bluuebunny/crossref_metadata_2025_split huggingface dataset:
T‐cell response to human papillomavirus type 52 L1, E6, and E7 peptides in women with transient infection, cervical intraepithelial neoplasia, and invasive cancer
Authors: Chan Paul K.S. , Liu Shih‐Jen , Cheung Jo L.K. , Cheung T.H. , Yeo Winnie , Chong Pele , Man Stephen 
Published: April 2011

AbstractThe E6 and E7 proteins encoded by human papillomaviruses (HPV) are prime targets for therapeutic vaccine development. Ninety‐five women with HPV 52 infection (33 transient infections, 17 cervical intraepithelial neoplasia grade II, 15 cervical intraepithelial neoplasia grade III, and 30 invasive cervical cancers) were examined for T‐cell responses using interferon‐γ enzyme‐linked immunospot (IFN‐γ ELISPOT) assay. Of the 29 peptides (13 L1, 10 E6, and 6 E7) screened positive by an in vitro peptide‐binding assay, 14 were positive by the IFN‐γ ELISPOT assay. Positive epitopes for HLA A11 were located at amino acid positions 103–111, 332–340, 342–350, and 373–381 of the L1 protein; and at 27–35 and 86–94 of the E6 protein; and at 1–9 and 27–35 of the E7 protein. A24‐specific epitopes included 60–68 and 98–106 of the L1 protein, 42–50 and 59–67 of the E6 protein, and 24–32 of the E7 protein. Only one epitope (99–107) of the E6 protein showed positive responses for HLA A2 subjects. Overall, T‐cell responses against L1 were observed mainly in subjects who had cleared infection; whereas responses against E6 and E7 were confined mainly to subjects who had developed cervical neoplasia. The proportion of subjects showing detectable T‐cell responses was low across all grades of cervical neoplasia suggesting that immune evasion mechanisms had set on early in the course of disease progression. This study provides the first set of T‐cell epitopes mapped for HPV 52, which can be considered for further evaluation as targets for immunotherapy. J. Med. Virol. 83:1023–1030, 2011. © 2011 Wiley‐Liss, Inc.
Prevalence, risk factors and virological profile of chronic hepatitis b virus infection in pregnant women in India
Authors: Pande Chandana , Sarin Shiv Kumar , Patra Sharda , Bhutia Kazila , Mishra Siddhartha Kumar , Pahuja Sangeeta , Jain Manjula , Srivastava Shikha , Dar Sadaf Bashir , Trivedi Shubha Sagar , Mukhopadhyay Chinmay K. , Kumar Ashish 
Published: April 2011

AbstractA large program was conducted by the Government of India to study the prevalence and profile of chronic hepatitis B virus (HBV) infection and its risk factors in pregnant women attending a tertiary care hospital in India. From September 2004 to December 2008 consecutive pregnant women attending the antenatal clinic were screened and those found positive for HBsAg were enrolled. Healthy non‐pregnant women of child‐bearing age, who presented for blood donation during the same period, served as controls. Women with symptoms of liver disease or those aware of their HBsAg status were excluded. Of the 20,104 pregnant women screened, 224 (1.1%) and of the 658 controls, 8 (1.2%) were HBsAg positive (P = ns). Previous blood transfusions and surgery were significant risk factors for infection with HBV. Of the women who were HBsAg positive, the ALT levels were normal in 54% of the women and HBV DNA levels were above 2,000 IU/ml in 71% of women. The median HBV DNA levels were higher in women who were HBeAg positive compared to the HBeAg negative group. The most common HBV genotype was D (84%) followed by A + D and A (8% each). In conclusion, the prevalence of HBsAg positivity among asymptomatic pregnant women in North India is 1.1% with 71% having high HBV DNA levels. These women may have a high risk of transmitting infection to their newborns. J. Med. Virol. 83:962–967, 2011. © 2011 Wiley‐Liss, Inc.
Occult hepatitis C virus infection in Iranian patients with cryptogenic liver disease
Authors: Bokharaei‐Salim Farah , Keyvani Hossein , Monavari Seyed Hamid Reza , Alavian Seyed Moayed , Madjd Zahra , Toosi Mohssen Nassiri , Alizadeh Amir Houshang Mohammad 
Published: April 2011

