Idiopathic pulmonary fibrosis (IPF) is the most common and most lethal type of idiopathic interstitial pneumonia. It is a chronic, aging-associated lung disease characterized by fibrotic foci and inflammatory infiltrates, with no cure and very limited therapeutic options. Although its etiology is unknown, several pathogenic pathways have been described that could explain this process, involving aging, environmental factors, genomic instability, loss of proteostasis, telomere attrition, epigenetic changes, mitochondrial dysfunction, cell senescence, and altered intercellular communication. One of the main prognostic factors for the development of IPF in broad epidemiological studies is age. The incidence increases with age, making this a disease that predominantly affects the elderly population, being exceptional under 45 years of age. However, the degree to which each of these mechanisms is involved in the etiology of the uncontrolled fibrogenesis that defines IPF is still unknown. Clarifying these questions is crucial to the development of points of intervention in the pathogenesis of the disease. This review briefly summarizes what is known about each possible etiological factor, and the questions that most urgently need to be addressed.

This is the first case of a patient taking aprepitant for a post‐acute COVID‐19 syndrome. This case may encourage researchers to look for the evidence for the efficacy and safety of a neurokinin 1 receptor antagonist in this frequent syndrome.

The study of the interaction between the SARS-CoV-2 spike protein and the angiotensin-converting enzyme 2 (ACE2) receptor is key to understanding binding affinity and stability. In the present report, we sought to investigate the differences between two already sequenced genome variants (Spanish and British) of SARS-CoV-2. Methods: In silico model evaluating the homology, identity and similarity in the genome sequence and the structure and alignment of the predictive spike by computational docking methods. Results: The identity results between the Spanish and British variants of the Spike protein were 28.67%. This close correspondence in the results between the Spanish and British SARS-CoV-2 variants shows that they are very similar (99.99%). The alignment obtained results in four deletions. There were 23 nucleotide substitutions also predicted which could affect the functionality of the proteins produced from this sequence. The interaction between the binding receptor domain from the spike protein and the ACE2 receptor produces some of the mutations found and, therefore, the energy of this ligand varies. However, the estimated antigenicity of the British variant is higher than its Spanish counterpart. Conclusions: Our results indicate that minimal mutations could interfere in the infectivity of the virus due to changes in the fitness between host cell recognition and interaction proteins. In particular, the N501Y substitution, situated in the RBD of the spike of the British variant, might be the reason for its extraordinary infective potential.

BACKGROUND Initial post SARS-CoV-2 (COVID-19) infection studies have demonstrated the presence of short- and medium-term functional and radiological pulmonary sequelae. Although some studies suggest that changes remain stable, there are already published data on radiological fibrotic - like progression. It is possible that fibrotic changes occur in a context of virus-mediated profibrotic biological activity. OBJECTIVE To describe the presence and progression of long-term (5-year) post-COVID pulmonary sequelae. METHODS This is an observational, prospective, multicenter and extension study based on an original cohort (COVID FIBROTIC, clinicaltrials.gov NCT04409275, patients admitted for bilateral COVID-19 pneumonia between March and June 2020) 5 years after the event. During the outreach visit, a clinical and functional assessment will be performed. Patients who have persistent radiological lesions at the end of the COVID FIBROTIC protocol, will undergo a computed tomography (CT) scan. In addition, in those centers with biobank availability, serum samples will be taken for the analysis of fibrosis biomarkers (metalloproteinase [MMP] 1, MMP7, periostin and KL-6). RESULTS This is the description of the design for an original study currently in progress. We have not yet received the results. CONCLUSIONS The results of the study are likely to provide a detailed description of the long-term evolution of persistent functional, clinical, and radiological sequelae following COVID-19, as well as the possible biological factors involved in their development. CLINICALTRIAL Extension study from clinicaltrials.gov NCT04409275