Simple Saliva Sample Collection for the Detection of SARS-CoV-2 Variants Compared With Nasopharyngeal Swab Sample.

CONTEXT.­: The use of saliva samples for diagnosis of SARS-CoV-2 infection offers several advantages, including ease of sample collection, feasibility of self-collection, and minimization of medical staff exposure to infection. The emergence of new SARS-CoV-2 variants has had an impact on the viral load of specimens and the results of real-time reverse transcription-polymerase chain reaction (rRT-PCR). OBJECTIVE.­: To compare nasopharyngeal swab and saliva samples for the diagnosis of SARS-CoV-2 using rRT-PCR. DESIGN.­: In this study, participants were recruited prospectively, and paired nasopharyngeal swab and saliva samples were collected simultaneously from each participant. After adding universal transport medium, RNA was extracted in an identical manner for both sample types, and samples were tested using rRT-PCR. In addition, samples with positive results were tested for SARS-CoV-2 variants. RESULTS.­: Of the 338 paired samples, 100 nasopharyngeal swab and 101 saliva samples tested positive for SARS-CoV-2. The rRT-PCR results of the saliva and nasopharyngeal swab samples showed a positive percent agreement of 95.0% (95% CI, 88.7%-98.4%), a negative percent agreement of 97.9% (95% CI, 95.2%-99.3%), and an overall percent agreement of 96.8% (95% CI, 94.3%-98.4%). SARS-CoV-2 was detected in the saliva samples of 6 participants with negative nasopharyngeal sample results. In addition, the sensitivity of saliva samples was similar to that of nasopharyngeal samples for detecting various SARS-CoV-2 variants, including the Omicron variant. CONCLUSIONS.­: Saliva samples can be used as an alternative to nasopharyngeal samples for convenient and effective detection of various SARS-CoV-2 variants.

Hepatocystin contributes to interferon-mediated antiviral response to hepatitis B virus by regulating hepatocyte nuclear factor 4α.

Hepatocystin/80K-H is known as a causative gene for autosomal dominant polycystic liver disease. However, the role of hepatocystin in hepatitis B virus-related liver disease remains unknown. Here, we investigated the role of hepatocystin on the cytokine-mediated antiviral response against hepatitis B virus infection. We investigated the antiviral effect and mechanism of hepatocystin by ectopic expression and RNAi knockdown in cell culture and mouse livers. Hepatocystin suppressed the replication of hepatitis B virus both in vitro and in vivo. This inhibitory effect was HBx-independent and mediated by the transcriptional regulation of viral genome via the activation of exogenous signal-regulated kinase 1/2 and the reduced expression of hepatocyte nuclear factor 4α, a transcription factor essential for hepatitis B virus replication. The amino-terminal region of hepatocystin was essential for regulation of this antiviral signaling pathway. We also found that hepatocystin acts as a critical component in interferon-mediated mitogen-activated protein kinase signaling pathway, and the interferon-induced antiviral activity against hepatitis B virus is associated with the expression levels of hepatocystin. We demonstrated that hepatocystin plays a critical role in modulating the susceptibility of hepatitis B virus to interferon, suggesting that the modulation of hepatocystin expression is important for cytokine-mediated viral clearance during hepatitis B virus infection.