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Find video protocols related to scientific articles indexed in Pubmed.
Hepatitis C Virus (HCV) NS3 sequence diversity and antiviral resistance-associated variant frequency in HCV/HIV coinfection.
Antimicrob. Agents Chemother.
PUBLISHED: 08-04-2014
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HIV coinfection accelerates disease progression in chronic hepatitis C and reduces sustained antiviral responses (SVR) to interferon-based therapy. New direct-acting antivirals (DAAs) promise higher SVR rates, but the selection of preexisting resistance-associated variants (RAVs) may lead to virologic breakthrough or relapse. Thus, pretreatment frequencies of RAVs are likely determinants of treatment outcome but typically are below levels at which the viral sequence can be accurately resolved. Moreover, it is not known how HIV coinfection influences RAV frequency. We adopted an accurate high-throughput sequencing strategy to compare nucleotide diversity in HCV NS3 protease-coding sequences in 20 monoinfected and 20 coinfected subjects with well-controlled HIV infection. Differences in mean pairwise nucleotide diversity (?), Tajima's D statistic, and Shannon entropy index suggested that the genetic diversity of HCV is reduced in coinfection. Among coinfected subjects, diversity correlated positively with increases in CD4(+) T cells on antiretroviral therapy, suggesting T cell responses are important determinants of diversity. At a median sequencing depth of 0.084%, preexisting RAVs were readily identified. Q80K, which negatively impacts clinical responses to simeprevir, was encoded by more than 99% of viral RNAs in 17 of the 40 subjects. RAVs other than Q80K were identified in 39 of 40 subjects, mostly at frequencies near 0.1%. RAV frequency did not differ significantly between monoinfected and coinfected subjects. We conclude that HCV genetic diversity is reduced in patients with well-controlled HIV infection, likely reflecting impaired T cell immunity. However, RAV frequency is not increased and should not adversely influence the outcome of DAA therapy.
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Tenofovir diphosphate and emtricitabine triphosphate concentrations in blood cells compared with isolated peripheral blood mononuclear cells: a new measure of antiretroviral adherence?
J. Acquir. Immune Defic. Syndr.
PUBLISHED: 08-21-2013
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The active metabolites of tenofovir (TFV) and emtricitabine (FTC) in peripheral blood mononuclear cells (PBMCs) have been used as markers of long-term antiretroviral (ARV) adherence. However, the process of isolating PBMCs is expensive, complex, and not feasible in many settings. We compared concentrations of TFV-diphosphate (TFV-DP) and FTC-triphosphate (FTC-TP) in the upper layer packed cells (ULPCs) obtained after whole blood centrifugation to isolated PBMCs as a possible alternative marker of adherence.
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Prevention and control of sexually transmissible infections among hotel-based female sex workers in Dhaka, Bangladesh.
Sex Health
PUBLISHED: 07-16-2013
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Background Hotel-based sex workers in Bangladesh have high rates of sexually transmissible infections (STIs), high client turnover and low condom use. Two monthly clinic-based strategies were compared: periodic presumptive treatment (PPT) and enhanced syndromic management (ESM) - one round of presumptive treatment followed by treatment based on assessment and laboratory tests. Methods: A randomised controlled trial compared PPT and ESM by prevalence and incidence, behaviour, retention, cost and STI incidence and prevalence. Demographic, behavioural and clinical data were collected from women at two clinics in Dhaka. All women received presumptive treatment and were randomised to receive PPT or ESM at nine monthly visits. Results: In total, 549 women (median age: <20 years) were enrolled. At baseline, the prevalence of chlamydia (Chlamydia trachomatis) and gonorrhoea (Neisseria gonorrhoeae) was 41% (ESM: 41%; PPT: 42%). After 9 months, chlamydia and gonorrhoea decreased to 7% overall, (ESM: 7.4%; PPT: 6.8%). At each visit, 98% of women receiving ESM met the therapy criteria and were treated. Retention was low (50%). Total costs were 50% lower per visit for each woman for PPT (ESM: $11.62 v. PPT: $5.80). The number of sex work sessions was reduced from 3.3 to 2.5 (P<0.001), but income did not change. Coercion was reduced but condom use at last sex did not change significantly. Conclusions: Monthly PPT and ESM were effective approaches for STI control. PPT offered a feasible, low-cost alternative to ESM. Educational aspects led to a reduction in coercion and fewer sessions. Implementation studies are needed to improve condom use and retention.
