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1.
Int J Environ Res Public Health ; 19(10)2022 05 17.
Article in English | MEDLINE | ID: covidwho-1862780

ABSTRACT

BACKGROUND: Antibody seroprevalence in rural communities remains poorly investigated. We compared the SARS-CoV-2 seroprevalence in two Greek communities in June and July 2021 after the end of the Delta-driven pandemic wave that started in November 2020. One community was affected worse than the other. METHODS: The SARS-CoV-2 IgG II Quant method (Architect, Abbott, IL, USA) was used for antibody testing. RESULTS: We found a high rate of SARS-CoV-2 seropositivity in both communities, approaching 77.5%. In the area with a higher burden of COVID-19, Malesina, seropositivity was achieved with vaccine-acquired and naturally acquired immunity, whereas in the low-burden context of Domokos, the high rates of seropositivity were achieved mainly with vaccination. Previously infected individuals were less likely to be vaccinated than previously uninfected adults. The antibody titers were significantly higher in previously infected, vaccinated participants than in unvaccinated ones. In total, 4% and 10% of the unvaccinated population were diagnosed seropositive for the first time while not knowing about the previous infection. Age and gender did not impact antibody titers in high- or low-burden contexts. CONCLUSIONS: Before the Omicron pandemic wave, herd immunity was reached in different contexts in Greece. Higher antibody titers were measured in infected vaccinated individuals than in infected unvaccinated ones.


Subject(s)
COVID-19 , Viral Vaccines , Adult , COVID-19/epidemiology , Greece/epidemiology , Humans , Pandemics , SARS-CoV-2 , Seroepidemiologic Studies
3.
Int J Environ Res Public Health ; 19(8)2022 04 12.
Article in English | MEDLINE | ID: covidwho-1785702

ABSTRACT

The aim of our study was to determine COVID-19 syndromic phenotypes in a data-driven manner using the survey results based on survey results from Carnegie Mellon University's Delphi Group. Monthly survey results (>1 million responders per month; 320,326 responders with a certain COVID-19 test status and disease duration <30 days were included in this study) were used sequentially in identifying and validating COVID-19 syndromic phenotypes. Logistic Regression-weighted multiple correspondence analysis (LRW-MCA) was used as a preprocessing procedure, in order to weigh and transform symptoms recorded by the survey to eigenspace coordinates, capturing a total variance of >75%. These scores, along with symptom duration, were subsequently used by the Two Step Clustering algorithm to produce symptom clusters. Post-hoc logistic regression models adjusting for age, gender, and comorbidities and confirmatory linear principal components analyses were used to further explore the data. Model creation, based on August's 66,165 included responders, was subsequently validated in data from March-December 2020. Five validated COVID-19 syndromes were identified in August: 1. Afebrile (0%), Non-Coughing (0%), Oligosymptomatic (ANCOS); 2. Febrile (100%) Multisymptomatic (FMS); 3. Afebrile (0%) Coughing (100%) Oligosymptomatic (ACOS); 4. Oligosymptomatic with additional self-described symptoms (100%; OSDS); 5. Olfaction/Gustatory Impairment Predominant (100%; OGIP). Our findings indicate that the COVID-19 spectrum may be undetectable when applying current disease definitions focusing on respiratory symptoms alone.


Subject(s)
COVID-19 , COVID-19/epidemiology , Comorbidity , Cough , Humans , Phenotype , SARS-CoV-2 , United States/epidemiology
4.
Int J Environ Res Public Health ; 19(2)2022 Jan 07.
Article in English | MEDLINE | ID: covidwho-1613788

ABSTRACT

Handgrip strength is an indirect indicator of physical fitness that is used in medical rehabilitation for its potential prognostic value. An increasing number of studies indicate that COVID-19 survivors experience impaired physical fitness for months following hospitalization. The aim of our study was to assess physical fitness indicator differences with another prevalent and hypoxia-driven disease, Obstructive Sleep Apnea Syndrome (OSAS). Our findings showed differences between post-COVID-19 and OSAS groups in cardiovascular responses, with post-COVID-19 patients exhibiting higher values for heart rate and in mean arterial blood pressure. Oxygen saturation (SpO2) was lower in post-COVID-19 patients during a six-minute walking test (6MWT), whereas the ΔSpO2 (the difference between the baseline to end of the 6MWT) was higher compared to OSAS patients. In patients of both groups, statistically significant correlations were detected between handgrip strength and distance during the 6MWT, anthropometric characteristics, and body composition parameters. In our study, COVID-19 survivors demonstrated a long-term reduction in muscle strength compared to OSAS patients. Lower handgrip strength has been independently associated with a prior COVID-19 hospitalization. The differences in muscle strength and oxygenation could be attributed to the abrupt onset of the disorder, which does not allow compensatory mechanisms to act effectively. Targeted rehabilitation focusing on such residual impairments may thus be indispensable within the setting of post-COVID-19 syndrome.


