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Background: Metabolic dysregulation and excessive inflammation are implicated in the pathogenesis of the highly infectious disease of coronavirus disease 2019 (COVID-19), which is caused by a newly emerging coronavirus (i.e., severe acute respiratory syndrome-coronavirus 2; SARS-CoV-2). The adenosine 5'-monophosphate-activated protein kinase (AMPK), an energy sensor regulating the metabolic pathways in diverse cells, exerts a regulatory role in the immune system. This study aims to examine the mRNA expression level of AMPK and the plasma levels of interleukin-6 (IL-6) and IL-10 cytokines in patients with different grades of COVID-19., Methods: Peripheral blood was collected from 60 patients with COVID-19 (Moderate, severe, and critical). The plasma levels of IL-6 and IL-10 were quantified by enzyme-linked immunosorbent assay (ELISA), and the mRNA expression level of AMPK was determined using real-time PCR., Results: The results showed that the plasma levels of IL-6 increased significantly in critical and severe patients compared to moderate cases of COVID-19 (P < 0.001). Moreover, IL-10 plasma concentrations were significantly higher in critical and severe cases than in moderate cases of COVID-19 (P < 0.01 and P < 0.05, respectively). Also, the gene expression of AMPK was meaningfully enhanced in critical patients relative to moderate and severe cases of COVID-19, in order (P < 0.001 and P < 0.01, respectively). There was a positive association between AMPK gene expression and plasma levels of IL-6 and IL-10 (P = 0.006, r = 0.348, P = 0.028, r = 0.283, respectively)., Conclusion: Increasing AMPK gene expression is likely a necessary effort of the immune system to inhibit inflammation in critical COVID-19. However, this effort seems to be inadequate, probably due to factors that induce inflammation, like erythrocyte sedimentation rate (ESR) and IL-6., (© 2023. The Author(s), under exclusive licence to Springer Nature B.V.)

Autoantibodies (AABs) play a critical role in the pathogenesis of autoimmune diseases (AIDs) and serve as a diagnostic and prognostic tool in assessing these complex disorders. Viral infections have long been recognized as a principal environmental factor affecting the production of AABs and the development of autoimmunity. COVID-19 has primarily been considered a hyperinflammatory syndrome triggered by a cytokine storm. In the following, the role of maladaptive B cell response and AABs became more apparent in COVID-19 pathogenesis. The current review will primarily focus on the role of extrafollicular B cell response, Toll-like receptor-7 (TLR-7) activation, and neutrophil extracellular traps (NETs) formation in the development of AABs following SARS-CoV-2 infection. In the following, this review will clarify how these AABs dysregulate immune response to SARS-CoV-2 by disrupting cytokine function and triggering neutrophil hyper-reactivity. Finally, the pathologic effects of these AABs will be further described in COVID-19 associate clinical manifestations, including venous and arterial thrombosis, a multisystem inflammatory syndrome in children (MIS-C), acute respiratory distress syndrome (ARDS), and recently described post-acute sequelae of COVID-19 (PASC) or long-COVID., (© 2022 John Wiley & Sons Ltd.)

Since COVID-19 vaccination started in December 2020, different side effects were reported. This case report describes the possibility of developing disseminated herpes simplex infection after COVID-19 vaccine in a patient with rheumatoid arthritis. In this case report, we describe a 63-year-old Iranian female. She was a known case of seronegative rheumatoid arthritis and presented with generalized papulo-pustular itchy and painful skin lesions which appeared about seven days after the second dose of Sinopharm BIBP COVID-19 vaccine (BIBP-CorV). A biopsy of the skin lesions revealed acantholysis, neutrophils, and enlarged keratinocytes with eosinophilic intra-nuclear inclusions. Findings were consistent with herpes simplex infection. She was successfully treated by acyclovir. Disseminated cutaneous herpes simplex infection may have been triggered by COVID-19 vaccination. Reactivation of herpes virus after COVID-19 vaccines was reported in both rheumatic patients and other individuals. Whether having an underlying autoimmune inflammatory disorder could be an additional risk factor is still unknown.

Neutrophilic myositis (NM) is an inflammatory disorder predominantly characterized by neutrophilic infiltration in the muscles, which is suggested to be an extracutaneous manifestation of neutrophilic dermatosis (ND). NM is a rare disorder which has been occasionally reported in association with hematologic and inflammatory disorders. This case report describes a 45-year-old woman who presented with gradual muscle weakness developed after coronavirus disease 2019 (COVID-19) infection. Electromyography and nerve conduction velocity findings were compatible with inflammatory myopathy and muscle biopsy revealed neutrophilic infiltration. She was successfully treated with intravenous immunoglobulin, prednisolone 1 mg/kg/day and azathioprine 150 mg/day. In conclusion, the COVID-19 infection itself and the drugs used to treat it can cause a number of muscle disorders. Awareness of muscular involvement in COVID-19 infected patients is important for early diagnosis and appropriate treatment.