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Systemically circulating viral and tumor-derived microRNAs in KSHV-associated malignancies.
PLoS Pathog.
PUBLISHED: 07-01-2013
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MicroRNAs (miRNAs) are stable, small non-coding RNAs that modulate many downstream target genes. Recently, circulating miRNAs have been detected in various body fluids and within exosomes, prompting their evaluation as candidate biomarkers of diseases, especially cancer. Kaposis sarcoma (KS) is the most common AIDS-associated cancer and remains prevalent despite Highly Active Anti-Retroviral Therapy (HAART). KS is caused by KS-associated herpesvirus (KSHV), a gamma herpesvirus also associated with Primary Effusion Lymphoma (PEL). We sought to determine the host and viral circulating miRNAs in plasma, pleural fluid or serum from patients with the KSHV-associated malignancies KS and PEL and from two mouse models of KS. Both KSHV-encoded miRNAs and host miRNAs, including members of the miR-17-92 cluster, were detectable within patient exosomes and circulating miRNA profiles from KSHV mouse models. Further characterization revealed a subset of miRNAs that seemed to be preferentially incorporated into exosomes. Gene ontology analysis of signature exosomal miRNA targets revealed several signaling pathways that are known to be important in KSHV pathogenesis. Functional analysis of endothelial cells exposed to patient-derived exosomes demonstrated enhanced cell migration and IL-6 secretion. This suggests that exosomes derived from KSHV-associated malignancies are functional and contain a distinct subset of miRNAs. These could represent candidate biomarkers of disease and may contribute to the paracrine phenotypes that are a characteristic of KS.
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Does HAART efficacy translate to effectiveness? Evidence for a trial effect.
PLoS ONE
PUBLISHED: 01-31-2011
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Patients who participate in clinical trials may experience better clinical outcomes than patients who initiate similar therapy within clinical care (trial effect), but no published studies have evaluated a trial effect in HIV clinical trials.
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The major genetic determinants of HIV-1 control affect HLA class I peptide presentation.
, Florencia Pereyra, Xiaoming Jia, Paul J McLaren, Amalio Telenti, Paul I W de Bakker, Bruce D Walker, Stephan Ripke, Chanson J Brumme, Sara L Pulit, Mary Carrington, Carl M Kadie, Jonathan M Carlson, David Heckerman, Robert R Graham, Robert M Plenge, Steven G Deeks, Lauren Gianniny, Gabriel Crawford, Jordan Sullivan, Elena González, Leela Davies, Amy Camargo, Jamie M Moore, Nicole Beattie, Supriya Gupta, Andrew Crenshaw, Noel P Burtt, Candace Guiducci, Namrata Gupta, Xiaojiang Gao, Ying Qi, Yuko Yuki, Alicja Piechocka-Trocha, Emily Cutrell, Rachel Rosenberg, Kristin L Moss, Paul Lemay, Jessica O'Leary, Todd Schaefer, Pranshu Verma, Ildikó Tóth, Brian Block, Brett Baker, Alissa Rothchild, Jeffrey Lian, Jacqueline Proudfoot, Donna Marie L Alvino, Seanna Vine, Marylyn M Addo, Todd M Allen, Marcus Altfeld, Matthew R Henn, Sylvie Le Gall, Hendrik Streeck, David W Haas, Daniel R Kuritzkes, Gregory K Robbins, Robert W Shafer, Roy M Gulick, Cecilia