice
Authors: Bertolini Luisa , Iacovacci Silvia , Bosman Cesare , Carloni Guido , Monaco Vincenzo , Bangrazi Caterina , Serafino Annalucia , Gualandi Giampiero , Prantera Giorgio , Fruscalzo Alberto 
Published: August 2002

AbstractIt has been suggested that an atypical course of primary infection by EBV and the reactivation of EBV infection in transplanted patients may induce hepatitis. We explored the possibility to dissect the infectious activity from the ability to promote B lymphocyte proliferation in vivo by injecting in nu/nu mice a low number (2 × 106–0.05 × 106) of cells from CE a normal human bone marrow–derived B cell line. This line carries an endogenous EBV in episomal and linear forms. Twenty nu/nu mice were inoculated subcutaneously with the B cell line CE and a matched group with the cell line RAG obtained by EBV in vitro infection of normal human peripheral blood. The mice injected with the CE line did not develop a lymphoproliferative disease, but 5 of them displayed typical histopathological lesions of chronic hepatitis without involvement of other organs. Similar results were obtained in 2 out of 20 animals in the RAG group. A close association between liver lesions and a previous EBV infection, by putative circulating B lymphoblastoid cells releasing their EBV, was established by PCR and by in situ hybridization with BamHI “W” DNA probe. This latter probe detected the presence of about 15% of positive cells only in affected livers. In addition, the rare detection in some hepatocytes of “A” type Cowdry bodies would suggest the occurrence of continuous EBV replication although at a very low level. These data show that we succeeded in dissecting the infectious from the proliferative activity of the endogenous EBV carrier CE cell line. This provides in addition a promising model for chronic EBV‐associated hepatitis. J. Med. Virol. 66:70–81, 2002. © 2002 Wiley‐Liss, Inc.
Early acquisition of TT virus in infants: Possible minor role of maternal transmission
Authors: Lin Ho‐Hsiung , Kao Jia‐Horng , Lee Ping‐Ing , Chen Ding‐Shinn 
Published: August 2002

AbstractThis study assessed the prevalence of TT virus (TTV) viremia in pregnant women and evaluated the role of maternal transmission in early acquisition of TTV in infants in Taiwan. Two groups of pregnant women were screened for TTV using polymerase chain reaction. The first group included 135 healthy pregnant women attending the obstetrics department for routine prenatal care and the second group from 25 GB virus‐C/hepatitis G virus (GBV‐C/HGV)‐infected mothers. In both groups, when TTV infection was found in mothers, serial serum samples were collected for the infants at regular intervals until 1 year of age and were tested for TTV DNA. The results showed that 40% (54/135) of the women undergoing routine prenatal care and 56% (14/25) of GBV‐C/HGV‐infected pregnant women were positive for TTV DNA (P = 0.137). Of the 54 TTV‐infected mothers in the routine prenatal group, 29 and their 30 infants received regular follow‐up. The positive rate of TTV DNA in infants was 40% (12/30) in the routine prenatal group and 29% (4/14) in the group with GBV‐C/HGV‐infected mothers (P = 0.463). All but 2 of the 16 TTV‐infected infants had normal serum alanine aminotransferase levels during follow‐up. The phylogenetic analysis in 7 mother‐infant pairs showed that the homology was diverse in each pair and a close genetic relatedness was found in 2 mother‐infant pairs. In conclusion, TTV viremia is common in pregnant Taiwanese women and their infants. However, the results suggest that maternal transmission may play only a minor role in early acquisition of TTV in infants. J. Med. Virol. 66:285–290, 2002. © 2002 Wiley‐Liss, Inc.
Factors predictive of response to interferon‐α therapy in hepatitis C virus type 1b infection
Authors: Yeh Byung‐Il , Han Kwang‐Hyub , Lee Hyean‐Woo , Sohn Joon Hyung , Ryu Wang‐Shick , Yoon Do‐Jun , Yoon Joonho , Kim Hyun‐Won , Kong In Deok , Chang Sei Jin , Choi Jong‐Whan 
Published: August 2002

AbstractInterferon‐α (IFN‐α) has been used to treat hepatitis C Virus (HCV)‐induced infection but has been effective in only about half of all patients. It is suggested that the different responses to IFN‐α treatment in HCV infection may be influenced by HCV genotypes, HCV RNA titer at the beginning of IFN‐α therapy, and the sequences of the interferon sensitivity determining region (ISDR). However, there have also been reports showing that these have no relation to an IFN‐α effect. In a previous study, it was found that the nucleotide sequence variation in the hypervariable region (HVR) 1 of the HCV could predict the effect of IFN‐α. In the present investigation, an attempt was made to determine the predictive factors of IFN‐α therapy. Twenty‐six patients with HCV infection were treated with IFN‐α. Among these, 13 patients recovered after 3 to 6 months of IFN‐α treatment, although the other 13 patients showed no response after 6 months of treatment with IFN‐α. In order to determine the predictive factors of IFN‐α therapy, the ALT levels, HCV genotypes, HCV serum titer, and the quasispecies of HVR 1 were compared between responders and non‐responders. It is suggested that the variation in the HVR 1 and HCV serum titer can be used to predict the effect of IFN‐α. J. Med. Virol. 66:481–187, 2002. © 2002 Wiley‐Liss, Inc.
Comparative analysis of two coxsackievirus B3 strains: Putative influence of virus‐receptor interactions on pathogenesis
Authors: Selinka H.‐C. , Wolde A. , Pasch A. , Klingel K. , Schnorr J.‐J. , Küpper J.‐H. , Lindberg A.M. , Kandolf R. 
Published: August 2002

