Strep A: At least 30 children have died in UK since mid-September

Since 19 September, 122 people in England have died from an invasive form of the bacterial infection, UKHSA data shows.

London Ambulance Service declares 'business continuity incident'

Mucosal Immunity After Novel COVID-19 Infection – Virus-Induced Immunosuppression: Preliminary Study - BioNanoScience

In recovered COVID-19 patients, the state of mucosal immunity remains understudied. Cytological, functional, and metabolic characteristics of neutrophils and the interleukin status will help to correctly assess the need for immunorehabilitation measures. The study objective is to assess the state of mucosal immunity after COVID-19. A comprehensive study of mucosal immunity included the assessment of nasal mucosal neutrophils with the monitoring of destructive and apoptotic changes as well as examination of the functional and metabolic activity of neutrophils entering the nasal secretions. Phagocytic activity was assessed using microbial suspension of Staphylococcus aureus, as well as intracellular oxygen-dependent biocidity, the functions of capturing, absorbing, and killing pathogens. Study of the secretory component included assessment of interleukin levels (TNF-α, IL-10, IFN-γ) and the content of sCD95 (sAPO-1/FAS), membrane marker of apoptosis, in the nasal secretions. Cell wall neutrophils in recovered COVID-19 patients show enhanced destructive and apoptotic processes within the cells. Functional disorders due to inhibited phagocytosis of autoflora are recorded. Functionally defective cells are brought into the nasal secretions; they demonstrate severely inhibited oxygen-dependent biocidity, rapid depletion of reserves, incomplete phagocytosis, and limited ability to capture pathogens, which can contribute to the growth of various pathogenic viruses and bacteria. In the nasal secretions, the concentration of sCD95 (sAPO-1/FAS), the membrane marker of apoptosis, is increased. Elevated level of pro- and anti-inflammatory cytokines (TNF-α, IL-10) downregulates IFN-γ, thus directly contributing to the formation of functionally defective neutrophils. Compensatory increase in the IL-10 anti-inflammatory cytokine under the influence of SARS-CoV-2 virus proteins downregulates IFN-γ and is a cofactor of depression of intracellular biocidity of neutrophils. An increased level of the TNF-α pro-inflammatory cytokine increases apoptotic and destructive changes in neutrophils entering the nasal secretion. Virus-induced, functional, and metabolic impairment of neutrophils of the mucosal immunity system develop in recovered COVID-19 patients, thus providing a scientific rationale for immunomodulatory therapy.