scholarly journals Involvement of Oxidative Stress and the Innate Immune System in SARS-CoV-2 Infection

Diseases ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 17
Author(s):  
Evgenii M. Kozlov ◽  
Ekaterina Ivanova ◽  
Andrey V. Grechko ◽  
Wei-Kai Wu ◽  
Antonina V. Starodubova ◽  
...  

The emergence of the novel coronavirus in December 2019 in China marked the beginning of a pandemic that impacted healthcare systems and economic life all over the world. The virus primarily targets the respiratory system causing severe acute respiratory syndrome (SARS) in some patients, and therefore received the name of SARS-CoV-2. The pathogen stands out among other coronaviruses by its rapid transmission from human to human, with the majority of infected individuals being asymptomatic or presenting with only minor illness, therefore facilitating the pathogen spread. At the same time, people from the risk groups, such as the elderly, patients suffering from chronic diseases, or obese individuals, have increased chances of developing a severe or even fatal disease. The search for risk factors explaining this phenomenon continues. In this review, we focus on the known mechanisms of SARS-CoV-2 infection affecting the functioning of the immune system and discuss potential risk factors responsible for the severe disease course. Oxidative stress is one of such factors, which plays a prominent role in innate immunity activity, and recent research has revealed its tight involvement in SARS-CoV-2 infection. We discuss these recent findings and the development of excessive inflammation and cytokine storm observed during SARS-CoV-2 infection. Finally, we consider potential use of antioxidant drugs for alleviating the severe symptoms in affected patients.

2021 ◽  
Vol 45 (1) ◽  
Author(s):  
Padmalochan Hembram

Abstract Background Coronavirus disease 19 is a viral infection caused by a novel coronavirus, SARS-CoV-2. It was first notified in Wuhan, China, is now spread into numerous part of the world. Thus, the world needs urgent support and encouragement to develop a vaccine or antiviral treatments to combat the atrocious outbreak. Main body of the abstract The origin of this virus is yet unknown; however, rapid transmission from human-to-human “Anthroponosis” has widely confirmed. The world is witnessing a continuous hike in SARS-CoV-2 infection. In light of the outbreak of coronavirus disease 19, we have aimed to highlight the basic and vital information about the novel coronavirus. We provide an overview of SARS-CoV-2 transmission, timeline and its pathophysiological properties which would be an aid for the development of therapeutic molecules and antiviral drugs. Immune system plays a crucial role in virus infection in order to control but may have dark side when becomes uncontrollable. The host and SARS-CoV-2 interaction describe how the virus exploits host machinery and how overactive host immune response can cause disease severity also addressed in this review. Short conclusion Safe and effective vaccines may be the game-changing tools, but in the near future wearing mask, washing hands at regular intervals, avoiding crowed, maintaining physical distancing and hygienic surrounding, must be good practices to reduce and break the transmission chain. Still, research is ongoing not only on how vaccines protect against disease, but also against infection and transmission.


2020 ◽  
Vol 13 ◽  
pp. 175628482097491
Author(s):  
Jonathan P. Segal ◽  
Joyce W. Y. Mak ◽  
Benjamin H. Mullish ◽  
James L. Alexander ◽  
Siew C. Ng ◽  
...  

The novel coronavirus infection (COVID-19) caused by the SARS-CoV-2 virus has spread rapidly across the globe, culminating in major global morbidity and mortality. As such, there has been a rapid escalation in scientific and clinical activity aimed at increasing our comprehension of this virus. This volume of work has led to early insights into risk factors associated with severity of disease, and mechanisms that underpin the virulence and dynamics involved in viral transmission. These insights ultimately may help guide potential therapeutics to reduce the human, economic and social impact of this pandemic. Importantly, the gastrointestinal (GI) tract has emerged as an important organ influencing propensity to, and potentially severity of, COVID-19 infection. Furthermore, the gut microbiome has been linked to a variety of risk factors for COVID-19 infection, and manipulation of the gut microbiome is an attractive potential therapeutic target for a number of diseases. While data profiling the gut microbiome in COVID-19 infection to date are limited, they support the possibility of several routes of interaction between COVID-19, the gut microbiome, angiotensin converting enzyme 2 (ACE-2) expression in the small bowel and colon and gut inflammation. This article will explore the evidence that implicates the gut microbiome as a contributing factor to the pathogenesis, severity and disease course of COVID-19, and speculate about the gut microbiome’s capability as a therapeutic avenue against COVID-19. Lay summary It has been noted that certain baseline gut profiles of COVID-19 patients are associated with a more severe disease course, and the gut microbiome impacts the disease course of several contributory risk factors to the severity of COVID-19. A protein called ACE-2, which is found in the small intestine among other sites, is a key receptor for COVID-19 virus entry; there is evidence that the gut microbiome influences ACE-2 receptor expression, and hence may play a role in influencing COVID-19 infectivity and disease severity. Furthermore, the gut microbiome plays a significant role in immune regulation, and hence may be pivotal in influencing the immune response to COVID-19. In terms of understanding COVID-19 treatments, the gut microbiome is known to interact with several drug classes being used to target COVID-19 and should be factored into our understanding of how patients respond to treatment. Importantly, our understanding of the role of the gut microbiome in COVID-19 infection remains in its infancy, but future research may potentially aid our mechanistic understanding of viral infection, and new ways in which we might approach treating it.


