ABSTRACT
The Covid-19 pandemic has provided a major innovative thrust to public services regarding their digitization to continue providing an effective response to the population's needs and to reduce management costs. However, there has been a partial lack of those welfare policies that can provide an adequate response to the elderly segment of the population, which is most affected by the introduction of new technologies into the public sphere. This study analyses the digital gap in health in the elderly living in remote areas of Italy and investigates the use of digital devices for health purposes. It compares the use of digital solutions for health with people's common digital competencies and their willingness to use them. A descriptive analysis of the sample was constructed to verify the different responses of the elderly by age, gender, educational qualification, and geographic area. Furthermore, regression analyses have been conducted to test whether there is any dependent effect among the elderly's characteristics or geographic areas. The results highlight the existence of a potential digital health gap among the elderly in remote areas of Italy both due to infrastructural issues and the lack of digital skills. The latter are positively correlated with educational qualification, such that it is also possible to highlight differences between age groups analysed and shape future welfare policies to reduce digital inequality.
Subject(s)
COVID-19 , Humans , Aged , COVID-19/epidemiology , Pandemics , Italy/epidemiology , Policy , Costs and Cost AnalysisABSTRACT
Identifying human proteins that interact with SARS-CoV-2 genome is important to understand its replication and to identify therapeutic strategies. Recent studies have unveiled protein interactions of SARS-COV-2 in different cell lines and through a number of high-throughput approaches. Here, we carried out a comparative analysis of four experimental and one computational studies to characterize the interactions of SARS-CoV-2 genomic RNA. Although hundreds of interactors have been identified, only twenty-one appear in all the experiments and show a strong propensity to bind. This set of interactors includes stress granule forming proteins, pre-mRNA regulators and elements involved in the replication process. Our calculations indicate that DDX3X and several editases bind the 5' end of SARS-CoV-2, a regulatory region previously reported to attract a large number of proteins. The small overlap among experimental datasets suggests that SARS-CoV-2 genome establishes stable interactions only with few interactors, while many proteins bind less tightly. In analogy to what has been previously reported for Xist non-coding RNA, we propose a mechanism of phase separation through which SARS-CoV-2 progressively sequesters human proteins hijacking the host immune response.
ABSTRACT
Specific elements of viral genomes regulate interactions within host cells. Here, we calculated the secondary structure content of >2000 coronaviruses and computed >100 000 human protein interactions with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The genomic regions display different degrees of conservation. SARS-CoV-2 domain encompassing nucleotides 22 500-23 000 is conserved both at the sequence and structural level. The regions upstream and downstream, however, vary significantly. This part of the viral sequence codes for the Spike S protein that interacts with the human receptor angiotensin-converting enzyme 2 (ACE2). Thus, variability of Spike S is connected to different levels of viral entry in human cells within the population. Our predictions indicate that the 5' end of SARS-CoV-2 is highly structured and interacts with several human proteins. The binding proteins are involved in viral RNA processing, include double-stranded RNA specific editases and ATP-dependent RNA-helicases and have strong propensity to form stress granules and phase-separated assemblies. We propose that these proteins, also implicated in viral infections such as HIV, are selectively recruited by SARS-CoV-2 genome to alter transcriptional and post-transcriptional regulation of host cells and to promote viral replication.