bluuebunny/crossref_metadata_2025_split huggingface dataset:
Genetic variability and phylogeny of the high‐risk HPV‐31, ‐33, ‐35, ‐52, and ‐58 in central Brazil
Authors: Raiol Tainá , Wyant Patrícia Soares , de Amorim Regina Maria Santos , Cerqueira Daniela Marreco , Milanezi Natália von Gal , Brígido Marcelo de Macedo , Sichero Laura , Martins Cláudia Renata Fernandes 
Published: February 2009

AbstractMore than 100 HPV types have been described, 13 of which are classified as high‐risk due to their association with the development of cervical cancer. The intratype genomic diversity of HPV‐16 and ‐18 has been studied extensively, while little data have been generated for other less common high‐risk types. The present study explores the nucleotide variability and phylogeny of the high‐risk HPV‐31, ‐33, ‐35, ‐52, and ‐58, in samples from Central Brazil. For this purpose, the LCR and the E6 and L1 genes were sequenced. Several variants of these HPV types were detected, some of which have been detected in other parts of the world. Furthermore, new variants of all types examined were characterized in a total of 13 new variants. Based on the E6 and L1 sequences, variants were described comprising conservative and non‐conservative amino acid changes. For phylogenetic tree construction, samples characterized in this study were compared to others described and submitted to GenBank previously. The phylogenetic analysis of HPV‐31, ‐33, ‐35, and ‐58 isolates did not reveal ethnic or geographical clustering as observed previously for HPV‐16 and ‐18. HPV‐35 analysis showed a dichotomic branching characteristic of viral subtypes. Interestingly, four clusters relative to the analysis of HPV‐52 isolates were identified, two of which could be classified as Asian and European branches. The genomic characterization of HPV variants is crucial for understanding the intrinsic geographical relatedness and biological differences of these viruses and contributes further to studies on their infectivity and pathogenicity. J. Med. Virol. 81:685–692, 2009 © 2009 Wiley‐Liss, Inc.
High prevalence of non‐B HIV‐1 subtypes in seamen and their sexual partners in Croatia
Authors: Ramirez‐Piedad Martha Kathleen , Lepej Snježana Židovec , Yerly Sabine , Begovac Josip 
Published: February 2009

AbstractTravel influences the spread of non‐B subtypes of HIV in Europe. The aim of this study was to assess whether the spread of non‐B subtypes occurred in Croatia, a country with a low level HIV infection. Phylogenetic analysis of the reverse transcriptase and protease genes was undertaken in 145 Croatian patients with the following risks for HIV‐infection: men who have sex with men (n = 64), heterosexual contact (n = 54), intravenous drug use (n = 21), bisexual contact (n = 4) and intravenous drug use plus heterosexual exposure (n = 2). The sample included 25 seamen and 13 steady female sexual partners of seamen. Overall, 38 (26%) of HIV‐patients were infected with non‐B subtypes. Non‐B subtype infections were found only in patients with a possible heterosexual exposure. Non‐B infections were most frequent in seamen and their regular female partners (in 27 of 38 seamen and their partners, 71%). The relative distribution of non‐B subtypes was as follows: A, 8%; C, 26%; F, 3%; CRF01_AE, 8%; CRF02_AG, 34%; CRF05_DF, 5%; CRF06_cpx, 3%; CRF10_CD 8%; and subtype U, 5%. There were altogether 19 heterosexual couples, phylogenetic analysis confirmed that the paired samples were related in all cases. Non‐B subtypes were found only in individuals with a heterosexual risk, mainly in seamen and their partners. J. Med. Virol. 81:573–577, 2009 © 2009 Wiley‐Liss, Inc.
Seroepidemiology of hepatitis A among Greek children indicates that the virus is still prevalent: Implications for universal vaccination
Authors: Kyrka A. , Tragiannidis A. , Cassimos D. , Pantelaki K. , Tzoufi M. , Mavrokosta M. , Pedeli X. , Athanassiadou F. , Hatzimichael A. , Konstantopoulos A. , Kafetzis D. , Papaevangelou V. 
Published: February 2009