Subject(s)
COVID-19 , Sarcopenia , Sleep Apnea, Obstructive , COVID-19/complications , Hand Strength , Humans , Hypoxia , Physical Fitness , SARS-CoV-2
5.
Alzheimer's & Dementia ; 17(S6):e057752, 2021.
Article in English | Wiley | ID: covidwho-1589193

ABSTRACT

Background The aim of our study was to investigate the prevalence and associations of cognitive impairment in previously COVID-19 patients 2 months after discharge. Method Our study included previously hospitalized, consecutive COVID-19 patients with mild to moderate disease, followed up 2 months post discharge at a tertiary hospital?s outpatient clinic during May 2021. Exclusion criteria included intensive care unit admission, intubation, or a history of neurodegenerative disease and stroke prior to COVID-19. Prior to inclusion, eligible patients had provided written informed consent. The full battery of measurements in our study included demographics, medical and family history, anthropometrics, the 6-minute walk test (6MWT), the Borg Dyspnea Scale, spirometry, the Pittsburgh Sleep Quality Index (PSQI), the Epworth Sleepiness Scale (ESS), the Short Form 36 health Survey (SF-36), the Montreal Cognitive Assessment (MoCA) and the Symptom Checklist 90-R (SLC90-R), reactive oxygen metabolites (dROMs) and plasma antioxidant capacity (PAT test;FRAS5, Parma, Italy). Cognitive impairment was considered on a MoCA cutoff ≤24. Data are presented as mean ±SD or Frequencies (%). Correlations between continuous data were assessed via the Spearman?s Rho correlation coefficient, whereas associations were assessed via multiple linear regression (MLR) models. For all tests, a p-value <0.05 was considered statistically significant. Results A total of 32 subjects were included in the study (35 Male, 17 Female;Mean age of 61.6±9.4). A total of 56.2% presented with cognitive decline (CD) as indicated by a MoCA score <24. Principal component analysis revealed that short-term memory impairments and multidomain impairment without short-term memory deficits were the predominant patterns of cognitive impairment. MoCA score correlated with age (?=-0.513, p=0.003), waist circumference (?=-0.388, p=0.028) waist to hip ratio (?=-0.361, p=0.042) and SpO2 during 6MWT (1st, 4th and 6th minute;p<0.05). MLR indicated that after adjusting for age and gender, SpO2 at the 6th minute of the 6MWT was independently associated with MoCA score (Beta=0.579, p-value=0.001). Conclusion Our findings indicated that among 32 outpatient clinic subjects, 56.2% presented with cognitive decline. The associations with oxygen saturation and physical condition as detected by the 6MWT may indicate overlap with post-COVID-19 fatigue and warrants further investigation.

6.
Int J Environ Res Public Health ; 19(1)2021 Dec 31.
Article in English | MEDLINE | ID: covidwho-1580777

ABSTRACT

BACKGROUND: In this work, we aimed to evaluate antibody-response longevity to SARS-CoV-2 infection and/or vaccination in one of the Greek communities that was worst hit by the pandemic, Deskati, five months after a previous serosurveillance and nine months after the pandemic wave initiation (October 2020). METHODS: The SARS-CoV-2 IgG II Quant method (Architect, Abbott, IL, USA) was used for antibody testing. RESULTS: A total of 69 subjects, who previously tested positive or negative for COVID-19 antibodies, participated in the study. We found that 48% of participants turned positive due to vaccination. 27% of participants were both previously infected and vaccinated. However, all previously infected participants retained antibodies to the virus, irrespective of their vaccination status. The antibody titers were significantly higher in previously infected participants that had been vaccinated than those who were unvaccinated and in those that had been previously hospitalized for COVID-19 than those with mild disease. CONCLUSIONS: Antibody responses to SARS-CoV-2 infection were maintained nine months after the pandemic. Vaccination alone had generated an immune response in almost half of the population. Higher antibody titers were found in the case of vaccination in previously infected subjects and especially in those with severe disease leading to hospitalization.