AbstractStrain‐specific differences in the interaction of coxsackievirus B3 (CVB3) with the coxsackievirus‐adenovirus receptor (CAR) and the decay‐accelerating factor (DAF) co‐receptor proteins were investigated using a non‐haemagglutinating (CVB3) and a haemagglutinating (CVB3‐HA) strain of CVB3. A panel of receptor‐transfected hamster CHO cells, expressing either CAR (CHOCAR cells), DAF (CHODAF cells), or both receptor proteins (CHODC cells) were used to study the interplay of CAR and DAF receptor molecules with regard to binding and infection with CVB3 and CVB3‐HA. Despite clear differences in their binding phenotypes, both virus strains were found to primarily depend on the CAR receptor protein for initialization of productive infections. Cytopathic effects induced by CVB3‐HA were influenced by co‐expression of DAF receptor proteins. The cardiotropic potential of both virus strains was investigated in A.BY/SnJ mice. Despite comparable virus replication of both CVB3 strains in individual myocytes, the number of infected heart muscle cells was significantly lower in CVB3‐HA infected mice. Infections of pancreata correlated with myocardial infections. Together these data suggest that even small differences in virus‐receptor interactions, influencing virus binding and virus spread, may have an impact on the pathogenesis of CVB‐induced diseases. J. Med. Virol. 67:224–233, 2002. © 2002 Wiley‐Liss, Inc.
New TLM nodes with PML absorbing boundary conditions for the characterization of axially symmetric antennas
Authors: Le Maguer S. 
Published: August 2002

AbstractAn efficient TLM algorithm for investigating body of revolution antennas is presented. This method requires a 2D‐mesh since azimuthal dependence of fields is known and introduced in the TLM scheme. Three major TLM nodes are presented (SCN (14 Voltages), HSCN (11 Voltages) and HHSCN (10 Voltages)) including their respective PML schemes (absorbing boundary conditions). For some cases, this method is found to be more attractive in terms of computer cost than the FDTD equivalent approach (BoR‐FDTD). Finally, the results found via antenna applications show the accuracy of the method. Copyright © 2001 John Wiley & Sons, Ltd.
Fast modelling of deeply and fully etched gratings based on the Bloch–Floquet theorem
Authors: Giorgio Agostino , Gina Perri Anna , Nicola Armenise Mario 
Published: August 2002

AbstractA model of deeply and fully etched gratings (also identified as one‐dimensional waveguide photonic bandgap structures), based on the Bloch–Floquet theorem, has been developed to perform a complete analysis of the electromagnetic (e.m.) wave propagation in the structure, assumed of finite extension, i.e. to determine mode propagation constants, electromagnetic field harmonics and total field distribution, transmission and reflection coefficients, total forward and backward power flow in the structure, guided power and total losses.Comparisons with other accurate numerical methods confirm the accuracy of the new one, whose main advantages are the quickness and the possibility to determine a great amount of information and figures of merit in a few seconds (for each operating wavelength). Moreover, the model allows the designer a complete view of the physical and geometrical device features, so it permits to draw design rules for optimization of photonic bandgap (PBG) waveguide device design. Copyright © 2001 John Wiley & Sons, Ltd.
Contact with astroglial membranes induces axonal and dendritic growth of human CNS model neurons and affects the distribution of the growth‐associated proteins MAP1B and GAP43
Authors: Piontek Jörg , Régnier‐Vigouroux Anne , Brandt Roland 
Published: August 2002

AbstractThe development of morphological complexity of CNS neurons is thought to be regulated by extracellular factors and cellular contact. To analyze the role of contact with astroglia in this process and to determine the intraneuronal mechanisms involved, an in vitro system was developed where terminally differentiated and polar human CNS model neurons (NT2‐N neurons) were cultured on a layer of mouse astrocytes or isolated membrane fractions in chemically defined medium. Morphometric analysis revealed that physical contact with living astrocytes increased the lengths of axonal and dendritic processes and lead to an increased number of branch points. Contact with astrocytes also resulted in a redistribution of the growth‐associated proteins MAP1b and GAP‐43 toward the growth cones of NT2‐N neurons. Astrocyte‐contact did not lead to a maturation of the neurons as would be detected by an increased expression of tau isoforms containing the adult‐specific exons 2 and 3. Culture on immobilized membrane fractions prepared from astrocytes also increased the morphological complexity of the neurons in a qualitatively similar manner. The results indicate that physical contact with astrocyte membranes increases the morphological complexity of CNS model neurons through a mechanism that involves a redistribution of growth‐associated proteins to neuronal growth cones. NT2‐N neurons may provide a useful cellular model to analyze cytoskeletal mechanisms during the development of terminally differentiated and polar human neurons. © 2002 Wiley‐Liss, Inc.
Preferential initiation of PC12 neurites in directions of changing substrate adhesivity
Authors: Murnane Aeneas C. , Brown Kimberly , Keith Charles H. 
Published: August 2002