AbstractA national cross‐sectional seroprevalence survey was conducted in order to evaluate the current seroepidemiology of hepatitis A among 1,383 children, aged 0–14 years, residing in Greece. Stratification of the study population was conducted according to age and area of residence. Sera from study participants were tested for the presence of anti‐HAV IgG antibodies. Immigrant children, as well as children residing in rural areas, had lower immunization rates. Among unvaccinated children, the seroprevalence rate of anti‐HAV was 17.1%. Nationality was shown to have a marginally significant effect since non‐immunized immigrant children had a higher seroprevalence rate (22.4% vs. 15.9%, OR = 1.52, P = 0.064). Significant differences between geographic areas for both vaccination coverage and natural immunity were observed. The study findings indicate that hepatitis A is prevalent in Greece and therefore universal infant hepatitis A immunization should be implemented. J. Med. Virol. 81:582–587, 2009 © 2009 Wiley‐Liss, Inc.
Detection of HPV types and neutralizing antibodies in Gansu province, China
Authors: Wu Xueling , Zhang Chuntao , Feng Shuxian , Liu Chunyu , Li Yanqin , Yang Yongxiu , Gao Jun , Li Hongfang , Meng Shufang , Li Liping , Zhang Yunzhong , Hu Xuemei , Wu Xiaolu , Lin Lin , Li Xun , Wang Youchun 
Published: February 2009

AbstractA total of 82 samples from patients with cervical cancer (Group 1) and 50 samples from patients with other genital diseases (Group 2) were collected in Gansu, China. All 132 samples were tested for HPV DNA with a typing kit that can detect 21 types of HPV, and also tested for neutralizing antibodies against HPV‐16, ‐18, ‐58, ‐45, ‐6, and ‐11 using pseudovirus‐based neutralization assays. The results revealed that 28% (23/82) of sera in Group 1 were positive for type‐specific neutralizing antibodies with a titer range of 160–640, of which 23.2% (19/82), 2.4% (2/82), 2.4% (2/82), 1.2% (1/82), and 1.2% (1/82) were against HPV‐16, ‐58, ‐6, ‐18, and ‐45, respectively. Only one serum (2%) in Group 2 was positive for neutralizing antibodies, which were against HPV‐6 with a titer of 2,560. Overall, 85.4% (70/82) of samples in Group 1 were HPV DNA‐positive, compared with 28% (14/50) of samples in Group 2. The seven most common types detected in Group 1 were HPV‐16 (80%), HPV‐52 (7.1%), HPV‐66 and HPV‐11 (5.7% each), and HPV‐58, HPV‐18, and HPV‐33 (4.3% each), while the four most common types in Group 2 were HPV‐16 (12%), HPV‐52 and HPV‐11 (6% each), and HPV‐68 (4%). The concordance between HPV DNA and corresponding neutralizing antibodies was 32.9% (27/82) with a significant difference (P < 0.005). More specifically, the concordance was 42.7% (35/82) for HPV‐16 in Group 1. The full‐length sequences of six HPV types (HPV‐16, ‐58, ‐33, ‐59, ‐11, and ‐68) were determined and showed 99% identities with their reported genomes. J. Med. Virol. 81:693–702, 2009 © 2009 Wiley‐Liss, Inc.
Randomized trial of high‐dose interferon‐α‐2b combined with ribavirin in patients with chronic hepatitis C: Correlation between amino acid substitutions in the core/NS5A region and virological response to interferon therapy
Authors: Mori Nami , Imamura Michio , Kawakami Yoshiiku , Saneto Hiromi , Kawaoka Tomokazu , Takaki Shintaro , Aikata Hiroshi , Takahashi Shoichi , Chayama Kazuaki 
Published: February 2009