AbstractThe diagnosis of cryptogenic liver disease is made when after extensive evaluations, recognizable etiologies of chronic liver disease are excluded. In this study, the presence of hepatitis C virus (HCV) RNA was tested in peripheral blood mononuclear cells (PBMCs) taken from Iranian patients who although were found negative for plasma HCV RNA and anti‐HCV antibodies, suffered from chronic liver disease of unknown etiology. From September 2007 to March 2010, 69 patients from Tehran with chronic liver disease of unknown etiology who were referred to our center were enrolled in the present study. PBMCs were isolated from 10 mL peripheral blood specimens. HCV‐RNA status was tested in plasma and PBMCs samples by reverse‐transcription polymerase chain reaction (RT‐PCR). HCV‐RNA was detected in HCV‐positive PBMCs specimens by RT‐PCR method. HCV genotypes were subsequently analyzed in HCV‐positive samples using restriction fragment length polymorphism (RFLP) assay; then HCV genotypes were confirmed by sequencing of 5′ non‐coding fragments after cloning PCR products into pJET1.2/blunt cloning vector. HCV‐RNA was detected in PBMCs specimens belonging to 7 (10%) out of 69 patients. Genotyping of the HCV‐RNA isolated from PBMCs showed that 3 (43%) patients with occult HCV infection had genotype 1b, 2 (29%) had genotype 1a, and another 2 (29%) had genotype 3a. The results of this study suggest that patients with chronic liver disease of unknown etiology may have occult HCV infection in the absence of anti‐HCV antibodies and plasma HCV‐RNA. It has been suggested that in the absence of liver biopsy specimens, analysis of PBMC sample for HCV‐RNA would be informative. J. Med. Virol. 83:989–995, 2011. © 2011 Wiley‐Liss, Inc.
T1846 and A/G1913 are associated with acute on chronic liver failure in patients infected with hepatitis B virus genotypes B and C
Authors: Yan Tao , Li Ke , Li Fan , Su Haibin , Mu Jinsong , Tong Shuping , Patel Mitul , Xia Jie , Wands Jack R. , Wang Huifen 
Published: April 2011

AbstractThe aim of this study was to determine whether mutations in the hepatitis B virus (HBV) genome are associated with the onset of acute on chronic liver failure (ACLF). For the longitudinal study, full‐length HBV genomes were cloned and sequenced from four ACLF patients and compared with sequences from matching samples collected before ACLF. For the cross‐sectional study, 166 serum samples were obtained, including 49 samples from patients with ACLF. The results of longitudinal study showed that C53T, A1846T, and G1896A were the most common mutations in association with ACLF. In the cross‐sectional study 61.2% patients with ACLF presented with T1846, which was higher than patients with chronic hepatitis B (CHB) (11.1%), liver cirrhosis (LC) (31.1%), and hepatocellular carcinoma (HCC) (33.3%). Prevalence of A/G1913 was 42.9% in patients with ACLF, also higher than patients with CHB (2.2%), LC (17.8%), and HCC (11.1%). There were no differences in HBV genotype and patients' HBeAg status among patients with ACLF, LC, and HCC. However, prevalence of T1846 was much higher in patients infected with genotype B (57.1%) than genotype C (30.4%). A/G1913 was higher in HBeAg negative patients (28%) than HBeAg positive patients (13.2%). Results of a multivariable analysis showed that T1846 and A/G1913 were independent factors for ACLF (OR = 3.373 and 4.244, respectively). Interestingly, T1846 destroys an ATG codon of a small open reading frame in the preC region, which may increase core protein expression. We conclude that T1846 and A/G1913 in the preC/C gene are closely associated with ACLF. J. Med. Virol. 83:996–1004, 2011. © 2011 Wiley‐Liss, Inc.
Molecular characterization of hepatitis C virus genotype 4 sequences in HIV‐coinfected patients from Argentina
Authors: Bolcic F. , Jones L.R. , Laufer N. , Quarleri J. 
Published: April 2011

AbstractThe prevalence of hepatitis C virus genotype 4 (HCV‐4) is increasing in different parts of the World but in Latin America the data are still scarce. We aimed to characterize HCV‐4 isolates from 383 HIV‐coinfected patients in Argentina. Sequence analyses were based on the non‐structural 5B region of HCV. Results from 18 patients indicated a genetic heterogeneity that involved three genotype 4 subtypes. Sequences were ascribed to subtype 4d (67%), 4a (22%), and 4m (11%). In spite of different sources of transmission were defined among patients, no statistical association was found with the genotype 4 subtype. The scenario is also compatible with multiple importation of the epidemic and there is no evidence for transmission‐specific clusters or network‐like transmission of HCV‐4. This HCV‐4 does not represent a recent introduction in Argentina, it circulates in all transmission groups and its presence is increasing among HIV‐infected patients. J. Med. Virol. 83:935–940, 2011. © 2011 Wiley‐Liss, Inc.
Rotavirus A genotype P[4]G2: Genetic diversity and reassortment events among strains circulating in Brazil between 2005 and 2009
Authors: Gómez Mariela Martínez , de Mendonça Marcos César Lima , Volotão Eduardo de Mello , Tort Luis Fernando López , da Silva Marcelle Figueira Marques , Cristina Juan , Leite Jose Paulo Gagliardi 
Published: April 2011

