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1.
Stem Cells and COVID-19 ; : 71-94, 2022.
Article in English | Scopus | ID: covidwho-2027796

ABSTRACT

From December 2019, COVID-19 pandemic has hit the human civilization in an unprecedented way. It has taken more than five million lives in just a span of two years. Two major mechanisms via which COVID-19 affects us are either via direct respiratory disorder and lung failure or otherwise via delayed flare of immune systems more prevalently known as the cytokine storm. Mesenchymal stem cells (MSCs) can be a potential therapeutic agent against mortality and morbidity of COVID-19 via direct differentiation into pulmonary epithelial cells as well as via antiinflammatory paracrine activities. MSCs are also can be useful to replicate COVID-19 infection in an in vitro organ model. In current study, we are systematically reviewing and finding out the potential applications of MSCs which could help mankind to combat COVID-19. © 2022 Elsevier Inc. All rights reserved.

2.
Stem Cells and COVID-19 ; : 7-22, 2022.
Article in English | Scopus | ID: covidwho-2027795

ABSTRACT

COVID-19 (coronavirus disease-2019) has been identified as a serious respiratory infection by the SARS-CoV2 virus (severe acute respiratory syndrome coronavirus 2), was first reported in Wuhan, Hubei Province, China in December 2019. World Health Organization (WHO) declared COVID 19 as a pandemic on March 11, 2020 considering the exponential spread and unmanageable mortality. It continues currently as the utmost urgent/critical ailment of global public health. Moreover, the COVID-19 pandemic has not only affected global health scenarios but also has heavily burdened the economic, financial, political, educational, and other dimensions of humanity across the world. Monitoring the COVID 19 pathology reveals a potential respiratory infection followed by severe pneumonia like clinical observations with greater chances of microvascular injuries and multiorgan failures in worse scenario. The preexisting comorbidities including type II diabetes, cardiovascular diseases, hypertension, and older age are other major aggravating factors. Rather than other flu viruses, the intricate interplay of SARS-CoV2 virus with the immune system underlies the pathological manifestations in both symptomatic and asymptomatic patients. This chapter highlights the role of heterogenous immune cell population, cytokine storm, immune cell activation, and potential signaling pathways associated with COVID 19 infection that are greatly appreciated to evolve novel translational therapeutic interventions. © 2022 Elsevier Inc. All rights reserved.

3.
Stem Cells and COVID-19 ; : 59-70, 2022.
Article in English | Scopus | ID: covidwho-2027793

ABSTRACT

Cytokine storms illustrate a robust, uncontrolled immune response that can severely disrupt the physiology of a person infected with a virus such as COVID-19. Cytokine storms during the most severe of COVID-19 infections are believed to be one of the major contributing factors to mortality and severe pathologic outcomes of the disease. Dysregulated levels of cytokines during a cytokine storm contribute to changes in different components of the local microenvironments including the stem cell components. Here, we review the pathophysiology of cytokine storms looking at different aspects of viral-induced cytokine release. In particular, we note the changes in the stem cell compartments that occur as well as therapeutic targets relying on targeting stem cells. © 2022 Elsevier Inc. All rights reserved.

4.
Stem Cells and COVID-19 ; : 47-57, 2022.
Article in English | Scopus | ID: covidwho-2027791

ABSTRACT

Coronavirus disease 2019 (COVID‐19) is an acute respiratory viral infection caused by SARS-CoV-2, an RNA virus. The first cluster of cases of COVID‐19 was reported from Wuhan, Hubei Province in China in December 2019. Soon after, the virus spread all over the world with 207 M confirmed cases, including 4.3 M deaths as of August 2021. Subsequently, the World Health Organization (WHO) declared the situation a public health emergency of international concern in January 2020 and later declared as a global pandemic threat. COVID‐19 mainly causes damage to the lung as well as other organs and systems such as the heart, the immune system, the nervous system, etc., and thus considered as a multisystem infection. Initial investigations provide insights about the pathogenesis of COVID‐19 and the role of ACE2 receptor has been elucidated. However, there is no complete treatment strategies proposed other than supportive care based on symptoms and severity. Though intense efforts are going on to vaccinate billions of people and at the time of writing 4462.8M vaccine doses have been administered, the pandemic continues spreading at a very fast rate. This chapter discusses the impact of COVID-19 in multisystem inflammation and multiorgan failure. Understanding the molecular and immunological aspects of this disease and diverse susceptibility in different patients would help to design better treatment methods in advance. COVID-19 is characterized by remarkable changes in the histology of multiple organs with high inflammation and necrosis. Along with that, the high imbalance in the immune system with abnormal secretion of proinflammatory cytokines and significant reduction in the circulating lymphocytes increases disease severity and organ damage. Addressing these scenarios carefully would help to discover blood markers or other analysis to predict the possible severity and chances of organ dysfunction in advance and design effective treatment. © 2022 Elsevier Inc. All rights reserved.

