COVID-19 Countermeasures: An Algorithm to Stay Unlocked.

We describe a visual algorithm to help prevent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) contagion as well as manage COVID-19 disease according to categories of clinical severity. The algorithm is timely, with multiple countries worldwide declaring repeat surges in SARS-CoV-2 infections following the easing of lockdown measures. Its flowchart assimilates key effective interventions in a visual manner that will assist healthcare workers to manage COVID-19 disease algorithmically, and policymakers to suppress further SARS-CoV-2 waves. Importantly, we include the innovative use of topical p-menthane-3,8-diol spray by the British Army for COVID-19 Support Force personnel, which in light of its coronavirucidal properties, deserves wider dissemination. This algorithm has the potential to be updated as numerous studies are concluded globally.

Adenoid-derived TH2 cells reactive to allergen and recall antigen express CC chemokine receptor 4.

BACKGROUND: Interrupting recruitment of allergen-specific T(H)2 cells to the airway is an attractive potential therapeutic strategy for allergic disease. CC chemokine receptor 4 (CCR4) is preferentially expressed on T(H)2 cells, and CCR4-expressing cells have been described at sites of allergic inflammation. However, whether selective recruitment of allergen-specific T(H)2 cells to the airways occurs through CCR4 or other chemokine receptors remains controversial. OBJECTIVE: We investigated the expression of the T(H)2-associated chemokine receptors (CCR3, CCR4, and CCR8) by primary antigen-specific human airway T(H)2 cells. METHODS: Children undergoing elective adenoidectomy were recruited, and their atopic status was determined. Adenoid cells were cultured with allergen or recall antigen. Flow cytometric analyses permitted identification of T(H) cells proliferating in response to antigen and characterization of chemokine receptor and cytokine expression. RESULTS: An increased proportion of airway CD4(+) T cells proliferated to allergen in atopic children (n = 6, of which 4 were given diagnoses of asthma or rhinitis) compared with nonatopic children (P =.0004). These cells were 44.7% (32.6% to 50.0%) IL-4(+) and only 2.5% (0.6% to 3.3%) IFN-(gamma) and showed a greater than 5-fold upregulation of CCR4 expression to 54.0% (40.7% to 67.8%) after culture, whereas CCR3 was expressed on 9.7% (7.4% to 18.9%) of allergen-reactive cells and CCR8 on less than 1%. Interestingly, increased expansion of recall antigen-specific cells was also seen in atopic children, and these cells were also predominantly of a T(H)2 CCR4(+) phenotype. CONCLUSION: We conclude that airway allergen-specific T(H)2 cells are CCR4(+), but in the atopic child CCR4 does not distinguish between recall antigen and allergen specificity.