Long COVID from rheumatology perspective — a narrative review

Sapkota, Hem; Nune, Arvind

doi:10.1007/s10067-021-06001-1

Cited by 65 publications

(59 citation statements)

References 75 publications

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“…There are many reports that the symptoms and laboratory data of patients with long COVID-19 are very similar to the symptoms of autoimmune rheumatic disease, mainly systemic lupus erythematosus, rheumatoid arthritis, and others [ 33 – 35 ]: fatigue, myalgia, arthralgia, low-grade fever, weakness, elevated levels of acute proteins, ESR, changes in general blood tests, etc. The role of EBV in the pathogenesis of autoimmune disorders due to the phenomenon of molecular mimicry and polyclonal activation of B-lymphocytes is also known [ 3 , 35 – 37 ]. It is becoming clear that reactivation of herpesviruses and especially EBV, triggered by SARS-CoV-2, can be an actual trigger for the formation of various autoimmune rheumatic diseases.…”

Section: Discussionmentioning

confidence: 99%

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Herpesvirus infections and post-COVID-19 manifestations: a pilot observational study

et al. 2022

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The global spread of SARS-CoV-2 points to unrivaled mutational variation of the virus, contributing to a variety of post-COVID sequelae in immunocompromised subjects and high mortality. Numerous studies have reported the reactivation of "sluggish" herpes virus infections in COVID-19, which exaggerate the course of the disease and complicate with lasting post-COVID manifestations CMV, EBV, HHV6). This study aimed to describe clinical and laboratory features of post-COVID manifestations accompanied by the reactivation of herpes virus infections (CMV, EBV, HHV6). 88 patients were recruited for this study, including subjects with reactivation of herpes viruses, 68 (72.3%) (main group) and 20 (27.7%) subjects without detectable DNA of herpesviruses (control group): 46 (52.3%) female and 42 (47.7%) male; median age was 41.4 ± 6.7 years. Patients with post-COVID manifestations presented with reactivation of EBV in 42.6%, HHV6 in 25.0%, and EBV plus HHV6 in 32.4%. Compared with controls, patients with herpes virus infections presented with more frequent slight fever temperature, headache, psycho-neurological disorders, pulmonary abnormalities and myalgia ( p < 0.01), activation of liver enzymes, elevated CRP and D-dimer, and suppressed cellular immune response ( p ≤ 0.05). Preliminary results indicate a likely involvement of reactivated herpes virus infections, primarily EBV infections in severe COVID-19 and the formation of the post-COVID syndrome. Patients with the post-COVID syndrome and reactivation of EBV and HHV6 infections are at high risk of developing various pathologies, including rheumatologic diseases.

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Section: Discussionmentioning

confidence: 99%

“…Short and long-term post-acute sequelae of COVID-19 (PASC) are frequently reported. Patients with the post-COVID disease have symptoms similar to systemic autoimmune disorders [ 3 – 5 ].…”

Section: Introductionmentioning

confidence: 99%

Herpesvirus infections and post-COVID-19 manifestations: a pilot observational study

et al. 2022

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“…Clinical Outcome: A recent systematic review assessing prevalence of symptoms of Long COVID affecting all body systems found fatigue to be the most reported ailment (58%). Effects on cognition were found to be 31% and 27% for persistent difficulty with concentrating and attention deficits, respectively [76,77]. Patients with brain fog who underwent cognitive testing as part of another study displayed short-term memory (32%) and attention (27%) deficits [9].…”

Section: Brain Fog and Long Covidmentioning

confidence: 99%

“…According to a study from Northwestern University's Neuro-COVID-19 Clinic, brain fog was the most reported persistent (>6 weeks) neurologic symptom in survivors (81%) without history of severe illness, hypoxia, or respiratory compromise [9]. Brain fog persisted as long as 5 months and females were much more likely than males (2.3:1) to exhibit "long hauler COVID-19" symptoms [9,76].…”