AbstractGroup A rotaviruses (RV‐A) are the leading cause of severe gastroenteritis in infants and young children worldwide. Due to the epidemiologic complexity of RV‐A, especially in developing countries, it is important to determine which genotypes are circulating, principally after the introduction in March 2006 of the monovalent (P[8]G1) Rotarix® vaccine in Brazil by the National Immunization Program. In Phase III trials with Rotarix®, the prevalence of genotype P[4]G2 was extremely low, and therefore, evaluation of heterotypic immunization against this genotype was performed by meta‐analysis statistics tests. Different studies have shown the re‐emergence of genotype P[4]G2 in Brazil, since 2005, as well as in other countries, suggesting that it could be a continental phenomenon related to the temporal variability in the genotype's naturally occurring distribution. It is important to note that genotype P[4]G2 does not share VP4 or VP7 antigens with the vaccine strain. Therefore, we performed a phylogenetic analysis based on VP4 (VP8*), VP7, VP6, and NSP4 genes of RV‐A genotype P[4]G2 samples isolated from the five regions of Brazil between 2005 and 2009. This study revealed that different genetic variants of RV‐A genotype P[4]G2 circulated in Brazil between 2005 and 2009, and that this variability is determined mainly by: occurrence of point mutations; reassortment events; and widespread global gene flow. The results obtained in this study are important to our understanding of the epidemiology and evolution of RV‐A genotype P[4]G2 and demonstrate the importance of continuous monitoring and molecular characterization of RV‐A strains circulating in human and animal populations. J. Med. Virol. 83:1093–1106, 2011. © 2011 Wiley‐Liss, Inc.
Effects of hepatitis C virus on suppressor of cytokine signaling mRNA levels: Comparison between different genotypes and core protein sequence analysis
Authors: Pascarella Stéphanie , Clément Sophie , Guilloux Kévin , Conzelmann Stéphanie , Penin François , Negro Francesco 
Published: April 2011

AbstractGlucose metabolism disturbances, including insulin resistance and type 2 diabetes, are frequent and important cofactors of hepatitis C. Increasing epidemiological and experimental data suggest that all major genotypes of hepatitis C virus (HCV), albeit to a different extent, cause insulin resistance. The HCV core protein has been shown to be sufficient to impair insulin signaling in vitro through several post‐receptorial mechanisms, mostly via the activation of suppressor of cytokine signaling (SOCS) family members and the consequent decrease of insulin receptor substrate‐1 (IRS‐1). The levels of IRS‐1 and SOCS were investigated upon expression of the core protein of HCV genotypes 1–4. Furthermore, the core protein sequences were analyzed to identify the amino acid residues responsible for IRS‐1 decrease, with particular regard to SOCS mRNA deregulation. The results suggest that the activation of SOCS family members is a general mechanism associated with the common HCV genotypes. A rare genotype 1b variant, however, failed to activate any of the SOCS tested: this allowed to analyze in detail the distinct amino acid sequences responsible for SOCS deregulation. By combining approaches using intergenotypic chimeras and site‐directed mutagenesis, genetic evidence was provided in favor of a role of amino acids 49 and 131 of the HCV core‐encoding sequence in mediating SOCS transactivation. J. Med. Virol. 83:1005–1015, 2011. © 2011 Wiley‐Liss, Inc.
Uteroglobulin‐related protein 1 and severity of respiratory syncytial virus infection in children admitted to hospital
Authors: Hashimoto Koichi , Katayose Masahiko , Sakuma Hiroko , Kawasaki Yukihiko , Sumikoshi Makoto , Sakata Hiroshi , Sato Masatoki , Ohara Shinichiro , Abe Yusaku , Watanabe Masahiro , Sato Toshiko , Ishibashi Kei , Suzutani Tatsuo , Munakata Mitsuru , Hosoya Mitsuaki 
Published: April 2011

