Point-of-care molecular diagnostics for the detection of group A Streptococcus in non-invasive skin and soft tissue infections: a validation study.

BACKGROUND: Skin and soft tissue infections (SSTIs) are commonly caused by group A Streptococcus (GAS). Rapid molecular assays for detecting GAS in wounds would help with clinical management. This study assessed a point-of-care system for the detection of GAS in non-severe SSTIs in a Native American community in the Southwest. METHODS: Patients presenting with a new non-severe SSTI were eligible if a swab was collected. The swab was tested by traditional culture methods and using the cobas® Liat® point-of-care (POC) system and results were compared. RESULTS: 399 samples were included. The final result from the POC assay was positive for 52.0% of samples. Compared to culture, the POC assay had a sensitivity of 100% and specificity of 99.5%. CONCLUSIONS: The cobas® Liat® system accurately and efficiently identified GAS in non-severe SSTIs. Having a POC test available to rapidly identify or rule out GAS could help to minimize overuse of antibiotics.

Interaction of SARS-CoV-2 and Other Coronavirus With ACE (Angiotensin-Converting Enzyme)-2 as Their Main Receptor: Therapeutic Implications.

Severe acute respiratory syndrome coronavirus (SARS-CoV)-2 originated from Wuhan, China, in December 2019 and rapidly spread to other areas worldwide. Since then, coronavirus disease 2019 (COVID-19) has reached pandemic proportions with >570 000 deaths globally by mid-July 2020. The magnitude of the outbreak and the potentially severe clinical course of COVID-19 has led to a burst of scientific research on this novel coronavirus and its host receptor ACE (angiotensin-converting enzyme)-2. ACE2 is a homolog of the ACE that acts on several substrates in the renin-Ang (angiotensin) system. With unprecedented speed, scientific research has solved the structure of SARS-CoV-2 and imaged its binding with the ACE2 receptor. In SARS-CoV-2 infection, the viral S (spike) protein receptor-binding domain binds to ACE2 to enter the host cell. ACE2 expression in the lungs is relatively low, but it is present in type II pneumocytes-a cell type also endowed with TMPRSS2 (transmembrane protease serine 2). This protease is critical for priming the SARS-CoV-2 S protein to complex with ACE2 and enter the cells. Herein, we review the current understanding of the interaction of SARS-CoV-2 with ACE2 as it has rapidly unfolded over the last months. While it should not be assumed that we have a complete picture of SARS-CoV-2 mechanism of infection and its interaction with ACE2, much has been learned with clear therapeutic implications. Potential therapies aimed at intercepting SARS-CoV-2 from reaching the full-length membrane-bound ACE2 receptor using soluble ACE2 protein and other potential approaches are briefly discussed as well.