2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Antoine Raberin ◽  
Philippe Connes ◽  
Jean-Claude Barthélémy ◽  
Pia Robert ◽  
Sébastien Celle ◽  
...  

Background. Cardiovascular diseases remain as the leading cause of morbidity and mortality in industrialized countries. Ageing and gender strongly modulate the risk to develop cardiovascular diseases but very few studies have investigated the impact of gender on cardiovascular diseases in the elderly, which represents a growing population. The purpose of this study was to test the impact of gender and physical activity level on several biochemical and clinical markers of cardiovascular risk in elderly individuals. Methods. Elderly individuals (318 women (75.8±1.2 years-old) and 227 men (75.8±1.1 years-old)) were recruited. Physical activity was measured by a questionnaire. Metabolic syndrome was defined using the National Cholesterol Education Program Expert Panel’s definition. Polysomnography and digital tonometry were used to detect obstructive sleep apnea and assess vascular reactivity, respectively. Blood was sampled to measure several oxidative stress markers and adhesion molecules. Results. The frequency of cardiovascular diseases was significantly higher in men (16.4%) than in women (6.1%) (p<0.001). Body mass index (25.0±4.3 vs. 25.8±3.13 kg.m−2) and glycaemia (94.9±16.5 vs. 101.5±22.6 mg.dL−1) were lower, and High Density Lipoprotein (HDL) (74.6±17.8 vs. 65.0±17.2 mg.dL−1) was higher in women compared to men (p<0.05). Oxidative stress was lower in women than in men (uric acid: 52.05±13.78 vs. 59.84±13.58, advanced oxidation protein products: 223±94 vs. 246±101 μmol.L−1, malondialdehyde: 22.44±6.81 vs. 23.88±9.74 nmol.L−1). Physical activity was not associated with lower cardiovascular risk factors in both genders. Multivariate analyses showed an independent effect of gender on acid uric (β=0.182; p=0.020), advanced oxidation protein products (β=0.257; p<0.001), and HDL concentration (β=−0.182; p=0.026). Conclusion. These findings suggest that biochemical cardiovascular risk factors are lower in women than men which could explain the lower cardiovascular disease proportion observed in women in the elderly.


2010 ◽  
Vol 8 (10) ◽  
pp. 2105-2112 ◽  
Author(s):  
M. J. ENGBERS ◽  
A. VAN HYLCKAMA VLIEG ◽  
F. R. ROSENDAAL

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3367
Author(s):  
Seodhna M. Lynch ◽  
Guangran Guo ◽  
David S. Gibson ◽  
Anthony J. Bjourson ◽  
Taranjit Singh Rai

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in a global pandemic associated with substantial morbidity and mortality worldwide, with particular risk for severe disease and mortality in the elderly population. SARS-CoV-2 infection is driven by a pathological hyperinflammatory response which results in a dysregulated immune response. Current advancements in aging research indicates that aging pathways have fundamental roles in dictating healthspan in addition to lifespan. Our review discusses the aging immune system and highlights that senescence and aging together, play a central role in COVID-19 pathogenesis. In our review, we primarily focus on the immune system response to SARS-CoV-2 infection, the interconnection between severe COVID-19, immunosenescence, aging, vaccination, and the emerging problem of Long-COVID. We hope to highlight the importance of identifying specific senescent endotypes (or “sendotypes”), which can used as determinants of COVID-19 severity and mortality. Indeed, identified sendotypes could be therapeutically exploited for therapeutic intervention. We highlight that senolytics, which eliminate senescent cells, can target aging-associated pathways and therefore are proving attractive as potential therapeutic options to alleviate symptoms, prevent severe infection, and reduce mortality burden in COVID-19 and thus ultimately enhance healthspan.