M Shikuma, Richard Haubrich, Sharon Riddler, Paul E Sax, Eric S Daar, Heather J Ribaudo, Brian Agan, Shanu Agarwal, Richard L Ahern, Brady L Allen, Sherly Altidor, Eric L Altschuler, Sujata Ambardar, Kathryn Anastos, Ben Anderson, Val Anderson, Ushan Andrady, Diana Antoniskis, David Bangsberg, Daniel Barbaro, William Barrie, J Bartczak, Simon Barton, Patricia Basden, Nesli Basgoz, Suzane Bazner, Nicholaos C Bellos, Anne M Benson, Judith Berger, Nicole F Bernard, Annette M Bernard, Christopher Birch, Stanley J Bodner, Robert K Bolan, Emilie T Boudreaux, Meg Bradley, James F Braun, Jon E Brndjar, Stephen J Brown, Katherine Brown, Sheldon T Brown, Jedidiah Burack, Larry M Bush, Virginia Cafaro, Omobolaji Campbell, John Campbell, Robert H Carlson, J Kevin Carmichael, Kathleen K Casey, Chris Cavacuiti, Gregory Celestin, Steven T Chambers, Nancy Chez, Lisa M Chirch, Paul J Cimoch, Daniel Cohen, Lillian E Cohn, Brian Conway, David A Cooper, Brian Cornelson, David T Cox, Michael V Cristofano, George Cuchural, Julie L Czartoski, Joseph M Dahman, Jennifer S Daly, Benjamin T Davis, Kristine Davis, Sheila M Davod, Edwin DeJesus, Craig A Dietz, Eleanor Dunham, Michael E Dunn, Todd B Ellerin, Joseph J Eron, John J W Fangman, Claire E Farel, Helen Ferlazzo, Sarah Fidler, Anita Fleenor-Ford, Renee Frankel, Kenneth A Freedberg, Neel K French, Jonathan D Fuchs, Jon D Fuller, Jonna Gaberman, Joel E Gallant, Rajesh T Gandhi, Efrain Garcia, Donald Garmon, Joseph C Gathe, Cyril R Gaultier, Wondwoosen Gebre, Frank D Gilman, Ian Gilson, Paul A Goepfert, Michael S Gottlieb, Claudia Goulston, Richard K Groger, T Douglas Gurley, Stuart Haber, Robin Hardwicke, W David Hardy, P Richard Harrigan, Trevor N Hawkins, Sonya Heath, Frederick M Hecht, W Keith Henry, Melissa Hladek, Robert P Hoffman, James M Horton, Ricky K Hsu, Gregory D Huhn, Peter Hunt, Mark J Hupert, Mark L Illeman, Hans Jaeger, Robert M Jellinger, Mina John, Jennifer A Johnson, Kristin L Johnson, Heather Johnson, Kay Johnson, Jennifer Joly, Wilbert C Jordan, Carol A Kauffman, Homayoon Khanlou, Robert K Killian, Arthur Y Kim, David D Kim, Clifford A Kinder, Jeffrey T Kirchner, Laura Kogelman, Erna Milunka Kojic, P Todd Korthuis, Wayne Kurisu, Douglas S Kwon, Melissa Lamar, Harry Lampiris, Massimiliano Lanzafame, Michael M Lederman, David M Lee, Jean M L Lee, Marah J Lee, Edward T Y Lee, Janice Lemoine, Jay A Levy, Josep M Llibre, Michael A Liguori, Susan J Little, Anne Y Liu, Alvaro J Lopez, Mono R Loutfy, Dawn Loy, Debbie Y Mohammed, Alan Man, Michael K Mansour, Vincent C Marconi, Martin Markowitz, Rui Marques, Jeffrey N Martin, Harold L Martin, Kenneth Hugh Mayer, M Juliana McElrath, Theresa A McGhee, Barbara H McGovern, Katherine McGowan, Dawn McIntyre, Gavin X Mcleod, Prema Menezes, Greg Mesa, Craig E Metroka, Dirk Meyer-Olson, Andy O Miller, Kate Montgomery, Karam C Mounzer, Ellen H Nagami, Iris Nagin, Ronald G Nahass, Margret O Nelson, Craig Nielsen, David L Norene, David H O'Connor, Bisola O Ojikutu, Jason Okulicz, Olakunle O Oladehin, Edward C Oldfield, Susan A Olender, Mario Ostrowski, William F Owen, Eunice Pae, Jeffrey Parsonnet, Andrew M Pavlatos, Aaron M Perlmutter, Michael N Pierce, Jonathan M Pincus, Leandro Pisani, Lawrence Jay Price, Laurie Proia, Richard C Prokesch, Heather Calderon Pujet, Moti Ramgopal, Almas Rathod, Michael Rausch, J