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SARS-CoV-2 causes a wide spectrum of clinical manifestations and significant mortality. Studies investigating underlying immune characteristics are needed to understand disease pathogenesis and inform vaccine design. In this study, we examined immune cell subsets in hospitalized and non-hospitalized individuals. In hospitalized patients, many adapt...
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... groups were compared to healthy, COVID-19 negative controls ("Healthy", n=20). An overview of the cohort demographics is shown in Table 1. Importantly, most individuals in the hospitalized group (n=36) were viremic and hospitalized at the time of sample collection; ...Context 2
... individuals in the non-hospitalized group were convalescent at the time of sample collection. As shown in Table 1, there were differences between age, race, and comorbidities. ...Context 3
... previously described (32), we found that hospitalized individuals in our study displayed normal WBC counts but distinctly lower numbers of lymphocytes ( Table 1). To further assess immune cells that remain during SARS-CoV-2 infection, we utilized a general . ...Context 4
... a marker for CD11c would have increased our ability to identify this population, we believe our gating strategy (CD3-CD19-CD14-CD56-CD16-HLADRhi) still identifies a relatively pure population of dendritic cells. Additionally, we acknowledge that there are substantial differences in age, race and sex between our hospitalized, non-hospitalized and healthy groups as summarized in Table 1. These differences reflect the nature of the COVID-19 pandemic, with numerous sources reporting increased hospitalizations and more severe clinical symptoms in elderly and African-American populations. ...Context 5
... the remaining relationships that were not significant by hospitalization status, there were also no significant findings to support that these relationships were driven by age, race, or sex. One exception to this was the finding that the decrease in CD16+ monocytes in our hospitalized group appears to be driven by sex (Supplemental Table 1). In addition, our hospitalized group had an increased frequency of existing comorbidities (shown in Table 1). ...Context 6
... exception to this was the finding that the decrease in CD16+ monocytes in our hospitalized group appears to be driven by sex (Supplemental Table 1). In addition, our hospitalized group had an increased frequency of existing comorbidities (shown in Table 1). This was expected since many of these risk factors have been found to correlate with worsening clinical outcomes in COVID-19 infection. ...Similar publications
SARS-CoV-2 causes a wide spectrum of clinical manifestations and significant mortality. Studies investigating underlying immune characteristics are needed to understand disease pathogenesis and inform vaccine design. In this study, we examined immune cell subsets in hospitalized and non-hospitalized individuals. In hospitalized patients, many adapt...
Citations
... Indeed, the predisposing conditions for hyperinflammatory COVID-19 are likely to overlap with at least some of those responsible for post-infection sequelae. Whether viral persistence occurs is uncertain, but post-infection inflammatory markers suggest ongoing low-grade innate immune activation linked to adaptive immune dysregulation and/or exhaustion (128). Chronic infection promotes the death of protective CD4+ cells through TLR7 and IRF5 (129). ...
Interleukin-1 receptor-associated kinase 4 (IRAK4) and interferon regulatory factor 5 (IRF5) lie sequentially on a signaling pathway activated by ligands of the IL-1 receptor and/or multiple TLRs located either on plasma or endosomal membranes. Activated IRF5, in conjunction with other synergistic transcription factors, notably NF-κB, is crucially required for the production of proinflammatory cytokines in the innate immune response to microbial infection. The IRAK4-IRF5 axis could therefore have a major role in the induction of the signature cytokines and chemokines of the hyperinflammatory state associated with severe morbidity and mortality in COVID-19. Here a case is made for considering IRAK4 or IRF5 inhibitors as potential therapies for the “cytokine storm” of COVID-19.
Objective. To study the vulnerability of a group of drug users to the HIV/COVID‑19 syndemic.
Methods and materials. We used data from personalized registration of patients with HIV infection in the Moscow region, which were ill with covid‑19 in 2020–2021.
Results. Alcohol and drug addiction are an additional factor that makes the course of COVID‑19 more severe in patients with HIV infection. The reasons for this additional influence, both in the vulnerability of this group due to behavioral risks, and in psychosocial problems affecting adherence to HIV treatment, and this factor does not allow achieving the immunological and virological effectiveness of antiretroviral therapy.
Conclusions. The article presents data showing that people living with HIV/AIDS, suffering from alcohol and drug addiction, are more vulnerable to COVID‑19 in terms of severity and mortality from the disease.
COVID-19 (Coronavirus Disease) is an infectious disease caused by the coronavirus SARS-CoV-2 (Severe acute respiratory syndrome Coronavirus 2), which belongs to the genus Betacoronavirus. It was first identified in patients with severe respiratory disease in December 2019 in Wuhan, China. It mainly affects the respiratory system, and in severe cases causes serious lung infection or pneumonia, which can lead to the death of the patient. Clinical studies show that SARS-CoV-2 infection in critical cases causes acute tissue damage due to a pathological immune response. The immune response to a new coronavirus is complex and involves many processes of specific and non-specific immunity. Analysis of available studies has shown various changes, especially in the area of specific cellular immunity, including lymphopenia, decreased T cells (CD3+, CD4+ and CD8+), changes in the T cell compartment associated with symptom progression, deterioration of the condition and development of lung damage. We provide a detailed review of the analyses of immune checkpoint molecules PD-1, TIM-3, LAG-3 CTLA-4, TIGIT, BTLA, CD223, IDO-1 and VISTA on exhausted T cells in patients with asymptomatic to symptomatic stages of COVID-19 infection. Furthermore, this review may help to better understand the pathological T cell immune response and improve the design of therapeutic strategies for patients with SARS-CoV-2 infection.