AbstractWhen PC12 cells are grown on substrates showing a gradient of nonspecific adhesion, they preferentially initiate neurites in directions of changing adhesivity, whether that change is in the direction of increasing or decreasing adhesivity. This preference for changing adhesivity is ablated both byC. difficiletoxin A, which inhibits all Rho‐family GTPases, and byC. botulinumC3 exoenzyme, which specifically inhibits Rho. © 2002 Wiley‐Liss, Inc.
Overexpression of S100β in transgenic mice does not protect from serotonergic denervation induced by 5,7‐dihydroxytryptamine
Authors: Bendotti C. , Cole S.E. , Gobbi M. , Hohmann C. , Reeves R.H. 
Published: August 2002

AbstractTransgenic mice overexpressing S100β were used to examine whether the chronic elevation of this protein alters the response to selective partial serotonergic lesions produced by bilateral intracerebroventricular injections of 5,7‐dihydroxytryptamine (5,7‐DHT). Basal levels of S100β mRNA examined by in situ hybridization were two‐ to threefold higher throughout the brain in transgenic than in control mice, whereas 5‐HT levels in forebrain were similar in both. After the 5,7‐DHT‐induced lesions, no differences were found in the S100β mRNA levels in either normal or transgenic mice. At 5 and 60 days after the lesion, forebrain 5‐HT levels were reduced by 56% and 35%, respectively, in control mice and by 51% and 35%, respectively, in the transgenic mice. Analysis of the 5‐HT immunostaining showed a marked decrease of the immunoreactivity in various brain regions, which was comparable at the two intervals postlesion. One exception was the medial hypothalamus, where an almost complete disappearance of 5‐HT immunoreactivity was observed in the medial region at 5 days after lesion, followed by a marked reinnervation 60 days later. These hypothalamic changes were seen in both controls and S100β‐overexpressing transgenic mice. Quantitative analysis of the density of 5‐HT transporter sites using [3H]citalopram binding, a marker of serotonergic terminals, showed a marked decrease in different brain regions at both 5 and 60 days after 5,7‐DHT injections. No difference in basal and postlesion levels of [3H]citalopram binding was seen between transgenic and control mice. In conclusion, this study demonstrates that constitutive overexpression of S100β in transgenic mice does not modify serotonin levels during development, nor does it protect the serotonergic neurons from selective neurotoxicity or modify the serotonergic sprouting induced by partial lesion. © 2002 Wiley‐Liss, Inc.
Chronic treatment with glutaric acid induces partial tolerance to excitotoxicity in neuronal cultures from chick embryo telencephalons
Authors: Kölker Stefan , Okun Jürgen G. , Ahlemeyer Barbara , Wyse Angela T.S. , Hörster Friederike , Wajner Moacir , Kohlmüller Dirk , Mayatepek Ertan , Krieglstein Josef , Hoffmann Georg F. 
Published: August 2002

AbstractGlutaryl‐CoA dehydrogenase deficiency (GDD) is characterized biochemically by an accumulation of glutaric (GA) and 3‐hydroxyglutaric (3‐OH‐GA) acids and clinically by the development of acute striatal degeneration. 3‐OH‐GA was recently shown to induce neuronal damage via N‐methyl‐D‐aspartate (NMDA) receptors. The pathogenetic role of GA, however, remains unclear. We demonstrate that GA exerts a dual action in cultured chick embryo neurons. Short‐term incubation with millimolar concentrations of GA induces a weak neuronal damage, adding to 3‐OH‐GA neurotoxicity. In contrast, chronic treatment with subtoxic, micromolar concentrations of GA results in partial tolerance to 3‐OH‐GA‐ and NMDA‐induced cell damage. A downregulation of NMDA receptors, in particular of the NR2B subunit, is critically involved in this GA‐induced effect, resulting in a reduced Ca2+ increase and generation of reactive oxygen species after acute exposure to NMDA or 3‐OH‐GA. Furthermore, GA decreases Na+/K+‐ATPase activity, which is prevented by glutathione, suggesting a modulation of NMDA receptor function via resting membrane potential and Na+‐dependent glutamate transport. In contrast, GA does not inhibit mitochondrial respiratory chain and β‐oxidation of fatty acids, virtually excluding an activation of NMDA receptors secondary to ATP depletion. These results strongly suggest that GA modulates the NMDA receptor‐mediated neurotoxicity of 3‐OH‐GA, providing an explanatory basis for the non‐linear relationship between organic acid concentrations and disease progression in GDD patients. Furthermore, GA‐induced downregulation of NMDA receptors might be involved in the delayed cerebral maturation of GDD patients, resulting in frontotemporal atrophy and a reduced opercularization, which are common neuroradiological findings in GDD patients. © 2002 Wiley‐Liss, Inc.