Short and Long-Term Impact of COVID-19 Infection on Previous Respiratory Diseases

SARS-CoV-2 Neuroinvasion, Inflammatory Neurodegeneration and Alzheimer's Disease

“…There is also evidence that a syntrophic consortium of complex microorganisms together, known as biofilms, may be involved and additionally contribute to the neuropathology of AD, however the combination of SARS-CoV-2 invasion with other microbes has not been well studied (Chakravarthi and Joshi, 2021;Piekut et al, 2022;Protto et al, 2022). Importantly, all microbial infections of nervous tissues as described above contribute to the development of a microbialor viral-induced cytokine storm, a smoldering and progressive inflammatory neurodegeneration and the appearance of neurofibrillary tangles (NFT), amyloid aggregation and related amyloidogenic processes as are observed during the course of AD (Ball et al, 2013;Hosseini et al, 2021; Chidambaram et al, 2022;Chiner-Vives et al, 2022;Visco et al, 2022). Interestingly, a pre-existing diagnosis of AD predicts the highest risk for COVID-19 yet found, driving the highest mortality rate amongst any classification of aged individuals (Nagu et al, 2020;Yu et al, 2021).…”

“…id=2448b930-1451-43e4-8634-c0c16707c749; last accessed 27 May 2022; Kallet et al, 2019;Lee et al, 2021;Zuin et al, 2021;Stefanou et al, 2022;Visco et al, 2022). It has been observed that about ∼75% of hospitalized COVID-19 patients have at least one COVID-19-associated comorbidity and COVID-19 patients with underlying chronic illnesses are more likely be affected with a more adverse and unfavorable prognosis (Chiner-Vives et al, 2022;Crivelli et al, 2022;Kirtipal et al, 2022).…”

“…SARS-CoV-2 virus therefore has potential to damage almost every tissue and organ system within the body and to induce a serious multi-organ system failure involving pulmonary, cardiovascular, endocrine, hematologic, renal, gastrointestinal, dermatologic, immunological, psychiatric and/or neurological manifestations. Cholesterol, sphingolipid and other lipid levels in the blood serum and cell membrane appear to modulate viral infectivity, and persons with underlying chronic lipid-associated diseases including cardiovascular disorders, cancer, obesity, chronic lung disease, diabetes or neurological disease have the worst prognosis for COVID-19, and are the most likely to develop acute respiratory distress syndrome and lethal pneumonia (Palacios-Rápalo et al, 2021;Chidambaram et al, 2022;Chiner-Vives et al, 2022). The remarkable and extraordinary capacity of SAR-CoV-2 to attack many different kinds of human host cells simultaneously may help explain the variability in symptoms and overall general feeling of malaise reported by COVID-19 infected patients.…”

“…FIGURE 1 | COVID-19 infections may have long-term effects termed "Long COVID' or "post-COVID-19 syndrome", especially in the elderly and persons with pre-existing disease. It is also evident that persons with underlying chronic disease have the worst prognosis for COVID-19 infection and are the most likely to develop acute respiratory distress syndrome, post-COVID-19-syndrome, a chronic or lethal pneumonia and/or neurological complications (see manuscript text; Palacios-Rápalo et al, 2021;Chidambaram et al, 2022;Chiner-Vives et al, 2022;Visco et al, 2022). Interestingly, a pre-existing diagnosis of AD predicts the highest risk for COVID-19 yet found, driving the highest mortality rate amongst any classification of aged individuals(Nagu et al, 2020;Yu et al, 2021).…”

Current Understanding of Post-COVID Pulmonary Fibrosis: Where Are We?

“…Elderly, obese, smokers and diabetics, and patients that required mechanical ventilation and had severe acute respiratory distress syndrome, with high levels of C-reactive protein, D-dimer and interleukin-6 seem to have a greater risk of long-term pulmonary involvement. 7 , 8 , 9 Additionally, the hyperstimulation of the immune system associated with systemic inflammation secondary to COVID-19 can trigger autoimmune responses, with production of cytokines and autoantibodies, which may contribute to the development and progression of pulmonary parenchymal lesions. 7 , 8 Genetic predisposition, such as the identification of shortening of leucocyte telomeres, is also speculated as a potential risk factor for the occurrence of definitive pulmonary fibrosis after COVID-19.…”