5.
Inflammation ; 2022.
Article in English | PubMed | ID: covidwho-2027559

ABSTRACT

A cytokine storm (CS) is an out-of-control inflammatory response closely associated with the progression of diseases, such as multiple organ failure (MOF), severe sepsis, and severe or critical COVID-19. However, there is currently a lack of reliable diagnostic markers to distinguish CS from normal inflammatory responses. Tumor necrosis factor-α (TNF-α) includes transmembrane TNF-α (tmTNF-α) and secreted TNF-α (sTNF-α). The MOF mouse model in this study showed that the tmTNF-α expression changes in the neutrophils differed from the serum TNF-α and serum IL-18, INF-γ, IL-4, and IL-6. Furthermore, tmTNF-α, instead of serum TNF-α, IL-18, INF-γ, IL-4, and IL-6, reflected liver and kidney tissue damage and increased with the aggravation of these injuries. Analysis of the ROC results showed that tmTNF-α effectively distinguished between inflammatory responses and CS and efficiently differentiated between surviving and dead mice. It also significantly improved the diagnostic value of the traditional CRP marker for CS. These results indicated that the tmTNF-α expressed in the neutrophils could be used to diagnose CS in MOF mice, providing an experimental basis to further develop tmTNF-α for diagnosing CS patients.

6.
Majallah-i Pizishki-i Danishgah-i ulum-i Pizishki-i Tabriz ; 44(3):189-199, 2022.
Article in Persian | Scopus | ID: covidwho-2026632

ABSTRACT

Background. The novel Coronavirus disease 2019 (COVID-19) was declared a global pandemic. There is an urgent need for finding efficient medical treatments to diminish the high mortality rate of the mutant variants of the virus. This study aimed to determine the efficacy of edaravone in patients with moderate COVID-19. Methods. This single-center non-randomized controlled clinical trial was performed on hospitalized patients with moderate COVID-19. The patients were divided into two groups of intervention (n=17) and control (n=16). Patients in the intervention group received three doses of edaravone (30 mg) for three interval days (Days 2, 4, and 6). Admission to the intensive care unit (ICU), need for intubation, and mortality were the primary outcomes. Results. All cases had 15-60% lung involvement. Although edaravone reduced the admission to ICU, need for intubation, and mortality rate in patients with moderate COVID-19, the results were not statistically significant. Baseline characteristics, admission days, and clinical parameters were similar between the two groups (P>0.05). Conclusion. Administration of edaravone 30 mg for three days had no significant effect on the overall outcome of patients with moderate COVID-19. Practical Implications. In this study, none of the COVID-19 patients receiving edaravone had ICU admission, intubation, and mortality. However, no significant difference was found between the clinical outcomes of the control and intervention groups. © 2022 The Authors.

