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Background. Although pandemic and avian influenza are known to be transmitted via human hands, there are minimal data regarding the effectiveness of routine hand hygiene (HH) protocols against pandemic and avian influenza. Methods. Twenty vaccinated, antibody-positive health care workers had their hands contaminated with 1 mL of 107 tissue culture infectious dose (TCID)>50/0.1 mL live human influenza A virus (H1N1; A/New Caledonia/20/99) before undertaking 1 of 5 HH protocols (no HH [control], soap and water hand washing [SW], or use of 1 of 3 alcohol-based hand rubs [61.5% ethanol gel, 70% ethanol plus 0.5% chlorhexidine solution, or 70% isopropanol plus 0.5% chlorhexidine solution]). H1N1 concentrations were assessed before and after each intervention by viral culture and real-time reverse-transcriptase polymerase chain reaction (PCR). The natural viability of H1N1 on hands for >60 min without HH was also assessed. Results. There was an immediate reduction in culture-detectable and PCR-detectable H1N1 after brief cutaneous air drying—14 of 20 health care workers had H1N1 detected by means of culture (mean reduction, 103–4 TCID>50/0.1 mL), whereas 6 of 20 had no viable H1N1 recovered; all 20 health care workers had similar changes in PCR test results. Marked antiviral efficacy was noted for all 4 HH protocols, on the basis of culture results (14 of 14 had no culturable H1N1; P<.002) and PCR results (P<.001; cycle threshold value range, 33.3–39.4), with SW statistically superior (P<.001) to all 3 alcohol-based hand rubs, although the actual difference was only 1–100 virus copies/µL. There was minimal reduction in H1N1 after 60 min without HH. Conclusions. HH with SW or alcohol-based hand rub is highly effective in reducing influenza A virus on human hands, although SW is the most effective intervention. Appropriate HH may be an important public health initiative to reduce pandemic and avian influenza transmission.

Background.The diagnosis of acute hepatitis C virus (HCV) infection is imprecise because antibody testing does not differentiate between acute and chronic infection. Although virologic features, such as viral load fluctuations and low levels of viremia, have been noted to be characteristic of acute HCV infection, these parameters have not been used for diagnosis. Methods.We validated the use of these novel parameters (ie, viral load fluctuations >1 log and HCV RNA levels <100,000 IU/mL) in a cohort of acute HCV seroconverters. We then applied standard diagnostic criteria for acute HCV infection in a cohort of high-risk injection drug users entering prison with suspected acute HCV infection (n=37). We subsequently assessed whether these novel virologic parameters, measured serially over a 10-week period, could enhance the diagnosis of acute infection. Results.Low-level viremia and viral load fluctuations were highly prevalent in our cohort of acute seroconverters (81% and 86%, respectively), whereas low-level viremia occurred in only 13% of control patients with chronic infection. With use of standard criteria, 37 inmates received a diagnosis of acute HCV infection. Among the 35 patients with HCV RNA detectable at baseline, we found low-level viremia to be highly prevalent (n=27; 77%); among patients with a minimum of 2 HCV RNA samples, we demonstrated viral fluctuations in more than one-third (n=9; 36%). Conclusions.The diagnosis of acute infection in HCV-seropositive patients is strengthened by the use of virologic parameters that are uncommon in chronic disease. Viral load fluctuations and low levels of HCV RNA should be incorporated into standard diagnostic criteria.

Since the advent of genetic analysis, electrode materials have played an irreplaceable role due to the easily-exploitable negatively-charged backbone of the DNA structure. Initially, the employment of electrophoretic movement lay only in the separation of DNA fragments of differing length; however, the widening utility of electrokinetic phenomena at the microscale in areas such as fluid transportation and multistep integration led researchers to capitalize further when translating processes to microfluidic or “lab-on-chip” devices. Over the following three decades, the field witnessed a plethora of ways in which the necessary voltages could be transmitted to the sample and reagents with many successes; however, additional demands were then placed on those hoping to bring their microdevices to the market place. A greater emphasis on the cost of all constituent parts along with the increased importance that fluidics be contained hermetically at all times meant groups would become more imaginative when incorporating electrode materials. This review will aim to exactly describe the evolution of how those materials have been employed in DNA-based microfluidic devices. It will focus on how developers began to explore other emerging uses and also discuss how their tactics reflected the progressive demands of their chosen industry.

In the last decade, the microfluidic community has witnessed an evolution in fabrication methodologies that deviate from using conventional glass and polymer-based materials. A leading example within this group is the print, cut and laminate (PCL) approach, which entails the laser cutting of microfluidic architecture into ink toner-laden polyester sheets, followed by the lamination of these layers for device assembly. Recent success when applying this method to human genetic fingerprinting has highlighted that it is now ripe for the refinements necessary to render it amenable to mass-manufacture. In this communication, we detail those modifications by identifying and implementing a suitable heat-sensitive adhesive (HSA) material to equip the devices with the durability and resilience required for commercialization and fieldwork. Importantly, this augmentation is achieved without sacrificing any of the characteristics which make the PCL approach attractive for prototyping. Exemplary HSA-devices performed DNA extraction, amplification and separation which, when combined, constitute the complete sequence necessary for human profiling and other DNA-based analyses.