AbstractThe aim of this study was to compare the efficacy of high‐dose interferon (IFN)‐α‐2b with standard dose of IFN‐α‐2b in combination with ribavirin (RBV) for patients with chronic hepatitis C virus (HCV) infection, and to investigate the predictive factors associated with virological response. Two hundred Japanese patients with high HCV viral load (>100 KIU/ml) were randomized to 6 or 10 mega units (MU) of 24‐week IFN‐α‐2b with RBV. Predictive factors were investigated; including pretreatment amino acid (aa) sequences of the core region and the IFN‐sensitive determining region (ISDR). The sustained virological response rate was not different in the two groups (24% vs. 30%) but the incidence of depression was significantly higher in the 10 MU group than 6 MU group (7% vs. 0%, P = 0.02). Younger age (<60) and HCV genotype (2a/b) were significant predictors of sustained virological response. In patients infected with genotype 1b, substitutions of core aa 70 and/or 91 were predictive for non‐virological response (P < 0.001), and substitutions in the ISDR was observed frequently in virological responders. Early viral kinetics study showed that serum HCV core antigen decreased more slowly in both patients with aa 70 and/or 91 substitutions in the core and with absence of substitutions in the ISDR. In conclusion, the use of a higher dose of IFN‐α‐2b in combination with RBV did not improve virological response but resulted in higher incidence of depression. Amino acid substitutions in the core and ISDR are predictive of virological response to the therapy in patients with genotype 1b and high viral load. J. Med. Virol. 81:640–649, 2009 © 2009 Wiley‐Liss, Inc.
Phylogenetic analysis of novel G12 rotaviruses in the United States: A molecular search for the origin of a new strain
Authors: Freeman M.M. , Kerin T. , Hull J. , Teel E. , Esona M. , Parashar U. , Glass R.I. , Gentsch J.R. 
Published: February 2009

AbstractRotavirus serotype G12 was initially identified in the Philippines in 1987 and was not described again until it reemerged more than 13 years later. G12 strains were first detected in the United States in 2002 and have recently assumed a worldwide distribution. The high similarity between the sequence of the major outer capsid VP7 gene of human G12 strains and the single porcine G12 isolate raised the prospect that human strains may have arisen through reassortment with porcine strains or, alternatively, that the porcine strain originally came from humans. We sequenced portions of the remaining 10 segments of two human G12 strains (G12P[8] and G12P[6]) and a currently circulating common strain (G1P[8]) identified during the 2005–2006 surveillance season and compared the sequences with those of strains available through GenBank. By comparison, the three strains were all Wa‐like and not porcine‐like. A newly outlined classification system proposed genotypes for each gene segment based on nucleotide similarity. Using this approach, gene segments VP1–3, VP6 and NSP1–5 grouped within the same genotype, indicating that the three strains analyzed were closely related. These results suggest that the novel G12P[8] strain could have been formed by the solitary introduction of a VP7 gene into a globally common rotavirus strain, G1P[8]. Classifying rotavirus strains based only on VP7 (G) and VP4 (P) genotype potentially underestimates diversity and sequence analysis of the other segments is required to assess the complete genetic relationships between strains. J. Med. Virol. 81:736–746, 2009 © 2009 Wiley‐Liss, Inc.
Hepatitis B e antigen‐negative mutations in the precore and core promoter regions in Korean patients
Authors: Choi Jong Won , Ahn Sang Hoon , Park Jun Yong , Chang Hye Young , Kim Ja Kyung , Baatarkhuu Oidov , Kim Do Young , Han Kwang‐Hyub , Chon Chae Yoon 
Published: February 2009