7.
Iranian Journal of Medical Microbiology ; 16(5):412-419, 2022.
Article in English | Scopus | ID: covidwho-2026442

ABSTRACT

Background and Aim: The COVID-19 disease is an emerging infectious disease that appeared in December 2019 in Wuhan, China. An uncontrolled systemic inflammatory response is one of the primary mechanisms causing death in this disease. In this study, the expression levels of some inflammatory cytokines, vitamin D, and some hematological and biochemical parameters were compared in patients with severe COVID-19 and mild types. Materials and Methods: In this cross-sectional study, 60 blood samples were taken from 30 severe coronavirus patients and 30 mild coronavirus patients. The expression levels of cytokines such as IL (interleukin)-6, interferon (IFN)-α, IL-12, transforming growth factor (TGF) β, IL-8 and tumor necrosis factor (TNF)-α were evaluated using Real-time PCR. A T-test was used for Statistical Analysis. Results: IL-6, IFN-α, IL-12, TGF-β, IL-8, and TNF-α cytokines in the peripheral blood of severe patients, were positive in 28/30 (93.33%), 27/30 (90%), 24/30 (80%), 25/30 (83.33%), 26/30 (86.66%), and 27/30 (90%) respectively. The positive rate of these cytokines in the mild patients were 20/30 (66.67%), 21/30 (70%), 18/30 (60%), 17/30 (56.67%), 19/30 (63.33%), 18/30 (60%), respectively. There was a statistically significant difference between these two groups in terms of cytokines biomarkers. A significant difference was found between both groups in terms of the serum level of lactate dehydrogenase (LDH), the mean number of lymphocytes and neutrophils as well as the mean percentage of neutrophils/ lymphocytes ratio (NLR). Conclusion: The expression of cytokine genes and their release into the peripheral blood was increased in both severe and mild patients with COVID-19. However, they were more intense in patients with severe symptoms than those with mild symptoms and can cause inflammatory and even destructive reactions. Vitamin D deficiency plays no role in causing severe COVID-19 in patients without risk factors. Severe COVID-19 is characterized by elevated serum levels of LDH and NLR≥3.45. © 2022. This is an original open-access article distributed under the terms of the Creative Commons Attribution-noncommercial 4.0 International License which permits copy and redistribution of the material just in noncommercial usages with proper citation.

8.
Bulletin of Siberian Medicine ; 21(2):207-211, 2022.
Article in English | Scopus | ID: covidwho-2026054

ABSTRACT

We presented a clinical case of the successful treatment of a severe course of polysegmental pneumonia caused by the novel coronavirus infection, that developed in the postoperative period after bariatric surgery in the patient with morbid obesity, comorbid type 2 diabetes mellitus, ischemic heart disease, arterial hypertension, pulmonary embolism (in past medical history), and stage 3 chronic obstructive pulmonary disease. The given clinical case demonstrates the possibility of successful treatment of coronavirus infection in the polymorbid patient at an extremely high risk of an unfavorable outcome, given timely diagnosis, combination therapy using drugs that block cytokine storm, and strict adherence to clinical recommendations. © 2022 Siberian State Medical University. All rights reserved.

9.
World Journal of Experimental Medicine ; 12(4):53-67, 2022.
Article in English | Scopus | ID: covidwho-2025163

ABSTRACT

Coronavirus disease 2019 (COVID-19) causes acute microvascular thrombosis in both venous and arterial structures which is highly associated with increased mortality. The mechanisms leading to thromboembolism are still under investigation. Current evidence suggests that excessive complement activation with severe amplification of the inflammatory response (cytokine storm) hastens disease progression and initiates complement-dependent cytotoxic tissue damage with resultant prothrombotic complications. The concept of thromboinflammation, involving overt inflammation and activation of the coagulation cascade causing thrombotic microangiopathy and end-organ damage, has emerged as one of the core components of COVID-19 pathogenesis. The complement system is a major mediator of the innate immune response and inflammation and thus an appealing treatment target. In this review, we discuss the role of complement in the development of thrombotic microangiopathy and summarize the current data on complement inhibitors as COVID-19 therapeutics. © The Author(s) 2022.

10.
Gülhane Tip Dergisi ; 64(3):208-216, 2022.
Article in English | ProQuest Central | ID: covidwho-2024906

ABSTRACT

We assessed the blood levels of the most important factors such as cytokines/chemokines in Coronavirus disease-2019 (COVID-19). PubMed/Medline and Scopus as two important databases were searched up to March 26, 2020. To analyze the data, we used Review Manager 5.3 software. Out of forty-two records retrieved from two databases, 10 studies were involved in the analysis. Thirty-three cytokines/chemokines were checked. The levels of 27 cytokines/chemokines in COVID-19 patients were higher than the healthy controls, and among 20 cytokines/chemokines;the levels of 10 cytokines/chemokines in severe COVID-19 patients were higher than non-severe COVID-19 patients. Also, out of three cytokines, one had a higher level in the intensive care unit (ICU) patients compared to the non-ICU patients. The findings showed the cytokine storm syndrome in COVID-19 patients, especially in patients with severe disease.

