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SARSNTdb offers a curated, nucleotide-centric database for users of varying levels of SARS-CoV-2 knowledge. Its user-friendly interface enables querying coding regions and coordinate intervals to find out the various functional and selective constraints that act upon the corresponding nucleotides and amino acids. Users can easily obtain information about viral genes and proteins, functional domains, repeats, secondary structure formation, intragenomic interactions, and mutation prevalence. Currently, many databases are focused on the phylogeny and amino acid substitutions, mainly in the spike protein. We took a novel, more nucleotide-focused approach as RNA does more than just code for proteins and many insights can be gleaned from its study. For example, RNA-targeted drug therapies for SARS-CoV-2 are currently being developed and it is essential to understand the features only visible at that level. This database enables the user to identify regions that are more prone to forming secondary structures that drugs can target. SARSNTdb also provides illustrative mutation data from a subset of ~25,000 patient samples with a reliable read coverage across the whole genome (from different locations and time points in the pandemic. Finally, the database allows for comparing SARS-CoV-2 and SARS-CoV domains and sequences. SARSNTdb can serve the research community by being a curated repository for information that gives a jump start to analyze a mutation’s effect far beyond just determining synonymous/non-synonymous substitutions in protein sequences. 

Abstract There is still a significant lack of knowledge regarding many aspects of the etiopathology and consequences of the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection in humans. For example, the variety of molecular mechanisms mediating this infection, and the long‐term consequences of the disease remain poorly understood. It first seemed like the SARS‐CoV‐2 infection primarily caused a serious respiratory syndrome. However, over the last years, an increasing number of studies also pointed towards the damaging effects of this infection has on the central nervous system (CNS). In fact, evidence suggests a possible disruption of the blood–brain barrier and deleterious effects on the CNS, especially in patients who already suffer from other pathologies, such as neurodegenerative disorders. The molecular mechanisms behind these effects on the CNS could involve the dysregulation of mitochondrial physiology, a well‐known early marker of neurodegeneration and a hallmark of aging. Moreover, mitochondria are involved in the activation of the inflammatory response, which has also been broadly described in the CNS in COVID‐19. Here, we critically review the current bibliography regarding the presence of neurodegenerative symptoms in COVID‐19 patients, with a special emphasis on the mitochondrial mechanisms of these disorders.