AbstractMost patients with hepatitis B e antigen (HBeAg)‐negative chronic hepatitis B have variants of the hepatitis B virus (HBV) that include mutations in the precore or core promoter regions of the HBV genome. The aim of this study was to investigate the patterns of precore and core promoter mutations and their relationship to HBeAg expression in Korean patients. Four hundred seventy‐five Korean patients with chronic HBV infection between February 1995 and December 2003 were enrolled in this study. There were 236 HBeAg‐positive and 239 HBeAg‐negative patients. Blood samples were tested for HBsAg, anti‐HBs, HBeAg, hepatitis B e antibody (anti‐HBe), liver function tests, and serum HBV DNA. Mutations in the precore and core promoter regions were determined by direct sequencing. In the core promoter region, the C1740, C1753, T1762/A1764, and T1766 mutations were associated with HBeAg escape (all; P < 0.05). In the precore region, a higher frequency of the C1802, A1828, T1846, A1850, C1858, T1862, and A1896 mutations was found in HBeAg‐negative patients (all; P < 0.05). In particular, the A1896 mutation was associated with high serum levels of ALT and HBV DNA in HBeAg‐negative patients (P = 0.014 and 0.026, respectively). Mutations around the Kozak sequence (nucleotides 1809–1812) were found in 6.7% of patients and were not associated with undetectable HBeAg (P = 0.13). In Korean patients, various mutations in the precore and core promoter regions were associated with HBeAg escape and amelioration of hepatic inflammation in HBeAg‐ negative patients. Only the A1896 mutation contributed to HBeAg‐negative chronic hepatitis B. J. Med. Virol. 81:594–601, 2009 © 2009 Wiley‐Liss, Inc.
Combined therapy of interferon plus ribavirin promotes multiple adaptive solutions in hepatitis C virus
Authors: Cuevas José M. , Torres‐Puente Manuela , Jiménez‐Hernández Nuria , Bracho María A. , García‐Robles Inmaculada , Carnicer Fernando , Olmo Juan del , Ortega Enrique , González‐Candelas Fernando , Moya Andrés 
Published: February 2009

AbstractHepatitis C virus (HCV) presents several regions involved potentially in evading antiviral treatment and host immune system. Two regions, known as PKR‐BD and V3 domains, have been proposed to be involved in resistance to interferon. Additionally, hypervariable regions in the envelope E2 glycoprotein are also good candidates to participate in evasion from the immune system. In this study, we have used a cohort of 22 non‐responder patients to combined therapy (interferon alpha‐2a plus ribavirin) for which samples obtained just before initiation of therapy and after 6 or/and 12 months of treatment were available. A range of 25–100 clones per patient, genome region and time sample were obtained. The predominant amino acid sequences for each time sample and patient were determined. Next, the sequences of the PKR‐BD and V3 domains and the hypervariable regions from different time samples were compared for each patient. The highest levels of variability were detected at the three hypervariable regions of the E2 protein and, to a lower extent, at the V3 domain of the NS5A protein. However, no clear patterns of adaptation to the host immune system or to antiviral treatment were detected. In summary, although high levels of variability are correlated to viral adaptive response, antiviral treatment does not seem to promote convergent adaptive changes. Consequently, other regions must be involved in evasion strategies likely based on a combination of multiple mechanisms, in which pools of changes along the HCV genome could confer viruses the ability to overcome strong selective pressures. J. Med. Virol. 81:650–656, 2009 © 2009 Wiley‐Liss, Inc.
Primary vasculitis of the central nervous system in patients infected with HIV‐1 in the HAART era
Authors: Melica Giovanna , Brugieres Pierre , Lascaux Anne‐Sophie , Levy Yves , Lelièvre Jean‐Daniel 
Published: February 2009

AbstractAngiitis of the central nervous system (CNS) in patients infected with HIV‐1‐is often associated with concomitant infection or lymphoproliferative disease of the CNS. Four HAART naïve patients infected with HIV‐1 with severe stroke are described. Evidence of vasculitis was found by magnetic resonance angiography. Extensive investigations excluded concomitant opportunistic, lymphoproliferative or autoimmune disorders leading to the diagnosis of primary angiitis of the CNS. Despite initiation of HAART and prolonged suppression of viral replication, these patients remained severely immunosuppressed. The addition of corticosteroids led to a significant improvement of clinical symptoms. Primary angiitis of the CNS should be considered in patients with HIV and stroke. The prognosis of these patients remain poor despite HAART. These observations suggest that the vascular inflammatory process persists despite the control of viral load under HAART in patients with persistent immunosuppression. J. Med. Virol. 81:578–581, 2009 © 2009 Wiley‐Liss, Inc.
Interleukin‐4 blocks thapsigargin‐induced cell death in rat rod photoreceptors: Involvement of cAMP/PKA pathway
Authors: Adão‐Novaes Juliana , Guterres Céulem de Cássia Belem , da Silva Ana Gabriela Ledo Santos , Campello‐Costa Paula , Linden Rafael , Sholl‐Franco Alfred 
Published: February 2009