Subject(s)
COVID-19 , Antibodies, Viral , Greece/epidemiology , Humans , SARS-CoV-2 , Seroepidemiologic Studies , Vaccination
7.
J Funct Morphol Kinesiol ; 6(4)2021 Dec 03.
Article in English | MEDLINE | ID: covidwho-1554987

ABSTRACT

The aim of our study was to assess the effect of 8 weeks of pulmonary rehabilitation (PR) in patients with pulmonary embolism (PE) during unsupervised PR (unSPRgroup) versus supervised PR (SPRgroup) on cardiopulmonary exercise testing (CPET) parameters, sleep quality, quality of life and cardiac biomarkers (NT-pro-BNP). Fourteen patients with PE (unSPRgroup, n = 7, vs. SPRgroup, n = 7) were included in our study (age, 50.7 ± 15.1 years; BMI, 30.0 ± 3.3 kg/m2). We recorded anthropometric characteristics and questionnaires (Quality of life (SF-36) and Pittsburg sleep quality index (PSQI)), we performed blood sampling for NT-pro-BNP measurement and underwent CPET until exhausting before and after the PR program. All patients were subjected to transthoracic echocardiography prior to PR. The SPRgroup differed in mean arterial pressure at rest before and after the PR program (87.6 ± 3.3 vs. 95.0 ± 5.5, respectively, p = 0.010). Patients showed increased levels of leg fatigue (rated after CPET) before and after PR (p = 0.043 for SPRgroup, p = 0.047 for unSPRgroup) while the two groups differed between each other (p = 0.006 for post PR score). Both groups showed increased levels in SF-36 scores (general health; p = 0.032 for SPRgroup, p = 0.010 for unSPRgroup; physical health; p = 0.009 for SPRgroup, p = 0.022 for unSPRgroup) and reduced levels in PSQI (cannot get to sleep within 30-min; p = 0.046 for SPRgroup, p = 0.007 for unSPRgroup; keep up enough enthusiasm to get things done; p = 0.005 for SPRgroup, p = 0.010 for unSPRgroup) following the PR program. The ΝT-pro-BNP was not significantly different before and after PR or between groups. PR may present a safe intervention in patients with PE. The PR results are similar in SPRgroup and unSPRgroup.

8.
EBioMedicine ; 74: 103722, 2021 Dec.
Article in English | MEDLINE | ID: covidwho-1536517

ABSTRACT

BACKGROUND: Numerous publications describe the clinical manifestations of post-acute sequelae of SARS-CoV-2 (PASC or "long COVID"), but they are difficult to integrate because of heterogeneous methods and the lack of a standard for denoting the many phenotypic manifestations. Patient-led studies are of particular importance for understanding the natural history of COVID-19, but integration is hampered because they often use different terms to describe the same symptom or condition. This significant disparity in patient versus clinical characterization motivated the proposed ontological approach to specifying manifestations, which will improve capture and integration of future long COVID studies. METHODS: The Human Phenotype Ontology (HPO) is a widely used standard for exchange and analysis of phenotypic abnormalities in human disease but has not yet been applied to the analysis of COVID-19. FUNDING: We identified 303 articles published before April 29, 2021, curated 59 relevant manuscripts that described clinical manifestations in 81 cohorts three weeks or more following acute COVID-19, and mapped 287 unique clinical findings to HPO terms. We present layperson synonyms and definitions that can be used to link patient self-report questionnaires to standard medical terminology. Long COVID clinical manifestations are not assessed consistently across studies, and most manifestations have been reported with a wide range of synonyms by different authors. Across at least 10 cohorts, authors reported 31 unique clinical features corresponding to HPO terms; the most commonly reported feature was Fatigue (median 45.1%) and the least commonly reported was Nausea (median 3.9%), but the reported percentages varied widely between studies. INTERPRETATION: Translating long COVID manifestations into computable HPO terms will improve analysis, data capture, and classification of long COVID patients. If researchers, clinicians, and patients share a common language, then studies can be compared/pooled more effectively. Furthermore, mapping lay terminology to HPO will help patients assist clinicians and researchers in creating phenotypic characterizations that are computationally accessible, thereby improving the stratification, diagnosis, and treatment of long COVID. FUNDING: U24TR002306; UL1TR001439; P30AG024832; GBMF4552; R01HG010067; UL1TR002535; K23HL128909; UL1TR002389; K99GM145411.