Section: Brain Fog and Long Covidmentioning

confidence: 99%

Neurological Sequelae of COVID-19

Ahmad¹,

Feigen²,

Vazquez³

et al. 2022

J. Integr. Neurosci.

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Background: Though primarily a pulmonary disease, Coronavirus disease 2019 caused by the SARS-CoV-2 virus can generate devastating disease states that affect multiple organ systems including the central nervous system (CNS). The various neurological disorders associated with COVID-19 range in severity from mild symptoms such as headache, or myalgias to more severe symptoms such as stroke, psychosis, and anosmia. While some of the COVID-19 associated neurological complications are mild and reversible, a significant number of patients suffer from stroke. Studies have shown that COVID-19 infection triggers a wave of inflammatory cytokines that induce endothelial cell dysfunction and generate coagulopathy that increases the risk of stroke or thromboses. Inflammation of the endothelium following infection may also destabilize atherosclerotic plaque and induce thrombotic stroke. Although uncommon, there have also been reports of hemorrhagic stroke associated with COVID-19. The proposed mechanisms include a blood pressure increase caused by infection leading to a reduction in angiotensin converting enzyme-2 (ACE-2) levels that results in an imbalance of the renin-angiotensin system ultimately manifesting inflammation and vasoconstriction. Coagulopathy, as demonstrated by elevated prothrombin time (PT), has also been posited as a factor contributing to hemorrhagics stroke in patients with COVID-19. Other neurological conditions associated with COVID-19 include encephalopathy, anosmia, encephalitis, psychosis, brain fog, headache, depression, and anxiety. Though there are several hypotheses reported in the literature, a unifying pathophysiological mechanism of many of these disorders remains unclear. Pulmonary dysfunction leading to poor oxygenation of the brain may explain encephalopathy and other disorders in COVID-19 patients. Alternatively, a direct invasion of the CNS by the virus or breach of the blood-brain barrier by the systemic cytokines released during infection may be responsible for these conditions. Notwithstanding, the relationship between the inflammatory cytokine levels and conditions such as depression and anxiety is contradictory and perhaps the social isolation during the pandemic may in part be a contributing factor to some of the reported CNS disorders. Objective: In this article, we review the current literature pertaining to some of the most significant and common neurological disorders such as ischemic and hemorrhagic stroke, encephalopathy, encephalitis, brain fog, Long COVID, headache, Guillain-Barre syndrome, depression, anxiety, and sleep disorders in the setting of COVID-19. We summarize some of the most relevant literature to provide a better understanding of the mechanistic details regarding these disorders in order to help physicians monitor and treat patients for significant COVID-19 associated neurologic impairments. Methods: A literature review was carried out by the authors using PubMed with the search terms "COVID-19" and "Neurology", "Neurological Manifestations", "Neuropsychiatric ...

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“…Patients infected by SARS-CoV-2 have also shown chronic sequelae for weeks or even months, a condition termed as "post COVID-19 syndrome" or "long COVID" (99,100). Following initial onset of COVID-19, an estimated 50% or more of COVID-19 survivors may develop multi-organ problems (e.g., pulmonary dysfunction and neurologic impairment) or have worsening concomitant chronic illness (100)(101)(102). Notably, a recent study found that circulating markers of NETs returned to comparable levels with healthy controls after 4 months of infection, implying that NETs are persistent and may be involved in post COVID-19 syndrome pathology (30,103,104).…”

Section: Post-covid-19 Syndromementioning

confidence: 99%

NETosis and Neutrophil Extracellular Traps in COVID-19: Immunothrombosis and Beyond

2022

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Infection with SARS-CoV-2, the causative agent of the Coronavirus disease 2019 (COVID-19) pandemic, causes respiratory problems and multifaceted organ dysfunction. A crucial mechanism of COVID-19 immunopathy is the recruitment and activation of neutrophils at the infection site, which also predicts disease severity and poor outcomes. The release of neutrophil extracellular traps (NETs), occurring during a regulated form of neutrophil cell death known as NETosis, is a key effector function that mediates harmful effects caused by neutrophils. Abundant NETosis and NET generation have been observed in the neutrophils of many COVID-19 patients, leading to unfavorable coagulopathy and immunothrombosis. Moreover, excessive NETosis and NET generation are now more widely recognized as mediators of additional pathophysiological abnormalities following SARS-CoV-2 infection. In this minireview, we introduce subtypes of NET-producing neutrophils (e.g., low-density granulocytes) and explain the biological importance of NETs and the protein cargos of NETs in COVID-19. In addition, we discuss the mechanisms by which SARS-CoV-2 causes NETosis by upregulating viral processes (e.g., viral entry and replication) as well as host pro-NET mechanisms (e.g., proinflammatory mediator release, platelet activation, and autoantibody production). Furthermore, we provide an update of the main findings of NETosis and NETs in immunothrombosis and other COVID-19-related disorders, such as aberrant immunity, neurological disorders, and post COVID-19 syndromes including lung fibrosis, neurological disorder, tumor progression, and deteriorated chronic illness. Finally, we address potential prospective COVID-19 treatment strategies that target dysregulated NETosis and NET formation via inhibition of NETosis and promotion of NET degradation, respectively.

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Long COVID from rheumatology perspective — a narrative review

Cited by 65 publications

References 75 publications

Herpesvirus infections and post-COVID-19 manifestations: a pilot observational study

Herpesvirus infections and post-COVID-19 manifestations: a pilot observational study

Neurological Sequelae of COVID-19

NETosis and Neutrophil Extracellular Traps in COVID-19: Immunothrombosis and Beyond

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