Point-of-care (POC) diagnostic testing platforms are a growing sector of the healthcare industry as they offer the advantages of rapid provision of results, ease of use, reduced cost, and the ability to link patients to care. While many POC tests are based on chromatographic flow assay technology, this technology suffers from a lack of sensitivity along with limited capacity for multiplexing and quantitative analysis. Several recent reports have begun to investigate the feasibility of coupling chromatographic flow platforms to more advanced read-out technologies which in turn enable on-site acquisition, storage, and transmission of important healthcare metrics. One such technology being explored is surface-enhanced Raman spectroscopy or SERS. In this work, SERS is coupled for the first time to a rapid vertical flow (RVF) immunotechnology for detection of anti-HCV antibodies in an effort to extend the capabilities of this commercially available diagnostic platform. High-quality and reproducible SERS spectra were obtained using reporter-modified gold nanoparticles (AuNPs). Serial dilution studies indicate that the coupling of SERS with RVF technology shows enormous potential for next-generation POC diagnostics.
Aims:To evaluate the anti-hepatitis B virus (anti-HBV) effects and mechanisms of recombinant human serum albumin-interferon-α-2b fusion protein (rHSA-IFNα-2b) in vitro and in vivo. Methods: The inhibiting effects on HBV replication were examined in the HepG2 2.2.15 cell line and in ducks, and the expressions of signal transducers and transactivator 1 (STAT1), IFN-stimulated gene factor 3 (ISGF3) and 2′,5′-oligoadenylate synthetase 1 (OAS1) were investigated by the reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis. Results: In vitro,at concentrations from 0.075 to 1.2 nmol/l, rHSA-IFNα-2b inhibited the releases of extracellular hepatitis B surface antigen, hepatitis B e antigen and HBV DNA in a dose-dependent manner; rHSA- IFNα-2b also increased the levels of STAT1, ISGF3 and OAS1. In vivo, rHSA-IFNα-2b reduced the levels of alanine aminotransferase, aspartate aminotransferase, total bilirubin and duck hepatitis B virus (DHBV) DNA in the sera of DHBV-infected ducks. Conclusions:We provide the first evidence that rHSA-IFNα-2b significantly inhibits HBV replication in HepG2 2.2.15 cells and in ducks, and that the antiviral effect of rHSA-IFNα-2b in vivo is more potent than that of IFNα-2b. The anti-HBV mechanism probably operates by triggering the JAK-STAT signaling pathway and increasing the expression of OAS1.
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