Subject(s)
COVID-19/complications , COVID-19/pathology , COVID-19/diagnosis , Humans , SARS-CoV-2
9.
Free Radic Biol Med ; 2020 Jul 15.
Article in English | MEDLINE | ID: covidwho-1385584

ABSTRACT

This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https://www.elsevier.com/about/our-business/policies/article-withdrawal.

12.
Infect Genet Evol ; 89: 104733, 2021 04.
Article in English | MEDLINE | ID: covidwho-1386288

ABSTRACT

OBJECTIVE: A recent study on the effects of SARS-CoV-2 infection on the host's transcriptome indicated the perturbation of several pathways associated with neurodegeneration, including but not limited to Parkinson's and Huntington's diseases. The purpose of this study was to determine overlapping pathways between iPD vs. Controls and those associated with SARS-CoV-2 infection. METHODS: Gene set enrichment analyses (GSEA) were performed on gene expression data from tissues donated by idiopathic Parkinson's disease patients (iPD). These included dorsal motor nucleus of the vagus (DMNV), substantia nigra (SN), whole blood (WB) and peripheral blood mononuclear cell samples (PBMC). Enriched pathways detected by GSEA results were subsequently compared to (a) those retrieved by two independently constructed SARS-CoV-2 - host interactomes, as well as (b) previously published pathway data. For all analyses, a false discovery rate (FDR) <0.05 was considered statistically significant. RESULTS: Analysis of iPD data revealed multiple immune response and viral parasitism -related pathways (FDR < 0.05). Head-to-head comparisons as well as confirmatory analyses revealed several pathways and gene ontology (GO) terms overlapping between iPD tissues and SARS-CoV-2 induced transcriptomic changes: "Parkinson's Disease" and "Huntington's Disease" (overlapping in DMNV, ION, SN, and WB; FDR < 0.05), "NAFLD" (overlapping in DMNV, SN, PBMC and WB; FDR < 0.05), mRNA surveillance and proteostasis pathways (All datasets; FDR < 0.5), among others. CONCLUSION: The overlap noted in this comparative transcriptomic study outlines the potential contribution of human coronaviruses in the pathogenesis of iPD. Furthermore, given SARS-CoV-2's neuroinvasive potential, closer scrutiny is warranted towards its contribution in the long-term development of neurodegenerative disease.


Subject(s)
COVID-19/virology , Parkinson Disease/virology , SARS-CoV-2/physiology , Transcriptome , Case-Control Studies , Gene Expression , Gene Ontology , Humans , Parkinson Disease/genetics
13.
Brain Disorders ; : 100022, 2021.
Article in English | ScienceDirect | ID: covidwho-1363981

ABSTRACT

Introduction (IFITM3) is an innate immune protein that has been identified as a novel γ-secretase (γs) modulator. FYN is a kinase that stabilizes IFITM3 on the membrane, primes APP for amyloidogenic γs processing and mediates tau oligomerization. The purpose of this study is to explore the role of FYN and IFITM3 in AD and COVID-19, expanding on previous research from our group. Methods A 520 gene signature containing FYN and IFITM3 (termed Ia) was extracted from a previously published meta-analysis of Alzheimer's disease (AD) bulk- and single nuclei sequencing data. Exploratory analyses involved meta-analysis of bulk and single cell RNA data for IFITM3 and FYN differential expression per CNS site and cellular type. Confirmatory analyses, gene set enrichment analysis (GSEA) on Ia was performed to detect overlapping enriched biological networks between COVID-19 with AD. Results Bulk RNA data analysis revealed that IFITM3 and FYN were overexpressed in two CNS regions in AD vs. Controls: the temporal cortex Wilcoxon p-value=1.3e-6) and the parahippocampal cortex Wilcoxon p-value=0.012). Correspondingly, single cell RNA analysis of IFITM3 and FYN revealed that it was differentially expressed in neurons, glial and endothelial cells donated b AD patients, when compared to controls. Discussion IFITM3 and FYN were found as interactors within biological networks overlapping between AD and SARS-CoV-2 infection. Within the context of SARS-CoV-2 induced tau aggregation and interactions between tau and Ab1-42, the FYN – IFITM3 regulome may outline an important innate immunity element responsive to viral infection and IFN-I signalling in both AD and COVID-19.