AbstractThere are several reports suggesting that genetic factors contribute to the severity of infection with the respiratory syncytial virus (RSV). Infants hospitalized with lower respiratory tract infection (LRTI) due to RSV are at a significantly increased risk for both recurrent wheezing and childhood asthma. Uteroglobin‐related protein 1 (UGRP1) is a secretory protein expressed in the airways, and speculated to have anti‐inflammatory activity. The presence of the −112G/A polymorphism in the UGRP1 promoter was found to have a significant correlation with asthma phenotype. Also plasma UGRP1 levels were shown to be associated both with this polymorphism and the severity of asthma. The study population consisted of 62 previously healthy infants, ≤12 months of age, who were hospitalized with RSV LRTI, and a control group of 99 healthy adults. Genotyping was performed by restriction fragment length polymorphism. UGRP1 serum levels were determined using ELISA. There were no significant differences in the overall distribution of UGRP1 −112G/A polymorphism genotypes or alleles between the hospitalized infants and healthy adults. A comparison of serum UGRP1 concentration measured at the time of admission and discharge between patients with and without the −112A allele revealed that there was no relation between the presence of the −112A allele and serum UGRP1 in hospitalized infants with RSV infection. Furthermore, there was no relationship between severity of RSV infection and genotype or serum UGRP1 concentration. These results suggest that UGRP1 does not have a major role in the development of severe RSV infection. J. Med. Virol. 83:1086–1092, 2011. © 2011 Wiley‐Liss, Inc.
Clinical and Molecular epidemiologic analyses of norovirus‐associated sporadic gastroenteritis in adults from Beijing, China
Authors: Gao Yan , Jin Miao , Cong Xv , Duan Zhaojun , Li Hui‐ying , Guo Xiaolin , Zuo Ying , Zhang Yanmin , Zhang Yi , Wei Lai 
Published: April 2011

AbstractNoroviruses (NoVs) are a major cause of nonbacterial acute gastroenteritis. The molecular epidemiology of NoV infections in China has not been well characterized. To study the incidence of NoV infections and the nature of the circulating NoV genotypes, 403 specimens were collected from adult outpatients with acute gastroenteritis in Beijing, China, between October 2007 and September 2008. Samples were examined for NoV by reverse transcriptase‐polymerase chain reaction (RT‐PCR) and sequences corresponding to both the NoV polymerase and capsid regions were characterized. Among the 403 specimens, 48 (11.9%) were positive for NoV and 1/3 NoV‐associated gastroenteritis cases occurred during the colder months (November and December). Based on polymerase region sequences, 6 NoV genotypes (GII‐4, GII‐b, GII‐6, GI‐2, GI‐3, and GI‐4) were identified with GII‐4 2006b being the most predominant genotype (37/48, 77.1%). Eleven distinct genotype sequences in polymerase and capsid regions were identified, indicating a genetic diversity among NoV isolates. This study suggested NoVs were an important pathogen responsible for sporadic acute gastroenteritis in adults in Beijing, China. J. Med. Virol. 83:1078–1085, 2011. © 2011 Wiley‐Liss, Inc.
Latent and lytic Epstein‐Barr virus gene expression in the peripheral blood of astronauts
Authors: Stowe Raymond P. , Kozlova Elena V. , Sams Clarence F. , Pierson Duane L. , Walling Dennis M. 
Published: April 2011

AbstractEpstein‐Barr virus (EBV) latent and replicative gene transcription was analyzed in peripheral blood B‐lymphocytes from astronauts who flew on short‐duration (∼11 days) Shuttle missions and long‐duration (∼180 days) International Space Station (ISS) missions. Latent, immediate‐early, and early gene replicative viral transcripts were detected in samples from six astronauts who flew on short‐duration Shuttle missions, whereas viral gene transcription was mostly absent in samples from 24 healthy donors. Samples from six astronauts who flew on long‐duration ISS missions were characterized by expanded expression of latent, immediate‐early, and early gene transcripts and new onset expression of late replicative transcription upon return to Earth. These data indicate that EBV‐infected cells are no longer expressing the restricted set of viral genes that characterize latency but are expressing latent and lytic gene transcripts. These data also suggest the possibility of EBV‐related complications in future long‐duration missions, in particular interplanetary travel. J. Med. Virol. 83:1071–1077, 2011. © 2011 Wiley‐Liss, Inc.
Distribution of human papillomavirus genotypes in cervical intraepithelial neoplasia and invasive cervical cancer in Canada
Authors: Coutlée François , Ratnam Samuel , Ramanakumar Agnihotram V. , Insinga Ralph R. , Bentley James , Escott Nicholas , Ghatage Prafull , Koushik Anita , Ferenczy Alex , Franco Eduardo L. 
Published: April 2011