AbstractAlthough the photoreceptors cell death is the main cause of some retinopathies diseases, the mechanisms involved in this process are poorly understood. The neuroprotective effects of interleukin‐4 (IL‐4) have been shown in several tissues, including retina. We demonstrate that treatment of rat retinal explants with IL‐4 completely inhibited the thapsigargin‐induced rod photoreceptor cell death after 24 hr in culture. We also showed that IL‐4 receptor α subunit (IL‐4Rα) is abundantly present in retina. Colocalization of IL‐4Rα and rhodopsin indicate a direct effect of this cytokine in rod photoreceptor cells. Moreover, IL‐4 increased the intracellular levels of cAMP in 7.4‐fold, indicating that the neuroprotective effect of this cytokine was completely blocked by RpcAMP, an inhibitor of protein kinase (PKA). Our data demonstrate, for the first time, the neuroprotective effect of IL‐4 through cAMP/PKA pathway in thapsigargin‐induced photoreceptor cell death. © 2009 Wiley‐Liss, Inc.
Induction of GAP‐43 modulates neuroplasticity in PBSC (CD34+) implanted‐Parkinson's model
Authors: Shyu Woei‐Cherng , Li Kuo‐Wei , Peng Hsiao‐Fen , Lin Shinn‐Zong , Liu Ren‐Shyan , Wang Hsiao‐Jung , Su Ching‐Yuan , Lee Yih‐Jing , Li Hung 
Published: February 2009

AbstractAs a result of the progressive decrease in efficacy of drugs used to treat Parkinson's disease (PD) and the rapid development of motor complications, effective alternative treatments for PD are required. In a 6‐hydroxydopamine (6‐OHDA)‐induced Parkinson's rat model, intracerebral peripheral blood stem cell (CD34+) (PBSC) transplantation significantly protected dopaminergic neurons from 6‐OHDA‐induced neurotoxicity, enhanced neural repair of tyrosine hydroxylase neurons through up‐regulation of Bcl‐2, facilitated stem cell plasticity, and attenuated activation of microglia, in comparison with vehicle‐control rats. The 6‐OHDA‐lesioned hemi‐Parkinsonian rats receiving intrastriatal transplantation of PBSCs also showed: 1) enhanced glucose metabolism in the lesioned striatum and thalamus, demonstrated by [18F]fluoro‐2‐deoxyglucose positron emission tomography (FDG‐PET), 2) improved neurochemical activity as shown by proton magnetic resonance spectroscopy (1H‐MRS), and 3) significantly reduced rotational behavior in comparison with control lesioned rats. These observations might be explained by an up‐regulation of growth‐associated protein 43 (GAP‐43) expression because improvements in neurological dysfunction were blocked by injection of MK‐801 in the PBSC‐treated group. In addition, a significant increase in neurotrophic factor expression was found in the ipsilateral hemisphere of the PBSC‐treated group. In summary, this protocol may be a useful strategy for the treatment of clinical PD. © 2009 Wiley‐Liss, Inc.
Vitamin K prevents oxidative cell death by inhibiting activation of 12‐lipoxygenase in developing oligodendrocytes
Authors: Li Jianrong , Wang Hong , Rosenberg Paul A. 
Published: February 2009