14.
J Pers Med ; 11(8)2021 Aug 18.
Article in English | MEDLINE | ID: covidwho-1360780

ABSTRACT

The aim of our study was to determine the impact of unsupervised Pulmonary Rehabilitation (uns-PR) on patients recovering from COVID-19, and determine its anthropometric, biological, demographic and fitness correlates. All patients (n = 20, age: 64.1 ± 9.9 years, 75% male) participated in unsupervised Pulmonary Rehabilitation program for eight weeks. We recorded anthropometric characteristics, pulmonary function parameters, while we performed 6 min walk test (6 MWT) and blood sampling for oxidative stress measurement before and after uns-PR. We observed differences before and after uns-PR during 6 MWT in hemodynamic parameters [systolic blood pressure in resting (138.7 ± 16.3 vs. 128.8 ± 8.6 mmHg, p = 0.005) and end of test (159.8 ± 13.5 vs. 152.0 ± 12.2 mmHg, p = 0.025), heart rate (5th min: 111.6 ± 16.9 vs. 105.4 ± 15.9 bpm, p = 0.049 and 6th min: 112.5 ± 18.3 vs. 106.9 ± 17.9 bpm, p = 0.039)], in oxygen saturation (4th min: 94.6 ± 2.9 vs. 95.8 ± 3.2%, p = 0.013 and 1st min of recovery: 97.8 ± 0.9 vs. 97.3 ± 0.9%), in dyspnea at the end of 6 MWT (1.3 ± 1.5 vs. 0.6 ± 0.9 score, p = 0.005), in distance (433.8 ± 102.2 vs. 519.2 ± 95.4 m, p < 0.001), in estimated O2 uptake (14.9 ± 2.4 vs. 16.9 ± 2.2 mL/min/kg, p < 0.001) in 30 s sit to stand (11.4 ± 3.2 vs. 14.1 ± 2.7 repetitions, p < 0.001)] Moreover, in plasma antioxidant capacity (2528.3 ± 303.2 vs. 2864.7 ± 574.8 U.cor., p = 0.027), in body composition parameters [body fat (32.2 ± 9.4 vs. 29.5 ± 8.2%, p = 0.003), visceral fat (14.0 ± 4.4 vs. 13.3 ± 4.2 score, p = 0.021), neck circumference (39.9 ± 3.4 vs. 37.8 ± 4.2 cm, p = 0.006) and muscle mass (30.1 ± 4.6 vs. 34.6 ± 7.4 kg, p = 0.030)] and sleep quality (6.7 ± 3.9 vs. 5.6 ± 3.3 score, p = 0.036) we observed differences before and after uns-PR. Our findings support the implementation of unsupervised pulmonary rehabilitation programs in patients following COVID-19 recovery, targeting the improvement of many aspects of long COVID-19 syndrome.

15.
J Pers Med ; 11(6)2021 May 23.
Article in English | MEDLINE | ID: covidwho-1244056

ABSTRACT

The fast-spreading coronavirus disease 2019 (COVID-19) pandemic forced countries to apply restrictive measures to counteract it. School closure was quickly adopted by health authorities. We aimed to investigate the compliance of children aged 4 to 12 years with the COVID-19 lockdown restrictions and evaluate the impact of school closure on the children's educational, social, economic, and psychological outcomes. An online survey was distributed through a social networking platform to parents of pre-primary and primary school-age children. The study period was defined as from 27 November 2020 to 3 December 2020, two weeks after the school closure due to the general lockdown in Greece. This study showed that the school units were well-informed and complied with the protection measures against COVID-19. The pupils quickly adopted the protection measures, even those whose parents suggested masks were less effective. The quarantine-forced school closure highly impacted primary school children's physical activity, quality of sleep, psychological status, eating habits, academic performance, and household income. Web use showed an increase, with the children over-spending extracurricular time in web activities. Our study highlights the need for long term monitoring of these aforementioned indices, and the development of COVID-19 mitigation measures that carefully incorporate effectiveness and societal impact.