AbstractInfection with high‐risk human papillomavirus (HPV) causes cervical intraepithelial neoplasia (CIN) and invasive cervical cancer (ICC). The distribution of HPV types in cervical diseases has been previously described in small studies for Canadian women. The prevalence of 36 HPV genotypes in 873 women with CIN and 252 women with ICC was assessed on cervical exfoliated cells analyzed with the Linear Array (Roche Molecular System). HPV16 was the most common genotype in CIN and ICC. The seven most frequent genotypes in order of decreasing frequency were HPV16, 51, 52, 31, 39, 18, and 56 in women with CIN1, HPV16, 52, 31, 18, 51, 39, and 33 in women with CIN2, HPV16, 31, 18, 52, 39, 33, and 58 in women with CIN3, and HPV16, 18, 45, 33, 31, 39, and 53 in women with ICC. HPV18 was detected more frequently in adenocarcinoma than squamous cell carcinoma (P = 0.013). Adjustment for multiple type infections resulted in a lower percentage attribution in CIN of HPV types other than 16 or 18. The proportion of samples containing at least one oncogenic type was greater in CIN2 (98.4%) or CIN3 (100%) than in CIN1 (80.1%; P < 0.001 for each comparison). Multiple type infections were demonstrated in 51 (20.2%) of 252 ICC in contrast to 146 (61.3%) of 238 women with CIN3 (P < 0.001). Adjusting for multiple HPV types, HPV16 accounted for 52.1% and HPV18 for 18.1% of ICCs, for a total of 70.2%. Current HPV vaccines should protect against HPV types responsible for 70% of ICCs in Canadian women. J. Med. Virol. 83:1034–1041, 2011. © 2011 Wiley‐Liss, Inc.
Monoclonal antibody‐based antigen capture immunoassay for detection of circulating non‐structural protein NS1: Implications for early diagnosis of japanese encephalitis virus infection
Authors: Kumar Jyoti S. , Parida Manmohan , Rao P.V. Lakshmana 
Published: April 2011

AbstractAn early diagnosis of Japanese encephalitis (JE) is important for timely clinical management and epidemiological control in areas where multiple flaviviruses are endemic. The NS1 antigen has an advantage over IgM enzyme‐linked immunosorbent assay (ELISA) for early confirmatory diagnosis of Japanese encephalitis virus (JEV) infection due to its proliferation on the surface of the host cells in the acute phase of infection. In this study, the development and evaluation of JE‐specific NS1 antigen capture ELISA is described using high‐affinity monoclonal antibody specific to the recombinant NS1 protein for early diagnosis of JE. The gene encoding NS1 protein was cloned and expressed in the pQE30UA expression vector followed by purification of the recombinant protein by affinity chromatography. A sandwich ELISA for antigen detection was developed using purified rabbit IgG antibody and mouse monoclonal antibody as the capture and detector antibody, respectively. The application of JE NS1 antigen ELISA for early diagnosis was evaluated with 120 acute phase sera and 80 CSF samples. The comparative evaluation of the JE NS1 antigen ELISA by real‐time RT‐PCR revealed 97% concordance with a sensitivity and specificity of 97% and 98%, respectively. The JE NS1 antigen was detectable in the blood from the first day up to day 9 after the onset of symptoms. These findings suggest that the JEV NS1 antigen capture ELISA may help early diagnosis of JE infection. J. Med. Virol. 83:1063–1070, 2011. © 2011 Wiley‐Liss, Inc.
Intersectin1‐s is involved in migration and invasion of human glioma cells
Authors: Ma Yongjie , Wang Bingbing , Li Wenliang , Liu Xiaoli , Wang Jing , Ding Ting , Zhang Jiao , Ying Guoguang , Fu Li , Gu Feng 
Published: April 2011

AbstractMalignant gliomas have a tendency to invade diffusely into surrounding healthy brain tissues, thereby precluding their successful surgical removal. Intersectin1 (ITSN1) as a molecular linker in the central nervous system is well known as an important regulator of endocytosis and exocytosis. ITSN1 has two isoforms: ITSN1‐l and ITSN1‐s. In this study, we show that siRNA‐mediated down regulation of ITSN1‐s inhibited migration and invasion of glioma cells. In addition, we demonstrate the possible mechanisms by which ITSN1‐s functions in migration and invasion. Several key proteins, including cofilin, LIMK, PAK, FAK, integrin β1, and MMP‐9, which are critical for cells migration and invasion, were probably involved in ITSN1‐s signaling pathways. These results suggest that ITSN1‐s contributes to glioma cells migration and invasion by regulating the formation of cytoskeleton, influencing adhesion and increasing expression of MMP‐9. Our results indicate that ITSN1‐s is a critical factor in glioms invasion and identify that ITSN1‐s is a new potentially antiinvasion target for therapeutic intervention in gliomas. © 2011 Wiley‐Liss, Inc.