ABSTRACT
One of the most effective ways to prevent the spread of the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is to develop accurate and rapid diagnostic tests. There are a number of molecular, serological, and imaging methods that are used to diagnose this infection in hospitals and clinical settings. The purpose of this review paper is to present the available approaches for detecting SARS-CoV-2 and address the advantages and limitations of each detection method. This work includes studies from recent literature publications along with information from the manufacturer's manuals of commercially available SARS-CoV-2 diagnostic products. Furthermore, supplementary information from the Food & Drug Administration (FDA), Centers for Disease Control and Prevention (CDC), and World Health Organization (WHO) is cited. The viral components targeted for virus detection, the principles of each diagnostic technique, and the detection efficiency of each approach are discussed. The potential of using diagnostic tests that were originally developed for previous epidemic viruses is also presented.
ABSTRACT
Hepatitis C virus (HCV) exploits an extensive network of host proteins to maintain chronic infection. Using RNA-Seq technology, we identified 30 host genes that were differentially expressed in cell culture grown HCV (HCVcc)-infected cells. Of these candidate genes, we selected solute carrier family 3 member 2 (SLC3A2) for further investigation. SLC3A2, also known as CD98hc, is a member of the solute carrier family and encodes a subunit of heterodimeric amino acid transporter. SLC3A2 and LAT1 constitute a heterodimeric transmembrane protein complex that catalyzes amino acid transport. In this study, we showed that HCV upregulated both mRNA and protein expression levels of SLC3A2 and this upregulation occurred through NS3/4A-mediated oxidative stress. HCV also elevated SLC3A2/LAT1 complex level and thus mammalian target of rapamycin complex 1 (mTORC1) signaling was activated. We further showed that L-leucine transport level was significantly increased in Jc1-infected cells as compared with mock-infected cells. Using RNA interference technology, we demonstrated that SLC3A2 was specifically required for the entry step but not for other stages of the HCV life cycle. These data suggest that SLC3A2 plays an important role in regulating HCV entry. Collectively, HCV exploits SLC3A2 for viral propagation and upregulation of SLC3A2 may contribute to HCV-mediated pathogenesis.