11.
Frontiers in Pharmacology ; 13, 2022.
Article in English | Web of Science | ID: covidwho-2022834

ABSTRACT

Background: The Janus kinase (JAK) 1/2 inhibitor ruxolitinib has been approved in an indication of myelofibrosis and is a candidate for the treatment of a number of inflammatory or autoimmune diseases. We assessed the effects of ruxolitinib on lipopolysaccharide (LPS)- and poly (I:C)-induced cytokine production by human lung macrophages (LMs) and on the LMs' phagocytic activity. Methods: Human LMs were isolated from patients operated on for lung carcinoma. The LMs were cultured with ruxolitinib (0.5 x 10(-7) M to 10(-5) M) or budesonide (10(-11) to 10(-8) M) and then stimulated with LPS (10 ng.ml(-1)) or poly (I:C) (10 mu g & BULL;ml(-1)) for 24 h. Cytokines released by the LMs into the supernatants were measured using ELISAs. The phagocytosis of labelled bioparticles was assessed using flow cytometry. Results: Ruxolitinib inhibited both the LPS- and poly (I:C)-stimulated production of tumor necrosis factor alpha, interleukin (IL)-6, IL-10, chemokines CCL2, and CXCL10 in a concentration-dependent manner. Ruxolitinib also inhibited the poly (I:C)- induced (but not the LPS-induced) production of IL-1ss. Budesonide inhibited cytokine production more strongly than ruxolitinib but failed to mitigate the production of CXCL10. The LMs' phagocytic activity was not impaired by the highest tested concentration (10(-5) M) of ruxolitinib. Conclusion: Clinically relevant concentrations of ruxolitinib inhibited the LPS- and poly (I:C)-stimulated production of cytokines by human LMs but did not impair their phagocytic activity. Overall, ruxolitinib's anti-inflammatory activities are less intense than (but somewhat different from) those of budesonide-particularly with regard to the production of the corticosteroid-resistant chemokine CXCL-10. Our results indicate that treatment with a JAK inhibitor might be a valuable anti-inflammatory strategy in chronic obstructive pulmonary disease, Th1-high asthma, and both viral and non-viral acute respiratory distress syndromes (including coronavirus disease 2019).

12.
Frontiers in Molecular Biosciences ; 9, 2022.
Article in English | Web of Science | ID: covidwho-2022799

ABSTRACT

Long non-coding RNAs (lncRNAs) are RNA transcripts that are over 200 nucleotides and rarely encode proteins or peptides. They regulate gene expression and protein activities and are heavily involved in many cellular processes such as cytokine secretion in respond to viral infection. In severe COVID-19 cases, hyperactivation of the immune system may cause an abnormally sharp increase in pro-inflammatory cytokines, known as cytokine release syndrome (CRS), which leads to severe tissue damage or even organ failure, raising COVID-19 mortality rate. In this review, we assessed the correlation between lncRNAs expression and cytokine release syndrome by comparing lncRNA profiles between COVID-19 patients and health controls, as well as between severe and non-severe cases. We also discussed the role of lncRNAs in CRS contributors and showed that the lncRNA profiles display consistency with patients' clinic symptoms, thus suggesting the potential of lncRNAs as drug targets or biomarkers in COVID-19 treatment.

13.
Frontiers in Molecular Biosciences ; 9, 2022.
Article in English | Web of Science | ID: covidwho-2022798

ABSTRACT

The coronavirus disease (COVID-19) caused by a coronavirus identified in December 2019 has caused a global pandemic. COVID-19 was declared a pandemic in March 2020 and has led to more than 6.3 million deaths. The pandemic has disrupted world travel, economies, and lifestyles worldwide. Although vaccination has been an effective tool to reduce the severity and spread of the disease there is a need for more concerted approaches to fighting the disease. COVID-19 is characterised as a severe acute respiratory syndrome . The severity of the disease is associated with a battery of comorbidities such as cardiovascular diseases, cancer, chronic lung disease, and renal disease. These underlying diseases are associated with general cellular stress. Thus, COVID-19 exacerbates outcomes of the underlying conditions. Consequently, coronavirus infection and the various underlying conditions converge to present a combined strain on the cellular response. While the host response to the stress is primarily intended to be of benefit, the outcomes are occasionally unpredictable because the cellular stress response is a function of complex factors. This review discusses the role of the host stress response as a convergent point for COVID-19 and several non-communicable diseases. We further discuss the merits of targeting the host stress response to manage the clinical outcomes of COVID-19.

