Editorial: Long- and post-COVID syndromes: immune mechanisms and therapeutic strategies
Long-term coronavirus disease (long-COVID) is an umbrella term that, according to the UK's National Institute for Health and Care Excellence, encompasses the debilitating effects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection lasting 4 to 12 weeks and 12 weeks or more, not explained by an alternative diagnosis; in the latter case, the term post-COVID syndrome can be adopted as a synonym (1). It is therefore a post-acute infection syndrome sharing similarities with post-Ebola syndrome and others (2). More rarely, it can also occur after the anti-SARS-CoV-2 vaccination (Limongelli et al.), although vaccination usually offers some protection against long-COVID (Guimarães et al.). Risk factors include, but are not limited to, female sex, older age, obesity, smoking (Alshammari et al.), concomitant respiratory diseases (asthma and chronic obstructive pulmonary disease), more severe infection at onset, and mental health problems (3,4). Common symptoms are represented by fatigue, myalgia, post-exertional malaise or dyspnea, chest pain, palpitations, cognitive and memory impairment ("brain fog"), initial loss of smell and taste, sleep disorders, headaches, depression and anxiety (Escrivá et al.). There is therefore an overlap in symptoms with myalgic encephalomyelitis/chronic fatigue syndrome, and patients report significant impairments in daily life and work ability, accompanied by a high psychological burden (Uecker et al.). As of 2025, the prevalence of long-COVID is estimated to be around 7% in adults and 1% in children having had COVID-19 (5); in practice, over 400 million people worldwide have experienced long-COVID in their lifetime (5). Various mechanisms play a role in the pathogenesis of long-COVID, including organ damage (4), endothelial dysfunction and blood clotting (6), persistent infection or reactivation of latent viruses (7), autoimmunity