Ravishankar, Frank S Rhame, Constance Shamuyarira Richards, Douglas D Richman, Berta Rodés, Milagros Rodriguez, Richard C Rose, Eric S Rosenberg, Daniel Rosenthal, Polly E Ross, David S Rubin, Elease Rumbaugh, Luis Saenz, Michelle R Salvaggio, William C Sanchez, Veeraf M Sanjana, Steven Santiago, Wolfgang Schmidt, Hanneke Schuitemaker, Philip M Sestak, Peter Shalit, William Shay, Vivian N Shirvani, Vanessa I Silebi, James M Sizemore, Paul R Skolnik, Marcia Sokol-Anderson, James M Sosman, Paul Stabile, Jack T Stapleton, Sheree Starrett, Francine Stein, Hans-Jürgen Stellbrink, F Lisa Sterman, Valerie E Stone, David R Stone, Giuseppe Tambussi, Randy A Taplitz, Ellen M Tedaldi, William Theisen, Richard Torres, Lorraine Tosiello, Cécile Tremblay, Marc A Tribble, Phuong D Trinh, Alice Tsao, Peggy Ueda, Anthony Vaccaro, Emília Valadas, Thanes J Vanig, Isabel Vecino, Vilma M Vega, Wenoah Veikley, Barbara H Wade, Charles Walworth, Chingchai Wanidworanun, Douglas J Ward, Daniel A Warner, Robert D Weber, Duncan Webster, Steve Weis, David A Wheeler, David J White, Ed Wilkins, Alan Winston, Clifford G Wlodaver, Angelique van't Wout, David P Wright, Otto O Yang, David L Yurdin, Brandon W Zabukovic, Kimon C Zachary, Beth Zeeman, Meng Zhao.
Science
PUBLISHED: 11-04-2010
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Infectious and inflammatory diseases have repeatedly shown strong genetic associations within the major histocompatibility complex (MHC); however, the basis for these associations remains elusive. To define host genetic effects on the outcome of a chronic viral infection, we performed genome-wide association analysis in a multiethnic cohort of HIV-1 controllers and progressors, and we analyzed the effects of individual amino acids within the classical human leukocyte antigen (HLA) proteins. We identified >300 genome-wide significant single-nucleotide polymorphisms (SNPs) within the MHC and none elsewhere. Specific amino acids in the HLA-B peptide binding groove, as well as an independent HLA-C effect, explain the SNP associations and reconcile both protective and risk HLA alleles. These results implicate the nature of the HLA-viral peptide interaction as the major factor modulating durable control of HIV infection.
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Good performance of rapid prostate-specific antigen test for detection of semen exposure in women: implications for qualitative research.
Sex Transm Dis
PUBLISHED: 05-21-2009
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Prostate-specific antigen (PSA) is a valid biomarker of semen exposure in women and has been used to assess reliability of self-reported sexual behavior as well as serve as a proxy measure for condom efficacy. Quantitative PSA tests are expensive and require specialized equipment. A simple, rapid, and inexpensive test for PSA would facilitate semen biomarker evaluation in a variety of research settings. This study evaluated the performance of a rapid PSA test compared with a quantitative assay to identify semen in vaginal swab specimens.
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Major coexisting human immunodeficiency virus type 1 env gene subpopulations in the peripheral blood are produced by cells with similar turnover rates and show little evidence of genetic compartmentalization.