Treatment of acute hepatitis C virus (HCV) infection leads to a sustained virologic response (SVR) in the vast majority of patients, although the clinical predictors of these favorable responses are not well understood. In chronic infection, the most potent predictor of a SVR is complete viral suppression after 4 weeks of treatment, also known as a rapid virologic response (RVR). However, few patients with HCV genotype 1 infection and high-level viremia ever achieve this benchmark. In 2 separate cohorts of patients with acute HCV infection, we demonstrate that rapid virologic clearance and low-level viremia (HCV RNA level, <400,000 IU/mL) are highly prevalent, regardless of HCV genotype

We report a case of acute hepatitis C virus infection that occurred after a traumatic altercation among prison inmates. This report has significant implications for infection control policies and procedures in prisons and jails, where the estimated prevalence of hepatitis C virus infection is ∼20 times that of the general population.

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 alíeles. These results implicate the nature of the HLA-viral peptide interaction as the major factor modulating durable control of HIV infection.

Background. Human immunodeficiency virus (HIV)–infected patients with hepatitis C virus (HCV) coinfection are at increased risk for drug-induced liver injury (DILI) compared with patients with HIV infection alone. The mechanism underlying this observation is unknown. We hypothesized that interferon (IFN) would induce biochemical improvement through its anti-inflammatory properties and thereby facilitate the reintroduction of antiretroviral therapy (ART) in patients with DILI. Methods. Patients with symptomatic DILI were referred for evaluation; biopsy of a liver sample was performed for all patients, except 1 with clinical cirrhosis. Results. Twelve patients with acquired immunodeficiency syndrome and symptomatic grade 3/4 hepatotoxicity received treatment with IFN and ribavirin (RBV). Seven of these patients had a history of recurrent DILI. The mean baseline CD4+ T cell counts and HIV RNA levels were 124 cells/mm3 and 115,369 copies/mL, respectively. Biopsies of liver samples demonstrated significant necroinflammation (mean grade, 10.3) and fibrosis (mean stage, 2.9). Three patients continued to receive ART when they began treatment with IFN-RBV; 9 reinitiated ART within an average of 12 weeks (range, 4–20 weeks) of HCV treatment initiation. All patients attained marked improvement in aminotransferases and continued to receive ART treatment during a mean follow-up regimen of 26.5 months, with subsequent virologic suppression and immunologic reconstitution (mean CD4+ cell count increase, 251/mm3). However, only 1 patient maintained HCV suppression after completion of treatment with IFN-RBV. Conclusions. In patients with symptomatic DILI, treatment with IFN-ribavirin (RBV) led to decreases in aminotransferase levels, which enabled the reinitiation of ART. The beneficial effects of IFN-based therapy may be modulated through the suppression of proinflammatory cytokines, even in virologic nonresponders. Herein, we propose a novel mechanism for DILI, whereby HCV- and HIV-associated inflammatory mediators induce liver injury synergistically.

Background. Existing severity assessment tools, such as the pneumonia severity index (PSI) and CURB-65 (tool based on confusion, urea level, respiratory rate, blood pressure, and age <65 years), predict 30-day mortality in community-acquired pneumonia (CAP) and have limited ability to predict which patients will require intensive respiratory or vasopressor support (IRVS). Methods. The Australian CAP Study (ACAPS) was a prospective study of 882 episodes in which each patient had a detailed assessment of severity features, etiology, and treatment outcomes. Multivariate logistic regression was performed to identify features at initial assessment that were associated with receipt of IRVS. These results were converted into a simple points-based severity tool that was validated in 5 external databases, totaling 7464 patients. Results. In ACAPS, 10.3% of patients received IRVS, and the 30-day mortality rate was 5.7%. The features statistically significantly associated with receipt of IRVS were low systolic blood pressure (2 points), multilobar chest radiography involvement (1 point), low albumin level (1 point), high respiratory rate (1 point), tachycardia (1 point), confusion (1 point), poor oxygenation (2 points), and low arterial pH (2 points): SMART-COP. A SMART-COP score of <3 points identified 92% of patients who received IRVS, including 84% of patients who did not need immediate admission to the intensive care unit. Accuracy was also high in the 5 validation databases. Sensitivities of PSI and CURB-65 for identifying the need for IRVS were 74% and 39%, respectively. Conclusions. SMART-COP is a simple, practical clinical tool for accurately predicting the need for IRVS that is likely to assist clinicians in determining CAP severity.