16.
Brain Behav Immun Health ; 14: 100243, 2021 Jul.
Article in English | MEDLINE | ID: covidwho-1157140

ABSTRACT

BACKGROUND: IFITM3 is a viral restriction protein that enables sequestration of viral particles and subsequent trafficking to lysosomes. Recently, IFITM3 upregulation was found to induce gamma - secretase activity and the production of amyloid beta. The purpose of this study was to determine whether dysregulation of IFITM3-dependent pathways was present in neurons and peripheral immune cells donated by AD patients. As a secondary aim, we sought to determine whether these perturbations could be induced by viruses, including SARS-CoV-2. METHODS: Gene set enrichment analyses (GSEA) previously performed on publicly available transcriptomic data from tissues donated by AD patients were screened for enriched pathways containing IFITM3. Subsequently, signature containing IFITM3, derived from entorhinal cortex (EC) neurons containing neurofibrillary tangles (NFT) was screened for overlap with curated, publicly available, viral infection-induced gene signatures (including SARS-CoV-2). RESULTS: GSEA determined that IFITM3 gene networks are significantly enriched both in CNS sites (entorhinal and hippocampal cortices) and in peripheral blood mononuclear cells (PBMCs) donated by AD patients. Overlap screening revealed that IFITM3 signatures are induced by several viruses, including SARS-CoV, MERS-CoV, SARS-CoV-2 and HIV-1 (adjusted p-value <0.001; Enrichr Database). DISCUSSION: A data-driven analysis of AD tissues revealed IFITM3 gene signatures both in the CNS and in peripheral immune cells. GSEA revealed that an IFITM3 derived gene signature extracted from EC/NFT neurons overlapped with those extracted from publicly available viral infection datasets, including SARS-CoV-2. Our results are in line with currently emerging evidence on IFITM3's role in AD, and SARS-CoV-2's potential contribution in the setting of an expanded antimicrobial protection hypothesis.

17.
Med Hypotheses ; 147: 110475, 2021 Feb.
Article in English | MEDLINE | ID: covidwho-988867

ABSTRACT

Coagulopathy has recently been recognized as a recurring complication of COVID-19, most typically associated with critical illness. There are epidemiological, mechanistic and transcriptomic evidence that link Selenium with SARS-CoV-2's intracellular latency. Taking into consideration the vital role of selenoproteins in maintaining an adequate immune response, endothelial homeostasis and a non-prothrombotic platelet activation status, we propose that impairment in selenocysteine synthesis, via perturbations in the aforementioned physiological functions, potentially constitutes a mechanism of coagulopathy in COVID 19 patients other than those developed in critical illness.


Subject(s)
Blood Coagulation Disorders/complications , COVID-19/complications , SARS-CoV-2/pathogenicity , Selenocysteine/biosynthesis , Blood Coagulation Disorders/virology , Blood Platelets/metabolism , Critical Illness , Endothelium, Vascular/metabolism , Homeostasis , Humans , Immune System , Inflammation , Models, Theoretical , Oxidative Stress , Platelet Activation , Selenium/chemistry , Selenocysteine/chemistry , Transcriptome
18.
Infect Genet Evol ; 86: 104602, 2020 12.
Article in English | MEDLINE | ID: covidwho-899330

ABSTRACT

BACKGROUND: SARS-CoV-2 coinfection with other viral and bacterial pathogens and their interactions are increasingly recognized in the literature as potential determinants of COVID-19 phenotypes. The aim of this study was to determine infection induced, host transcriptomic overlap between SARS-CoV-2 and other pathogens. MATERIALS AND METHODS: SARS-CoV-2 infection induced gene expression data were used for gene set enrichment analysis (GSEA) via the Enrichr platform. GSEA compared the extracted signature to VirusMINT, Virus and Microbe perturbations from Gene Expression Omnibus (GEO) in order to detect overlap with other pathogen induced host gene signatures. For all analyses, a false discovery rate (FDR) <0.05 was considered statistically significant. RESULTS: GSEA via Enrichr revealed several significantly enriched sub-signatures associated with HSV1, EBV, HIV1, IAV, RSV, P.Aeruginosa, Staph. Aureus and Strep. Pneumoniae infections, among other pathogens (FDR < 0.05). These signatures were detected in at least 6 infection-induced transcriptomic studies from GEO and involved both bronchial epithelial and peripheral blood immune cells. DISCUSSION: SARS-CoV-2 infection may function synergistically with other viral and bacterial pathogens at the transcriptomic level. Notably, several meta-analyses of COVID-19 cohorts have furthermore corroborated viral and bacterial pathogens reported herein as coinfections with SARS-CoV-2. The identification of common, perturbed gene networks outlines a common host targetome for these pathogens, and furthermore provides candidates for biomarker discovery and drug design.


