Early Insights into Immune Responses during COVID-19

John, Ashley L. St.; Rathore, Abhay P. S.

doi:10.4049/jimmunol.2000526

Cited by 55 publications

(52 citation statements)

References 100 publications

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“…Additionally, very little is known about potential common dysregulated signaling pathways regarding immune cell dysfunction and inflammation between adverse psychosocial or neighborhood environmental conditions and other comorbidities known to affect COVID-19 severity. An understanding of the pathophysiology of COVID-19 requires an understanding of the interplay of SARS-CoV-2 virus with immune cells and inflammation which is slowly emerging in the literature ( 23 ). This understanding may guide therapeutics, translational studies, and multidisciplinary interventions that may mitigate some effects of COVID-19, while also elucidating mechanisms by which health disparities influence outcomes during pandemics and beyond for future targeted treatment.…”

Section: Introductionmentioning

confidence: 99%

Health Disparities in COVID-19: Addressing the Role of Social Determinants of Health in Immune System Dysfunction to Turn the Tide

Baumer

Farmer

Premeaux

et al. 2020

Front. Public Health

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It is evident that health disparities exist during the COVID-19 pandemic, a pandemic caused by the novel coronavirus SARS-CoV-2. Underlying reasons for COVID-19 health disparities are multi-factorial. However, social determinants, including those regarding socioeconomic status, social inequalities, health behaviors, and stress, may have implications on these disparities. Exposure to one or more of these social determinants is associated with heightened inflammatory responses, particularly increases in the cytokine interleukin-6 (IL-6), as well as immune system dysfunction. Thus, an amplified effect during COVID-19 could occur, potentially resulting in vulnerable patients experiencing an intensified cytokine storm due to a hyperactive and dysfunctional immune response. Further understanding how social determinants play a mechanistic role in COVID-19 disparities could potentially help reduce health disparities overall and in future pandemics.

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Section: Introductionmentioning

confidence: 99%

Health Disparities in COVID-19: Addressing the Role of Social Determinants of Health in Immune System Dysfunction to Turn the Tide

Baumer

Farmer

Premeaux

et al. 2020

Front. Public Health

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“…Moreover, both SARS-CoV-2 and IAV are airborne transmitted pathogens that infect the same human tissues such as the respiratory tract, nasal, bronchial, and alveolar epithelial cultures (3,4). Besides, alveolar type II cells (AT2 pneumocytes) appeared to be preferentially infected by SARS-CoV-2, which were also the primary site of IAV replication (5,6).…”

Section: Introductionmentioning

confidence: 99%

Co-infection of influenza A virus enhances SARS-CoV-2 infectivity

Bai

Zhao

Dong

et al. 2020

Preprint

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The upcoming flu season in the northern hemisphere merging with the current COVID-19 pandemic may raise a potentially severe threat to public health. However, little is known about the consequences of the co-infection of influenza A virus (IAV) and SARS-CoV-2. Through experimental co-infection of IAV with either pseudotyped or SARS-CoV-2 live virus, we found that IAV pre-infection significantly promoted the infectivity of SARS-CoV-2 in a broad range of cell types. Intriguingly, such enhancement of SARS-CoV-2 infectivity was only seen under co-infection with IAV but not with several other viruses including Sendai virus, human rhinovirus, human parainfluenza virus, human respiratory syncytial virus, or human enterovirus 71. IAV infection rather than interferon signaling induced elevated expression of ACE2 essential for such enhancement of SARS-CoV-2 infectivity. Remarkably, we further confirmed that the pre-infection of IAV indeed resulted in an increased SARS-CoV-2 viral load and more severe lung damage in hACE2-transgenic mice. This study illustrates that the co-infection of IAV aggravates SARS-CoV-2 infection and disease severity, which in turn suggests that preventing the convergence of flu season and COVID-19 pandemic would be of great significance.

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“…Nonetheless, since its introduction in human populations SARS-CoV-2 must have been subject to the selective pressure imposed by the human immune system. In fact, as with most other viruses, data from SARS,and MERS patients indicate that both B and T lymphocytes play a role in controlling infection (Channappanavar et al, 2014;St John and Rathore, 2020;Vabret et al, 2020).…”

Section: Introductionmentioning

confidence: 94%

“…Potential epitopes were predicted using Immune Epitope Database (IEDB) tools, as previously described (Grifoni et al, 2020a). Specifically, because they are the major targets of the humoral immune response (Channappanavar et al, 2014;St John and Rathore, 2020;Vabret et al, 2020), we predicted both linear and conformational B epitopes for the S and N proteins, whereas only linear epitopes were predicted for the other viral proteins (Table S1). A good correspondence was observed between B cell epitope predictions for the S protein and epitopes identified in two works that systematically mapped antibody responses in the sera of convalescent COVID-19 patients (Farrera et al, 2020;Poh et al, 2020) (Figure 1).…”

Section: Antigenic Variability Of Sars-cov-2 Proteinsmentioning

confidence: 99%

“…In fact, whereas the majority of COVID-19 cases are relatively mild, a significant proportion of patients develop a serious, often fatal illness, characterized by acute respiratory distress syndrome (Wu and McGoogan, 2020). Both viral-induced lung pathology and overactive immune responses are thought to contribute to disease severity (St John and Rathore, 2020;Vabret et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

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Antigenic variation of SARS-CoV-2 in response to immune pressure

Forni

Cagliani

Pontremoli

et al. 2020

Preprint

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SummaryThe ongoing evolution of SARS-CoV-2 is expected to be at least partially driven by the selective pressure imposed by the human immune system. We exploited the availability of a large number of high-quality SARS-CoV-2 genomes, as well as of validated epitope predictions, to show that B cell epitopes in the spike glycoprotein (S) and in the nucleocapsid protein (N) have higher diversity than non-epitope positions. Similar results were obtained for other human coronaviruses. Conversely, in the SARS-CoV-2 population, epitopes for CD4+ and CD8+ T cells were not more variable than non-epitope positions. A significant reduction in epitope variability was instead observed for some of the most immunogenic proteins (S, N, ORF8, and ORF3a). Analysis over longer evolutionary time-frames indicated that this effect is not due to differential constraints. These data indicate that SARS-CoV-2 is evolving to elude the host humoral immune response, whereas recognition by T cells might benefit the virus.

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Early Insights into Immune Responses during COVID-19

Cited by 55 publications

References 100 publications

Health Disparities in COVID-19: Addressing the Role of Social Determinants of Health in Immune System Dysfunction to Turn the Tide

Health Disparities in COVID-19: Addressing the Role of Social Determinants of Health in Immune System Dysfunction to Turn the Tide

Co-infection of influenza A virus enhances SARS-CoV-2 infectivity

Antigenic variation of SARS-CoV-2 in response to immune pressure

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