J. Virol.
PUBLISHED: 02-11-2009
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A distinctive feature of chronic human immunodeficiency virus type 1 (HIV-1) infection is the presence of multiple coexisting genetic variants, or subpopulations, that comprise the HIV-1 population detected in the peripheral blood. Analysis of HIV-1 RNA decay dynamics during the initiation of highly active antiretroviral therapy (HAART) has been a valuable tool for modeling the life span of infected cells that produce the bulk HIV-1 population. However, different HIV-1 target cells may have different turnover rates, and it is not clear whether the bulk HIV-1 RNA decay rate actually represents a composite of the decay rates of viral subpopulations compartmentalized in different cellular subsets with different life spans. Using heteroduplex tracking assays targeting the highly variable V3 or V4-V5 regions of the HIV-1 env gene in eight subjects, we found that all detectable coexisting HIV-1 variants in the peripheral blood generally decayed at similar rates during the initiation of HAART, suggesting that all of the variants were produced by cells with similar life spans. Furthermore, single genome amplification and coreceptor phenotyping revealed that in two subjects coexisting HIV-1 variants with distinct CXCR4 or CCR5 coreceptor phenotypes decayed with similar rates. Also, in nine additional subjects, recombination and a lack of genetic compartmentalization between X4 and R5 variants were observed, suggesting an overlap in host cell range. Our results suggest that the HIV-1 env subpopulations detectable in the peripheral blood are produced by cells with similar life spans and are not genetically isolated within particular cell types.
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Low prevalence of antiretroviral resistance among HIV type 1-positive prisoners in the Southeast United States.
AIDS Res. Hum. Retroviruses
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Drug-resistant HIV complicates management of HIV infection. Although an estimated 14% of all HIV-positive persons pass through a prison or jail in the United States each year, little is known about the overall prevalence of antiretroviral (ARV) resistance in incarcerated persons. All genotypic sequence data on HIV-positive prisoners in the North Carolina (NC) Department of Corrections (DOC) were obtained from LabCorp. Screening for major resistance mutations in protease (PI) and reverse transcriptase (NRTI and NNRTI) was done using Genosure and the Stanford HIV Database. For subjects with multiple genotype reports, each mutation was counted only once and considered present on all subsequent genotypes. Between October 2006 and February 2010, the NC DOC incarcerated 1,911 HIV(+) individuals of whom 19.2% (n=367) had at least one genotype performed. The overall prevalence of a major resistance mutation was 28.3% (95% CI 23.7, 33.0). Among prisoners ever exposed to an ARV during incarceration (n=329) prevalence of a major resistance mutation was 29.8% (95% CI 24.9, 34.7); resistance by class was 20.4% (95% CI 16.0, 24.7) for NRTIs, 19.8% (95% CI 15.5, 24.1) for NNRTIs, and 8.8% (95% CI 5.8,11.9) for PIs. Single class drug resistance was most prevalent at 14.2% (10.2,17.7) followed by dual 12.5% (I8.9,16.0) and triple class 3.3% (1.4,5.3) resistance. The three most prevalent mutations were K103N 15.8% (12.0, 20.2), M184V 14.3% (10.7,18.5), and M41L 4.9% (2.8,7.8). In the NC DOC ARV resistance prevalence, dual and triple class drug resistance was moderate over the study period. Resistance to PIs was lower than NNRTIs and NRTIs, likely reflecting higher usage of these two classes or a lower barrier to resistance.
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Expression of p16(INK4a) as a biomarker of T-cell aging in HIV-infected patients prior to and during antiretroviral therapy.
Aging Cell
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The p16(INK4a) tumor suppressor gene is a mediator of cellular senescence and has been suggested to be a biomarker of molecular age in several tissues including T cells. To determine the association of both active and suppressed HIV infection with T-cell aging, T-cell p16(INK4a) expression was compared between 60 HIV+ suppressed subjects, 23 HIV+ untreated subjects, and 18 contemporaneously collected HIV-negative controls, as well as 148 HIV-negative historical samples. Expression did not correlate with chronologic age in untreated HIV+ patients, consistent with an effect of active HIV replication on p16(INK4a) expression. In patients on cART with suppressed viral loads, however, p16(INK4a) levels were similar to uninfected controls and correlated with chronologic age, with a trend toward an inverse correlation with CD4 count. These data show that p16(INK4a) is a reliable biomarker of T-cell aging in HIV+ patients with suppressed viral loads and suggest that poor CD4 cell recovery on cART may be associated with increased T-cell expression of p16(INK4a), a marker of cellular senescence.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.