Hi everyone,
In this issue, we cover a wide range of topics, including the impact of Long Covid on insurance claims, and the potential link between severe pneumonia and neurological disorders. We also explore breakthrough research on immunological indicators for identifying Covid-19 progressors and the effect of the urban exposome on Covid-19 health outcomes.
Also important to note - The PolyBio Symposium was last week! Please check out this thread for more detail on what was presented.
Media
DEFINITIONS:
Post-acute infection syndrome: chronic illnesses that occur after an infection from a virus, bacteria, or parasite.
SUMMARY:
Long COVID and other post-acute infection syndromes are receiving more attention from researchers.
A recent study found that those who had been infected with COVID or other respiratory infections were more likely to have new or continuing symptoms compared to those who had not been infected.
Yale School of Medicine and Yale Medicine have been actively working to treat people affected by Long COVID and other post-acute infection syndromes.
The Center for Infection & Immunity at Yale aims to understand the underlying biological mechanisms that cause these diseases in order to develop effective treatments.
Article: Lessons learned from adjusting Long COVID insurance claims | PropertyCasualty360
SUMMARY:
In the pandemic's aftermath, more insurance and health care professionals have been presented with an unusual and complicated set of novel claims involving cases of long COVID-19.
This diagnosis has introduced new challenges to the insurance world.
My Take:
The article highlights the need for insurance adjusters to understand the evolving COVID-19 landscape in order to evaluate and treat long COVID claims responsibly and compassionately.
This is important as it ensures that individuals suffering from long COVID receive the necessary support and compensation they deserve.
Article: Long covid: Researchers “extremely angry” at Boris Johnson’s “bollocks” comment | The BMJ
SUMMARY:
Clinicians who led research on long covid from early on in the pandemic and who met government members to discuss the condition have expressed sadness and anger after messages emerged in which the then prime minister, Boris Johnson, described the condition as “bollocks.”
Chris Brightling and Rachael Evans, two of the investigators leading the Post-Hospitalisation Covid (Phosp-Covid) study, a national study looking at the long term effects of Covid-19 on hospital patients, said they were “shocked” and “angry” by the messages and raised concerns over how much Johnson’s views had influenced the government’s decision making.
Article: Researchers explore possible ties between long Covid, menopause
DEFINITIONS:
Menopause: the period of natural cessation of menstruation and reproductive activity, usually occurring between the ages of 45 and 55.
SUMMARY:
Women have been reporting period disturbances after a Covid infection or after receiving a Covid vaccine, though research has often minimized the relevance of such symptoms.
Lab results found markers for autoimmune disease and Epstein-Barr virus in women experiencing menstrual disturbances after Covid infection.
Women experiencing symptoms such as fatigue, chronic pain, and difficulty focusing may have long Covid, according to a gynecologist specializing in menopause.
Menopausal women who have been stable for years are starting to experience symptoms again, possibly due to long Covid.
The impact of the Covid infection on the female reproductive system is gaining more attention.
Research
DEFINITIONS:
Endogenous bacteria: Bacteria that normally reside in the body, specifically in the lungs in this context.
Lung-blood barrier: A barrier that separates the blood circulation from the lung tissue, preventing the movement of substances between them.
Blood-brain barrier (BBB): A highly selective barrier that separates the blood circulation from the brain tissue, protecting the brain from potentially harmful substances.
SUMMARY:
Neurological disorders are a common feature in patients who recover from severe acute pneumonia, but the underlying mechanisms remain poorly understood.
Bacterial translocation from the lung to the brain during pneumonia is associated with the development of neurological syndromes.
Principal components analysis revealed similarities between the bacteria found in the brain and those in the lungs, suggesting that the bacteria in the brain may originate from the lungs.
Impairment of both the lung-blood and brain-blood barriers allows endogenous lung bacteria to invade the brain during pneumonia.
Activation of microglia and astrocytes via bacterial infection–related pathways disrupts brain homeostasis, contributing to neurological symptoms after severe pneumonia.
My Take:
Understanding the connection between pneumonia and neurological disorders is crucial for improving patient outcomes.
