Lessons learned from the COVID-19 pandemic for improved influenza control.

The World Health Organization noted that COVID-19 vaccination programmes could be leveraged to deliver influenza vaccination. In 2008, the International Federation of Pharmaceutical Manufacturers and Associations' (IFPMA) Influenza Vaccine Supply International Task Force (IVS) developed a survey method using the number of influenza vaccine doses distributed globally to estimate vaccination coverage rates. Seven hundred and ninety-seven million doses were distributed in 2021, representing a 205% increase over the 262 million doses distributed in 2004, exceeding the number of doses distributed during and after the 2009-2010 influenza pandemic. The most obvious explanation for the global increase is the enabling of critical elements of the vaccine ecosystem by decision-makers during the COVID-19 pandemic to reinforce implementation of influenza vaccination programs. Most of the improvements in performance of influenza programs during the COVID-19 pandemic can be classified in four categories: 1) promoting vaccination using tailored approaches for specific populations; 2) improving convenient access to influenza vaccines in COVID-safe settings; 3) improving reimbursement of seasonal influenza vaccination for priority groups; 4) maintaining the timing of vaccination to the autumn. In spite of the increase in rates of seasonal influenza vaccines distributed during the COVID-19 pandemic, globally, the rate of influenza dose distribution is sub-optimal, and a considerable proportion of the influenza infections remains preventable. To sustain the benefits from increased uptake of influenza vaccines, governments need to sustain the efforts made during the COVID-19 pandemic, and a number of global policy endeavours should be undertaken, including developing a clear global roadmap for achieving influenza control objectives, adopted by a WHA resolution, in line with the strategic objective 3 of the Global Influenza Strategy 2030, embedded in the Immunization Agenda 2030 (IA2030).

Ketamine stimulates secretion of beta-endorphin from a mouse pituitary cell line.

BACKGROUND AND OBJECTIVES: beta-endorphin is an endogenous opioid that mediates pain-induced analgesia. Propofol inhibits in vitro secretion of beta-endorphin from a mouse pituitary cell line (AtT-20). We hypothesized that ketamine would also alter secretion of beta-endorphin. METHODS: AtT-20 cells were exposed to the intravenous anesthetic ketamine (10 to 40 micromol/L). Secretion of beta-endorphin was determined by enzyme-linked immunosorbent assay. Long-term effects were determined by exposing the cells to ketamine, allowing the cells to recover overnight, then stimulating the secretion of beta-endorphin. AtT-20 cells were stimulated with secretagogues to induce secretion of beta-endorphin. The effect of ketamine on stimulated secretion was determined. Cultures of AtT-20 cells were grown for 5 days in the presence of ketamine. Cell numbers were determined on each day. RESULTS: Ketamine increased secretion of beta-endorphin to levels that were up to 3 times greater than baseline secretion. Stimulation of beta-endorphin secretion by ketamine persisted into the subsequent day. Ketamine caused increased secretion from cells stimulated with secretagogues. Ketamine was not toxic to these cells; AtT-20 cells grew normally for 5 days in the presence of up to 40 micromol/L ketamine. CONCLUSIONS: Clinically relevant concentrations of ketamine stimulated both immediate and delayed secretion of beta-endorphin. This suggests that the prolonged analgesia observed in some clinical situations with ketamine could be in part caused by increased release of an endogenous opioid.