SARS-CoV-2, immunosenescence and inflammaging: partners in the COVID-19 crime

Domingues, Renato; Lippi, Alice; Setz, Cristian; Outeiro, Tiago F.; Kriško, Anita

doi:10.18632/aging.103989

Cited by 48 publications

(45 citation statements)

References 97 publications

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“…Immunosenescence is a gradual decline in immune function that interferes with pathogen recognition, alert signaling, and clearance, causing increased susceptibility to infections and other immune-related chronic disorders, such as autoimmune diseases and cancer. 44 , 45 Inflammaging, in turn, is an increase in systemic inflammation that arises from an overactive yet ineffective alert system whereby a decline in cellular repair mechanisms causes an accumulation of genome and proteome damage, leading to systemic changes in the immune system and increased production of proinflammatory cytokines. 46 …”

Section: Methodsmentioning

confidence: 99%

The immune response to SARS-CoV-2 and COVID-19 immunopathology – Current perspectives

et al. 2021

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SARS-CoV-2 is a new beta coronavirus, similar to SARS-CoV-1, that emerged at the end of 2019 in the Hubei province of China. It is responsible for coronavirus disease 2019 (COVID-19), which was declared a pandemic by the World Health Organization on March 11, 2020. The ability to gain quick control of the pandemic has been hampered by a lack of detailed knowledge about SARS-CoV-2-host interactions, mainly in relation to viral biology and host immune response. The rapid clinical course seen in COVID-19 indicates that infection control in asymptomatic patients or patients with mild disease is probably due to the innate immune response, as, considering that SARS-CoV-2 is new to humans, an effective adaptive response would not be expected to occur until approximately 2–3 weeks after contact with the virus. Antiviral innate immunity has humoral components (complement and coagulation-fibrinolysis systems, soluble proteins that recognize glycans on cell surface, interferons, chemokines, and naturally occurring antibodies) and cellular components (natural killer cells and other innate lymphocytes). Failure of this system would pave the way for uncontrolled viral replication in the airways and the mounting of an adaptive immune response, potentially amplified by an inflammatory cascade. Severe COVID-19 appears to be due not only to viral infection but also to a dysregulated immune and inflammatory response. In this paper, the authors review the most recent publications on the immunobiology of SARS-CoV-2, virus interactions with target cells, and host immune responses, and highlight possible associations between deficient innate and acquired immune responses and disease progression and mortality. Immunotherapeutic strategies targeting both the virus and dysfunctional immune responses are also addressed.

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Section: Methodsmentioning

confidence: 99%

The immune response to SARS-CoV-2 and COVID-19 immunopathology – Current perspectives

et al. 2021

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“…Indeed, our investigations have shown that in mice with thymic involution, there was increased lymphocyte infiltration into self-tissues, including the lung [ 67 ]. Although there is increasing interest in the correlation between immunosenescence and the increased risk of COVID-19 mortality in the elderly, more research is needed to fully elucidate the role of pre-existing lung inflammation and infiltration of potentially self-reactive T cells during COVID-19 pathogenesis [ 73 , 74 , 75 , 76 ].…”

Section: How Does Age-related Thymic Involution and Subsequent T-cmentioning

confidence: 99%

Thymic Aging May Be Associated with COVID-19 Pathophysiology in the Elderly

Wang

Thomas

et al. 2021

Cells

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused the global pandemic of coronavirus disease 2019 (COVID-19) and particularly exhibits severe symptoms and mortality in elderly individuals. Mounting evidence shows that the characteristics of the age-related clinical severity of COVID-19 are attributed to insufficient antiviral immune function and excessive self-damaging immune reaction, involving T cell immunity and associated with pre-existing basal inflammation in the elderly. Age-related changes to T cell immunosenescence is characterized by not only restricted T cell receptor (TCR) repertoire diversity, accumulation of exhausted and/or senescent memory T cells, but also by increased self-reactive T cell- and innate immune cell-induced chronic inflammation, and accumulated and functionally enhanced polyclonal regulatory T (Treg) cells. Many of these changes can be traced back to age-related thymic involution/degeneration. How these changes contribute to differences in COVID-19 disease severity between young and aged patients is an urgent area of investigation. Therefore, we attempt to connect various clues in this field by reviewing and discussing recent research on the role of the thymus and T cells in COVID-19 immunity during aging (a synergistic effect of diminished responses to pathogens and enhanced responses to self) impacting age-related clinical severity of COVID-19. We also address potential combinational strategies to rejuvenate multiple aging-impacted immune system checkpoints by revival of aged thymic function, boosting peripheral T cell responses, and alleviating chronic, basal inflammation to improve the efficiency of anti-SARS-CoV-2 immunity and vaccination in the elderly.

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“…Liver biopsy of the deceased patients showed mild lobular and portal vein activity and moderate microvascular steatosis [ 11 ]. Previous studies have demonstrated that a cytokine storm is triggered when the immune system overreacts to infection [ 34 , 35 ]. And cytokine storm is considered to be an important factor leading to acute respiratory distress syndrome and multiple organ dysfunction syndrome [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Clinical characteristics and peripheral immunocyte subsets alteration of 85 COVID-19 deaths

Xiong

Zang

Gao

et al. 2021

Aging

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Objectives: To retrospectively evaluate the clinical and immunological characteristics of patients who died of COVID-19 and to identify patients at high risk of death at an early stage and reduce their mortality. Results: Total white blood cell count, neutrophil count and C-reactive protein were significantly higher in patients who died of COVID-19 than those who recovered from it (p < 0.05), but the total lymphocyte count, CD4 + T cells, CD8 + T cells, B cells and natural killer cells were significantly lower when compared in the same groups. Multiple logistic regression analysis showed that increased D-dimer, decreased CD4 + T cells and increased neutrophils were risk factors for mortality. Further multiple COX regression demonstrated that neutrophil ≥ 5.27 × 109/L increased the risk of death in COVID-19 patients after adjustment for age and gender. However, CD4 + T cells ≥ 260/μL appeared to reduce the risk of death. Conclusion: SARS-CoV-2 infection led to a significant decrease of lymphocytes, and decreased CD4 + T cell count was a risk factor for COVID-19 patients to develop severe disease and death. Methods: This study included 190 hospitalized COVID-19 patients from January 30, 2020 to March 4, 2020 in Wuhan, China, of whom 85 died and 105 recovered. Two researchers independently collected the clinical and laboratory data from electronic medical records.

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SARS-CoV-2, immunosenescence and inflammaging: partners in the COVID-19 crime

Cited by 48 publications

References 97 publications

The immune response to SARS-CoV-2 and COVID-19 immunopathology – Current perspectives

The immune response to SARS-CoV-2 and COVID-19 immunopathology – Current perspectives

Thymic Aging May Be Associated with COVID-19 Pathophysiology in the Elderly

Clinical characteristics and peripheral immunocyte subsets alteration of 85 COVID-19 deaths

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