AbstractOxidative mechanisms of injury are important in many neurological disorders. Developing oligodendrocytes (pre‐OLs) are particularly sensitive to oxidative stress‐mediated injury. We previously demonstrated a novel function of phylloquinone (vitamin K1) and menaquinone 4 (MK‐4; a major form of vitamin K2) in protecting pre‐OLs and immature neurons against glutathione depletion‐induced oxidative damage (Li et al. [ 2003] J. Neurosci. 23:5816–5826). Here we report that vitamin K at nanomolar concentrations prevents arachidonic acid‐induced oxidative injury to pre‐OLs through blocking the activation of 12‐lipoxygenase (12‐LOX). Arachidonic acid metabolism is a potential source for reactive oxygen species (ROS) generation during ischemia and reperfusion. Exposure of pre‐OLs to arachidonic acid resulted in oxidative cell death in a concentration‐dependent manner. Administration of vitamin K (K1 and MK‐4) completely prevented the toxicity. Consistent with our previous findings, inhibitors of 12‐LOX abolished ROS production and cell death, indicating that activation of 12‐LOX is a key event in arachidonic acid‐induced pre‐OL death. Vitamin K1 and MK‐4 significantly blocked 12‐LOX activation and prevented ROS accumulation in pre‐OLs challenged with arachidonic acid. However, vitamin K itself did not directly inhibit 12‐LOX enzymatic activity when assayed with purified 12‐LOX in vitro. These results suggest that vitamin K, or likely its metabolites, acts upstream of activation of 12‐LOX in pre‐OLs. In summary, our data indicate that vitamin K prevents oxidative cell death by blocking activation of 12‐LOX and ROS generation. © 2009 Wiley‐Liss, Inc.
Contribution of a mitochondrial pathway to excitotoxic neuronal necrosis
Authors: Seo Dae‐Won , Lopez‐Meraz Maria‐Leonor , Allen Suni , Wasterlain Claude Guy , Niquet Jerome 
Published: February 2009

AbstractIt is traditionally thought that excitotoxic necrosis is a passive mechanism that does not require the activation of a cell death program. In this study, we examined the contribution of the cytochrome c‐dependent mitochondrial death pathway to excitotoxic neuronal necrosis, induced by exposing cultured cortical neurons to 1 mM glutamate for 6 hr and blocked by the NMDA antagonist, dizocilpine. Glutamate treatment induced early cytochrome c release, followed by activation of caspase‐9 and caspase‐3. Preincubation with the caspase‐9 inhibitor z‐LEHD‐fmk, the caspase‐3 inhibitor z‐DEVD‐fmk, or the specific pan‐caspase inhibitor Q‐VD‐oph decreased the percentage of propidium iodide‐positive neurons (52.5% ± 3.1%, 39.4% ± 3.5%, 44.6% ± 3%, respectively, vs. 65% ± 3% in glutamate + vehicle). EM studies showed mitochondrial release of cytochrome c in neurons in the early stages of necrosis and cleaved caspase‐3 immunoreactivity in morphologically necrotic neurons. These results suggest that an active mechanism contributes to the demise of a subpopulation of excitotoxic necrotic neurons. © 2009 Wiley‐Liss, Inc.
Lipopolysaccharides enhance the action of bradykinin in enteric neurons via secretion of interleukin‐1β from enteric glial cells
Authors: Murakami Matsuka , Ohta Toshio , Ito Shigeo 
Published: February 2009

AbstractFunctional changes of the enteric nervous system have been observed under inflammatory states of inflammatory bowel disease increasing the endotoxin level. The aim of the present study was to determine the effect of lipopolysaccharides (LPS) on myenteric neuron–glia interaction in vitro. We examined the increase of the intracellular Ca2+ concentration ([Ca2+]i) and the release of interleukin‐1β (IL‐1β) or prostaglandin E2 (PGE2) and COX‐2 expression in myenteric plexus cells from the rat intestine induced by LPS. LPS potentiated BK‐induced [Ca2+]i increases in both myenteric neurons and enteric glial cells, which were suppressed by a B1R antagonist. Only in enteric glial cells, a B1R agonist increased [Ca2+]i. The effects of LPS were blocked by pretreatment with an interleukin‐1 receptor antagonist or by reducing the density of enteric glial cells in culture. LPS prompted the release of IL‐1β from enteric glial cells. The augmenting effects of IL‐1β on the BK‐induced neural [Ca2+]i increase and PGE2 release from enteric glial cells were abolished by a phospholipase A2 (PLA2) inhibitor and a COX inhibitor, and partly suppressed by a COX‐2 inhibitor. IL‐1β up‐regulated the COX‐2 expression in enteric glial cells. LPS promotes IL‐1β secretion from enteric glial cells, resulting in augmentation of the neural response to BK through PGE2 release via glial PLA2 and COX‐2. The alteration of the regulatory effect of glial cells may be the cause of the changes in neural function in the enteric nervous system in inflammatory bowel disease. © 2009 Wiley‐Liss, Inc.