Comparison of SARS-CoV-2 detection with the Cobas® 6800/8800 system on gargle samples using two sample processing methods with combined oropharyngeal/nasopharyngeal swab.

BACKGROUND: Gargle samples have been proposed as a noninvasive method for detection of SARS-CoV-2 RNA. The clinical performance of gargle specimens diluted in Cobas® PCR Media and in Cobas® Omni Lysis Reagent was compared to oropharyngeal/nasopharyngeal swab (ONPS) for the detection of SARS-CoV-2 RNA. STUDY DESIGN: Participants were recruited prospectively in two COVID-19 screening clinics. In addition to the ONPS, participants gargled with 5 ml of natural spring water split in the laboratory as follows: 1 ml was added to 4.3 ml of polymerase chain reaction (PCR) media and 400 µl was added to 200 µl of lysis buffer. Testing was performed with the Cobas® SARS-CoV-2 test on the Cobas® 6800 or 8800 platforms. RESULTS: Overall, 134/647 (20.7%) participants were considered infected because the ONPS or at least one gargle test was positive. ONPS had, respectively, a sensitivity of 96.3% (95% confidence interval [CI]: 91.3-98.5); both gargle processing methods were slightly less but equally sensitive (90.3% [95% CI: 83.9-94.3]). When ONPS and gargle specimens were both positive, the mean cycle threshold (Ct ) was significantly higher for gargles, suggesting lower viral loads. CONCLUSION: Gargle specimens directly added in PCR Media provide a similar clinical sensitivity to chemical lysis, both having a slightly, not significantly, lower sensitivity to ONPS.

Molecular Regulation of Cellular Senescence by MicroRNAs: Implications in Cancer and Age-Related Diseases.

Cellular senescence is a tumor suppressor response that acts as a barrier to cancer development and progression. In normal cells, diverse stimuli, including excessive mitogenic signaling, DNA damage or telomere shortening, trigger a senescence response characterized by stable growth arrest. Cellular senescence is orchestrated by tumor suppressor pathways, which have to be inactivated in order to impair the establishment of senescence and promote cancer. Consequently, by overcoming or bypassing this cellular response, cancer cells evade cell cycle checkpoint control leading to genomic instability and uncontrolled proliferation. MicroRNAs (MiRs) have emerged as essential factors contributing to or preventing cellular senescence. Here we detail the molecular mechanisms underlying the fine-tuning of cellular senescence signals by MiRs, and how the senescence response itself contributes to modulation of MiR expression, with a special focus on cancer and pathologies associated with aging.