Metabolic Syndrome and Viral Pathogenesis: Lessons from Influenza and Coronaviruses

Smith, Maria A.; Honce, Rebekah; Schultz‐Cherry, Stacey

doi:10.1128/jvi.00665-20

Cited by 44 publications

(35 citation statements)

References 23 publications

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“…The high early viral replication in a given host is likely a reflection of failed innate immune responses including interferon-mediated antiviral defense. Indeed, impaired innate antiviral defense is seen with the COVID-19 risk factors including advanced age 44 , metabolic syndrome 45 , cancer 46 ,and in immunocompromised status. In addition, recent work has also shown increased expression of ACE2 in the lungs of individuals with COVID-19 risk factors 47 , which may further predispose those with pre-existing conditions to higher viral replication.…”

Section: Discussionmentioning

confidence: 99%

Saliva viral load is a dynamic unifying correlate of COVID-19 severity and mortality

Silva

Lucas

Sundaram

et al. 2021

Preprint

100

103

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While several clinical and immunological parameters correlate with disease severity and mortality in SARS-CoV-2 infection, work remains in identifying unifying correlates of coronavirus disease 2019 (COVID-19) that can be used to guide clinical practice. Here, we examine saliva and nasopharyngeal (NP) viral load over time and correlate them with patient demographics, and cellular and immune profiling. We found that saliva viral load was significantly higher in those with COVID-19 risk factors; that it correlated with increasing levels of disease severity and showed a superior ability over nasopharyngeal viral load as a predictor of mortality over time (AUC=0.90). A comprehensive analysis of immune factors and cell subsets revealed strong predictors of high and low saliva viral load, which were associated with increased disease severity or better overall outcomes, respectively. Saliva viral load was positively associated with many known COVID-19 inflammatory markers such as IL-6, IL-18, IL-10, and CXCL10, as well as type 1 immune response cytokines. Higher saliva viral loads strongly correlated with the progressive depletion of platelets, lymphocytes, and effector T cell subsets including circulating follicular CD4 T cells (cTfh). Anti-spike (S) and anti-receptor binding domain (RBD) IgG levels were negatively correlated with saliva viral load showing a strong temporal association that could help distinguish severity and mortality in COVID-19. Finally, patients with fatal COVID-19 exhibited higher viral loads, which correlated with the depletion of cTfh cells, and lower production of anti-RBD and anti-S IgG levels. Together these results demonstrated that viral load – as measured by saliva but not nasopharyngeal — is a dynamic unifying correlate of disease presentation, severity, and mortality over time.

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Section: Discussionmentioning

confidence: 99%

Saliva viral load is a dynamic unifying correlate of COVID-19 severity and mortality

Silva

Lucas

Sundaram

et al. 2021

Preprint

100

103

View full text Add to dashboard Cite

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“…Men appear to have disproportionate hospitalization rates compared with non-pregnant women 37 , presumably related to differences in immune responses mediated by sex hormones, which may be age-dependent 24,38 . Comorbid chronic health conditions, including metabolic syndrome 39 , heart failure 40 and chronic obstructive pulmonary disease 41 , also increase an individual's risk of severe disease. Finally, environmental factors, such as cigarette smoke exposure, contribute to disease severity 42 , potentially as a result of alterations in epithelial and immune cell function 43 as well as in fibroblast repair responses to viral infection 44 .…”

Section: Global (Who Data)mentioning

confidence: 99%

Influenza virus and SARS-CoV-2: pathogenesis and host responses in the respiratory tract

et al. 2021

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“…This has become an important issue in the case of coronavirus disease 2019 (COVID- 19) infection where diabetics are more likely to suffer from more severe disease (5). In addition, accumulating evidence shows that the state of nutrition can influence the outcome of a viral infection by causing changes in one or more aspect of metabolism (6). All of these observations imply that adjusting metabolic events during the course of a viral infection could represent a valuable approach to reshape the outcome of infections (7,8).…”

Section: Introductionmentioning

confidence: 99%

Virus Infections and Host Metabolism—Can We Manage the Interactions?

et al. 2021

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When viruses infect cells, they almost invariably cause metabolic changes in the infected cell as well as in several host cell types that react to the infection. Such metabolic changes provide potential targets for therapeutic approaches that could reduce the impact of infection. Several examples are discussed in this review, which include effects on energy metabolism, glutaminolysis and fatty acid metabolism. The response of the immune system also involves metabolic changes and manipulating these may change the outcome of infection. This could include changing the status of herpesviruses infections from productive to latency. The consequences of viral infections which include coronavirus disease 2019 (COVID-19), may also differ in patients with metabolic problems, such as diabetes mellitus (DM), obesity, and endocrine diseases. Nutrition status may also affect the pattern of events following viral infection and examples that impact on the pattern of human and experimental animal viral diseases and the mechanisms involved are discussed. Finally, we discuss the so far few published reports that have manipulated metabolic events in-vivo to change the outcome of virus infection. The topic is expected to expand in relevance as an approach used alone or in combination with other therapies to shape the nature of virus induced diseases.

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Metabolic Syndrome and Viral Pathogenesis: Lessons from Influenza and Coronaviruses

Cited by 44 publications

References 23 publications

Saliva viral load is a dynamic unifying correlate of COVID-19 severity and mortality

Saliva viral load is a dynamic unifying correlate of COVID-19 severity and mortality

Influenza virus and SARS-CoV-2: pathogenesis and host responses in the respiratory tract

Virus Infections and Host Metabolism—Can We Manage the Interactions?

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