Last data update: Oct 28, 2024. (Total: 48004 publications since 2009)
Records 1-6 (of 6 Records) |
Query Trace: Shaw MW[original query] |
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Lessons from the reestablishment of Public Health Laboratory activities in Puerto Rico after Hurricane Maria
Hardy MC , Stinnett RC , Kines KJ , Rivera-Nazario DM , Lowe DE , Mercante AM , Gonzalez Jimenez N , Cuevas Ruiz RI , Rivera Arbolay HI , Gonzalez Pena RL , Toro M , Trujillo AA , Pappas CL , Llewellyn AC , Candal F , Burgos Garay M , Gomez GA , Concepcion Acevedo J , Ansbro M , Moura H , Shaw MW , Muehlenbachs A , Romanoff LC , Sunshine BJ , Rose DA , Patel A , Shapiro CN , Luna-Pinto SC , Pillai SK , O'Neill E . Nat Commun 2019 10 (1) 2720 Public Health Laboratories (PHLs) in Puerto Rico did not escape the devastation caused by Hurricane Maria. We implemented a quality management system (QMS) approach to systematically reestablish laboratory testing, after evaluating structural and functional damage. PHLs were inoperable immediately after the storm. Our QMS-based approach began in October 2017, ended in May 2018, and resulted in the reestablishment of 92% of baseline laboratory testing capacity. Here, we share lessons learned from the historic recovery of the largest United States' jurisdiction to lose its PHL capacity, and provide broadly applicable tools for other jurisdictions to enhance preparedness for public health emergencies. |
Identification of cellular proteins required for replication of human immunodeficiency virus type 1
Dziuba N , Ferguson MR , O'Brien WA , Sanchez A , Prussia AJ , McDonald NJ , Friedrich BM , Li G , Shaw MW , Sheng J , Hodge TW , Rubin DH , Murray JL . AIDS Res Hum Retroviruses 2012 28 (10) 1329-39 Cellular proteins are essential for human immunodeficiency virus type 1 (HIV-1) replication and may serve as viable new targets for treating infection. Using gene trap insertional mutagenesis, a high-throughput approach based on random inactivation of cellular genes, candidate genes were found that limit virus replication when mutated. Disrupted genes (N=87) conferring resistance to lytic infection with several viruses were queried for an affect on HIV-1 replication by utilizing small interfering RNA (siRNA) screens in TZM-bl cells. Several genes regulating diverse pathways were found to be required for HIV-1 replication, including DHX8, DNAJA1, GTF2E1, GTF2E2, HAP1, KALRN, UBA3, UBE2E3, and VMP1. Candidate genes were independently tested in primary human macrophages, toxicity assays, and/or Tat-dependent beta-galactosidase reporter assays. Bioinformatics analyses indicated that several host factors present in this study participate in canonical pathways and functional processes implicated in prior genome-wide studies. However, the genes presented in this study did not share identity with those found previously. Novel antiviral targets identified in this study should open new avenues for mechanistic investigation. |
Detecting 2009 pandemic influenza A (H1N1) virus infection: availability of diagnostic testing led to rapid pandemic response
Jernigan DB , Lindstrom SL , Johnson JR , Miller JD , Hoelscher M , Humes R , Shively R , Brammer L , Burke SA , Villanueva JM , Balish A , Uyeki T , Mustaquim D , Bishop A , Handsfield JH , Astles R , Xu X , Klimov AI , Cox NJ , Shaw MW . Clin Infect Dis 2011 52 S36-S43 Diagnostic tests for detecting emerging influenza virus strains with pandemic potential are critical for directing global influenza prevention and control activities. In 2008, the Centers for Disease Control and Prevention received US Food and Drug Administration approval for a highly sensitive influenza polymerase chain reaction (PCR) assay. Devices were deployed to public health laboratories in the United States and globally. Within 2 weeks of the first recognition of 2009 pandemic influenza H1N1, the Centers for Disease Control and Prevention developed and began distributing a new approved pandemic influenza H1N1 PCR assay, which used the previously deployed device platform to meet a >8-fold increase in specimen submissions. Rapid antigen tests were widely used by clinicians at the point of care; however, test sensitivity was low (40%-69%). Many clinical laboratories developed their own pandemic influenza H1N1 PCR assays to meet clinician demand. Future planning efforts should identify ways to improve availability of reliable testing to manage patient care and approaches for optimal use of molecular testing for detecting and controlling emerging influenza virus strains. |
Comprehensive assessment of 2009 pandemic influenza A (H1N1) virus drug susceptibility in vitro