14.
Frontiers in Immunology ; 13, 2022.
Article in English | Scopus | ID: covidwho-2022745

ABSTRACT

Influenza vaccines remain the most effective tools to prevent flu and its complications. Trivalent or quadrivalent inactivated influenza vaccines primarily elicit antibodies towards haemagglutinin and neuraminidase. These vaccines fail to induce high protective efficacy, in particular in older adults and immunocompromised individuals and require annual updates to keep up with evolving influenza strains (antigenic drift). Vaccine efficacy declines when there is a mismatch between its content and circulating strains. Current correlates of protection are merely based on serological parameters determined by haemagglutination inhibition or single radial haemolysis assays. However, there is ample evidence showing that these serological correlates of protection can both over- or underestimate the protective efficacy of influenza vaccines. Next-generation universal influenza vaccines that induce cross-reactive cellular immune responses (CD4+ and/or CD8+ T-cell responses) against conserved epitopes may overcome some of the shortcomings of the current inactivated vaccines by eliciting broader protection that lasts for several influenza seasons and potentially enhances pandemic preparedness. Assessment of cellular immune responses in clinical trials that evaluate the immunogenicity of these new generation vaccines is thus of utmost importance. Moreover, studies are needed to examine whether these cross-reactive cellular immune responses can be considered as new or complementary correlates of protection in the evaluation of traditional and next-generation influenza vaccines. An overview of the assays that can be applied to measure cell-mediated immune responses to influenza with their strengths and weaknesses is provided here. Copyright © 2022 Janssens, Joye, Waerlop, Clement, Leroux-Roels and Leroux-Roels.

15.
Frontiers in Immunology ; 13, 2022.
Article in English | Web of Science | ID: covidwho-2022702

ABSTRACT

Coronavirus disease 2019 (COVID-19) has been a pandemic for the past two years. Predicting patient prognosis is critical. Although immune checkpoints (ICs) were shown to be involved in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, quantitative studies of ICs in clinical practice are limited. In this study, various soluble ICs (sICs) and cytokine levels in patients with SARS-CoV-2 infection at different time points were compared between survivors and deaths;we also examined whether sICs are useful for predicting prognosis. sICs and cytokines were measured in serum samples from 38 patients diagnosed with COVID-19 in the first and second week post-diagnosis. All assays were performed by bead-based multiplexed immunoassay system using Luminex Bio-Plex 200 system. The correlation of sICs and cytokines with laboratory markers was evaluated, and the levels of sICs in survivors were compared with those in deaths. Among the sICs, the second-week levels of soluble cluster of differentiation (sCD27, p = 0.012), sCD40 (p< 0.001), cytotoxic T-lymphocyte-associated protein 4 (sCTLA-4, p< 0.001), herpes virus entry mediator (sHVEM, p = 0.026), and T-cell immunoglobulin and mucin-domain containing-3 (sTIM-3, p = 0.002) were significantly higher in deaths than in survivors. The levels of nine cytokines assessed in the second week of deaths were significantly higher than those in survivors. The sICs sCD27, sCD40, sCTLA-4, and sTIM-3 and cytokines chemokine CC motif ligand 2 (CCL2), GM-CSF, IL-10, and IL-8 showed significant positive correlations with the levels of C-reactive protein (CRP) and procalcitonin and were negatively correlated with the absolute lymphocyte count and platelet values. Increased levels of sICs including sCD27, sCD40, sCTLA-4, and sTIM-3 and cytokines were significant factors for poor prognosis. sICs, together with cytokines and inflammatory markers, may be useful as prognostic stratification markers in SARS-CoV-2-infected patients.

16.
Curr Alzheimer Res ; 2022.
Article in English | PubMed | ID: covidwho-2022271

ABSTRACT

The COVID-19 pandemic is caused by the severe acute respiratory syndrome coronavirus (SARS-CoV-2), a respiratory pathogen with neuroinvasive potential. Neurological COVID-19 manifestations include loss of smell and taste, headache, dizziness, stroke, and potentially fatal encephalitis. Several studies found elevated proinflammatory cytokines such as TNF-α, IFN-γ, IL-6 IL-8, IL-10 IL-16, IL-17A, and IL-18 in severely and critically ill COVID-19 patients, which may persist even after apparent recovery from infection. Biomarker studies on CSF and plasma and serum from COVID-19 patients have also shown a high level of IL-6, intrathecal IgG, neurofilament light chain (NFL), glial fibrillary acidic protein (GFAP), and tau protein. Emerging evidence on the matter has established the concept of COVID-19 associated neuroinflammation, in the context of COVID-19 associated cytokine storm. While the short-term implications of this condition are extensively documented, its long-term implications are yet to be understood. The association of the aforementioned cytokines with the pathogenesis of neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, Huntington disease, and amyotrophic lateral sclerosis, may increase COVID-19 patients' risk to develop neurodegenerative diseases. Analysis of proinflammatory cytokines and CSF biomarkers in patients with COVID-19 can contribute to the early detection of the disease's exacerbation, monitoring the neurological implications of the disease and devising risk scales, and identifying treatment targets.