Subject(s)
COVID-19 , Host-Pathogen Interactions/genetics , SARS-CoV-2/pathogenicity , Transcriptome , Virus Diseases , COVID-19/genetics , COVID-19/metabolism , COVID-19/virology , Cells, Cultured , Coinfection , Computer Simulation , Humans , Systems Biology , Transcriptome/genetics , Transcriptome/physiology , Virus Diseases/genetics , Virus Diseases/metabolism , Virus Diseases/virology , Viruses/pathogenicity
19.
Med Hypotheses ; 144: 110275, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-773391

ABSTRACT

There is a growing body of evidence on the significance of interactions between comorbidities, their treatments and COVID-19 clinical phenotypes. The hypothesis explored herein is that pharmaceutical compounds currently in use are affecting COVID-19 susceptibility and phenotypes by overlapping transcriptional networks. Using two distinct SARS-CoV-2 - host interactomes, gene set enrichment analysis is used to discover compounds and assorted gene signatures derived from SARS-CoV-2 interactomes. Micronutrients, antiplatelets, ACE2 inhibitors, NSAIDs, corticosteroids and tyrosine kinase inhibitors are among the compounds discovered. Considering the implication of their associated comorbidities such as diabetes and cardiovascular disease that are associated with severe COVID-19, this study outlines the need to consider specific compounds as modulators of the observed COVID-19 spectrum. Furthermore, given that micronutrient trafficking may be targeted by viral processes, and display synergism with other enriched compounds, such as statins, studies assessing their levels prior and during infection are more than warranted.


Subject(s)
COVID-19/physiopathology , COVID-19/virology , Host-Pathogen Interactions , SARS-CoV-2/drug effects , Angiotensin-Converting Enzyme 2/metabolism , Antiviral Agents/therapeutic use , Disease Susceptibility , Gene Expression Regulation, Viral , Humans , Immune System , Inflammation , Micronutrients , Models, Biological , Models, Theoretical , Phenotype , SARS-CoV-2/genetics , Transcription, Genetic
20.
Med Hypotheses ; 144: 110212, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-733695

ABSTRACT

SARS-CoV-2 neurotropism has been increasingly recognized by its imaging and syndromic manifestations in the literature. The purpose of this report is to explore the limited yet salient current evidence that SARS-CoV-2's host genomic targets PTBP1 and the 14-3-3 protein isoform encoding genes YWHAE and YWHAZ may be hold the key to understanding how neurotropism triggers neurodegeneration and how it may contribute to the onset of neurodegenerative disease. Considering that PTBP1 silencing in particular has recently been shown to reverse clinical parkinsonism and induce neurogenesis, as well as the known interactions of PTBP1 and YWHAE/Z with coronaviruses - most notably 14-3-3 and SARS-CoV, recent studies reinvigorate the infectious etiology hypotheses on major neurodegenerative disease such as AD and iPD. Considering that human coronaviruses with definite neurotropism have been shown to achieve long-term latency within the mammalian CNS as a result of specific accommodating mutations, the corroboration of genomic-level evidence with neuroimaging has vast potential implications for neurodegenerative disease.


Subject(s)
14-3-3 Proteins/genetics , COVID-19/complications , COVID-19/genetics , Heterogeneous-Nuclear Ribonucleoproteins/genetics , Neurodegenerative Diseases/etiology , Neurodegenerative Diseases/genetics , Polypyrimidine Tract-Binding Protein/genetics , COVID-19/virology , Gene Expression Regulation , Host Microbial Interactions/genetics , Humans , Models, Neurological , Nerve Degeneration/etiology , Nerve Degeneration/genetics , Pandemics , SARS-CoV-2/pathogenicity
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