Gubareva LV , Trujillo AA , Okomo-Adhiambo M , Mishin VP , Deyde VM , Sleeman K , Nguyen HT , Sheu TG , Garten RJ , Shaw MW , Fry AM , Klimov AI . Antivir Ther 2010 15 (8) 1151-9 BACKGROUND: Antiviral drugs are an important option for managing infections caused by influenza viruses. This study assessed the drug susceptibility of 2009 pandemic influenza A (H1N1) viruses collected globally between April 2009 and January 2010. METHODS: Virus isolates were tested for adamantane susceptibility, using pyrosequencing to detect the S31N marker of adamantane resistance in the M2 protein and biological assays to assess viral replication in cell culture. To assess neuraminidase (NA) inhibitor (NAI) susceptibility, virus isolates were tested in chemiluminescent NA inhibition assays and by pyrosequencing to detect the H275Y (H274Y in N2 numbering) marker of oseltamivir resistance in the NA. RESULTS: With the exception of three, all viruses that were tested for adamantane susceptibility (n=3,362) were resistant to this class of drugs. All viruses tested for NAI susceptibility (n=3,359) were sensitive to two US Food and Drug Administration-approved NAIs, oseltamivir (mean +/-sd 50% inhibitory concentration [IC(50)] 0.25 +/-0.12 nM) and zanamivir (mean IC(50) 0.29 +/-0.09 nM), except 23 (0.7%), which were resistant to oseltamivir, but sensitive to zanamivir. Oseltamivir-resistant viruses had the H275Y mutation in their NA and were detected in patients exposed to the drug through prophylaxis or treatment. NA activity of all viruses was inhibited by the NAIs peramivir, laninamivir (R-125489) and A-315675, except for H275Y variants, which exhibited approximately 100-fold reduction in peramivir susceptibility. CONCLUSIONS: This report provides data regarding antiviral susceptibility of 2009 pandemic influenza A (H1N1) surveillance viruses, the majority of which were resistant to adamantanes and sensitive to NAIs. These findings provide information essential for antiviral resistance monitoring and development of novel diagnostic tests for detecting influenza antiviral resistance. |
Validation of a method for preparing influenza H5N1 simulated samples
Lednicky JA , Villanueva JM , Burke SA , Shively R , Shaw MW , Daniels DE , Hamilton SB , Donis RO . J Virol Methods 2010 167 (2) 125-131 Avian influenza virus type A subtype H5N1 and potentially other novel influenza A viruses continue to pose a concern with mutation into a form easily transmitted between humans. The ability to rapidly detect and characterize influenza viruses, and distinguish seasonal and novel influenza A viruses such as H5N1, remains important to minimize morbidity and mortality in humans. As with other rare and emerging viral pathogens, clinical specimens from persons with H5N1 infections are extremely rare. Consequently, development of standardized methods and accepted criteria are necessary for both ensuring the validity of available diagnostic methods and for assessing the potential of new diagnostic tests that can detect and differentiate H5N1 and other novel influenza A viruses. Additionally, genotypic and antigenic evolution of H5N1 poses a challenge with maintaining updated reference virus strains. In this report, a method for preparing simulated samples using defined procedures and carefully selected H5N1 virus strains is described, and the reliability for using these samples in an evaluation protocol with a laboratory test for differentiating H5N1 virus from other influenza A viruses is evaluated. |
Host cell selection of influenza neuraminidase variants: implications for drug resistance monitoring in A(H1N1) viruses
Okomo-Adhiambo M , Nguyen HT , Sleeman K , Sheu TG , Deyde VM , Garten RJ , Xu X , Shaw MW , Klimov AI , Gubareva LV . Antiviral Res 2009 85 (2) 381-8 The neuraminidase inhibitors (NAIs), oseltamivir and zanamivir, are essential for treatment and prevention of influenza A and B infections. Oseltamivir resistance among influenza A (H1N1) viruses rapidly emerged and spread globally during the 2007-2008 and 2008-2009 influenza seasons. Approximately 20% and 90% of viruses tested for NAI susceptibility at CDC during these seasons, respectively, were resistant to oseltamivir (IC(50) approximately 100-3000 time>those of sensitive viruses), based on the chemiluminescent NA inhibition assay. Pyrosequencing analysis confirmed H274Y mutation (H275Y in N1 numbering) in the neuraminidase (NA) gene of oseltamivir-resistant viruses. Full NA sequence analysis of a subset of oseltamivir-resistant and sensitive virus isolates from both seasons (n=725) showed that 53 (7.3%) had mutations at residue D151 (D-->E/G/N), while 9 (1.2%) had mutations at Q136 (Q-->K) and 2 (0.3%) had mutations at both residues. Viruses with very high IC(50) for oseltamivir and peramivir, and elevated IC(50) for zanamivir, had H274Y in addition to mutations at D151 and/or Q136, residues which can potentially confer NAI-resistance based on recent N1 NA crystal structure data. Mutations at D151 without H274Y, did not elevate IC(50) for any tested NAI, however, Q136K alone significantly reduced susceptibility to zanamivir (36-fold), peramivir (80-fold) and A-315675 (114-fold) but not oseltamivir. Mutations at D151 and Q136 were present only in MDCK-grown viruses but not in matching original clinical specimens (n=33) which were available for testing, suggesting that these variants were the result of cell culture selection or they were present in very low proportions. Our findings provide evidence that propagation of influenza virus outside its natural host may lead to selection of virus variants with mutations in the NA that affect sensitivity to NAIs and thus poses implications for drug resistance monitoring and diagnostics. |
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