17.
Current Pharmaceutical Design ; 28(22):1779, 2022.
Article in English | MEDLINE | ID: covidwho-2022254
18.
Gut ; 71(Suppl 2):A148, 2022.
Article in English | ProQuest Central | ID: covidwho-2020135

ABSTRACT

BackgroundCoronavirus disease 2019 (COVID-19), which was first reported in Wuhan City, China, is a major public health burden worldwide. Systemic corticosteroid therapy is an effective treatment for severe COVID-19 with ARDS. It ameliorates COVID-19-induced cytokine storm and improves patient outcomes;however, it can trigger immunosuppression, which causes a myriad of secondary infections.MethodsFifteen patients suffering from gastrointestinal complaints during COVID-19 related illness underwent gastroscopic/colonoscopic examination.ResultsWe report 15 cases of gastrointestinal (GI) Cytomegalovirus (CMV) infection diagnosed on biopsy. The mean age at diagnosis was 57 years;13 were males and 2 were females. The most common presentation was bleeding per rectum in 12 patients, dysphagia in 2 patients and abdominal pain in 1 patient. The most common site was the colon seen in 10 patients, 1 patient had Ileo-caecal valve involvement, and 2 each had gastric and esophageal involvement. Among colonic involvement, 2 patients had pan-colonic involvement. Out of 15 patients, 9 patients had either past history of steroid intake or ongoing intake for COVID-19 associated lung injury. Nine patients were diabetic, and 2 were suffering from chronic liver disease.ConclusionsImmunosuppressive state inhibits the activity of crucial transcriptional regulators of proinflammatory genes and reducing lymphocyte levels. Therefore, exposure to systemic corticosteroids can be a risk factor for CMV infection in patients with severe COVID-19.

19.
Thoracic Cancer ; : 1, 2022.
Article in English | Academic Search Complete | ID: covidwho-2019069

ABSTRACT

Cytokine release syndrome (CRS) is a systemic inflammatory disease caused by a variety of factors, including infections and certain drugs. A 70‐year‐old man who was diagnosed with a postoperative recurrence of lung adenocarcinoma received nivolumab, ipilimumab, pemetrexed and carboplatin every 3 weeks for two cycles followed by nivolumab and ipilimumab, which resulted in a partial response. Four days after the dose of nivolumab, the patient returned with diarrhea and fever. The patient was diagnosed with COVID‐19 infection accompanied by severe colitis. Although intensive care was performed, the patient suddenly went into cardiopulmonary arrest. Examination revealed an abnormally high interleukin‐6 level, suggesting CRS. This is the first report of a patient with CRS accompanied with COVID‐19 infection during treatment with ICIs. Cytokine release syndrome (CRS) is a systemic inflammatory disease caused by a variety of factors, including infections and certain drugs. Here, we report a case of non‐small cell lung cancer with CRS caused by COVID‐19 infection during treatment with nivolumab and ipilimumab. Fever is a common event in cancer patients, especially in COVID‐19‐infected patients, but when fever develops during cancer immunotherapy, CRS should always be kept in mind. [ FROM AUTHOR] Copyright of Thoracic Cancer is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)

20.
Brain ; 2022.
Article in English | Web of Science | ID: covidwho-2017742

ABSTRACT

Infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is associated with acute and postacute cognitive and neuropsychiatric symptoms including impaired memory, concentration, attention, sleep and affect. Mechanisms underlying these brain symptoms remain understudied. Here we report that SARS-CoV-2-infected hamsters exhibit a lack of viral neuroinvasion despite aberrant blood-brain barrier permeability. Hamsters and patients deceased from coronavirus disease 2019 (COVID-19) also exhibit microglial activation and expression of interleukin (IL)-1beta and IL-6, especially within the hippocampus and the medulla oblongata, when compared with non-COVID control hamsters and humans who died from other infections, cardiovascular disease, uraemia or trauma. In the hippocampal dentate gyrus of both COVID-19 hamsters and humans, we observed fewer neuroblasts and immature neurons. Protracted inflammation, blood-brain barrier disruption and microglia activation may result in altered neurotransmission, neurogenesis and neuronal damage, explaining neuropsychiatric presentations of COVID-19. The involvement of the hippocampus may explain learning, memory and executive dysfunctions in COVID-19 patients.

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