2020 ◽  
Vol 71 (8) ◽  
pp. 1962-1968 ◽  
Author(s):  
Ashish Bhargava ◽  
Elisa Akagi Fukushima ◽  
Miriam Levine ◽  
Wei Zhao ◽  
Farah Tanveer ◽  
...  

Abstract Background COVID-19 is a pandemic disease caused by a novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Predictors for severe COVID-19 infection have not been well defined. Determination of risk factors for severe infection would enable identifying patients who may benefit from aggressive supportive care and early intervention. Methods We conducted a retrospective observational study of 197 patients with confirmed COVID-19 admitted to a tertiary academic medical center. Results Of 197 hospitalized patients, the mean (SD) age of the cohort was 60.6 (16.2) years, 103 (52.3%) were male, and 156 (82.1%) were black. Severe COVID-19 infection was noted in 74 (37.6%) patients, requiring intubation. Patients aged above 60 were significantly more likely to have severe infection. Patients with severe infection were significantly more likely to have diabetes, renal disease, and chronic pulmonary disease and had significantly higher white blood cell counts, lower lymphocyte counts, and increased C-reactive protein (CRP) than patients with nonsevere infection. In multivariable logistic regression analysis, risk factors for severe infection included pre-existing renal disease (odds ratio [OR], 7.4; 95% CI, 2.5–22.0), oxygen requirement at hospitalization (OR, 2.9; 95% CI, 1.3–6.7), acute renal injury (OR, 2.7; 95% CI, 1.3–5.6), and CRP on admission (OR, 1.006; 95% CI, 1.001–1.01). Race, age, and socioeconomic status were not independent predictors. Conclusions Acute or pre-existing renal disease, supplemental oxygen upon hospitalization, and admission CRP were independent predictors for the development of severe COVID-19. Every 1-unit increase in CRP increased the risk of severe disease by 0.06%.


2010 ◽  
Vol 138 (11) ◽  
pp. 1559-1568 ◽  
Author(s):  
J. M. GRAN ◽  
B. IVERSEN ◽  
O. HUNGNES ◽  
O. O. AALEN

SUMMARYInfluenza can be a serious, sometimes deadly, disease, especially for people in high-risk groups such as the elderly and patients with underlying, severe disease. In this paper we estimated the influenza-related excess mortality in Norway for 1975–2004, comparing it with dominant virus types and estimates of the reproduction number. Analysis was done using Poisson regression, explaining the weekly all-cause mortality by rates of reported influenza-like illness, together with markers for seasonal and year-to-year variation. The estimated excess mortality was the difference between the observed and predicted mortality, removing the influenza contribution from the prediction. We estimated the overall influenza-related excess mortality as 910 deaths per season, or 2·08% of the overall deaths. Age-grouped analyses indicated that the major part of the excess mortality occurred in the ⩾65 years age group, but that there was also a significant contribution to mortality in the 0–4 years age group. Estimates of the reproduction number R, ranged from about 1 to 1·69.


2020 ◽  
pp. jech-2020-214297 ◽  
Author(s):  
Saman Khalatbari-Soltani ◽  
Robert G Cumming ◽  
Cyrille Delpierre ◽  
Michelle Kelly-Irving

Disadvantaged socioeconomic position (SEP) is widely associated with disease and mortality, and there is no reason to think this will not be the case for the newly emerged coronavirus disease 2019 (COVID-19) that has reached a pandemic level. Individuals with a more disadvantaged SEP are more likely to be affected by most of the known risk factors of COVID-19. SEP has been previously established as a potential determinant of infectious diseases in general. We hypothesise that SEP plays an important role in the COVID-19 pandemic either directly or indirectly via occupation, living conditions, health-related behaviours, presence of comorbidities and immune functioning. However, the influence of socioeconomic factors on COVID-19 transmission, severity and outcomes is not yet known and is subject to scrutiny and investigation. Here we briefly review the extent to which SEP has been considered as one of the potential risk factors of COVID-19. From 29 eligible studies that reported the characteristics of patients with COVID-19 and their potential risk factors, only one study reported the occupational position of patients with mild or severe disease. This brief overview of the literature highlights that important socioeconomic characteristics are being overlooked when data are collected. As COVID-19 spreads worldwide, it is crucial to collect and report data on socioeconomic determinants as well as race/ethnicity to identify high-risk populations. A systematic recording of socioeconomic characteristics of patients with COVID-19 will be beneficial to identify most vulnerable groups, to identify how SEP relates to COVID-19 and to develop equitable public health prevention measures, guidelines and interventions.


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