This study suggests that the translocation of endogenous bacteria from the lungs to the brain plays a role in the development of neurological syndromes after severe pneumonia.
The impaired lung-blood barrier and BBB allow bacteria to invade the brain, disrupting brain homeostasis.
DEFINITIONS:
Transcriptomic: Referring to the study and analysis of all the RNA molecules produced by the cells of an organism.
Epigenomic: Relating to the study and analysis of changes in gene expression that are caused by chemical modifications of DNA or associated proteins, rather than by changes in the DNA sequence itself.
SUMMARY:
Multi-omic analyses identified differences in immune cell composition, cytokine levels, and cell subset-specific transcriptomic and epigenomic signatures between individuals on a more serious disease trajectory (Progressors) as compared to those on a milder course (Non-progressors).
Higher levels of multiple cytokines were observed in Progressors, with IL-6 showing the largest difference.
Blood monocyte cell subsets were also skewed, showing a comparative decrease in non-classical CD14−CD16+ and intermediate CD14+CD16+ monocytes.
In lymphocytes, the CD8+ T effector memory cells displayed a gene expression signature consistent with stronger T cell activation in Progressors.
These early stage observations could serve as the basis for the development of prognostic biomarkers of disease risk and interventional strategies to improve the management of severe COVID-19.
DEFINITIONS:
Antibody escape: The ability of a viral strain to evade the neutralizing antibodies produced by the immune system, rendering antibodies and immune-based therapies ineffective.
Cross-immunity: The protection against infection or disease provided by the immune response to a previous infection or exposure to a related strain of a pathogen.
Serotype formation: The co-circulation of antigenically distinct strains of a virus, resulting in the emergence of multiple serotypes.
SUMMARY:
The emergence of immune-evading strains of SARS-CoV-2 is a major driver of transmission trends in the pandemic.
The extent of immune evasion and the level of cross-immunity between emerging strains and pre-existing strains play a crucial role in determining invasion success and transmission levels.
Strains with antibody escape that weakens pre-existing immunity are likely to be strongly selected for and drive significant increases in short-term transmission.
Long-term co-circulation of multiple SARS-CoV-2 strains, known as serotype formation, may increase disease burden and complicate control efforts.
My Take:
This research emphasizes the need for early data on immune evasion and cross-immunity to inform vaccination strategies and other interventions.
Article: Long COVID research risks losing momentum – we need a moonshot
!Important Article!
SUMMARY:
Investing $1 billion every year for the next ten years into long COVID research could improve the lives of millions and save trillions in economic costs.
Long COVID is likely to have most impact on those populations that have been disproportionately affected throughout the pandemic — communities of color, with less access to health care, and a higher prevalence of comorbidities.
When it comes to COVID-19, millions of previously healthy people were infected with SARS-CoV-2 at the same time, and many of those infections were confirmed through testing.
Since the earliest days of the pandemic, we have been on the front lines of care, research and advocacy concerning long COVID — defined here as symptoms, such as cognitive dysfunction, fatigue, breathlessness and pain, that persist for months or years after SARS-CoV-2 infection.
We call for a moonshot for long COVID, a commitment — from the US government — to invest at least $1 billion annually over the next ten years to address the problem.
My Take:
The authors of this article argue for a US government commitment of $1 billion annually over the next ten years to address long COVID.
In my opinion, there definitely needs to be an allocated budget for LC - this is something I have argued for in prior editions.
DEFINITIONS:
DCLK1: Doublecortin-like kinase 1, a protein associated with cancer stem cells that is highly expressed in the lungs of COVID-19 patients and enhances viral production and hyperinflammatory responses.
kinase: An enzyme that transfers a phosphate group from ATP to a target protein molecule, regulating its function and activity.
SUMMARY:
DCLK1 is a protein that plays a crucial role in the replication cycle of SARS-CoV-2 and the dysregulation of cell signaling that contributes to COVID-19 severity.
Inhibition of DCLK1 using a small molecule kinase inhibitor effectively blocked viral replication and restored normal cell signaling pathways.
Treatment with the DCLK1 inhibitor reduced viral RNA levels, downregulated inflammatory cytokines, and improved lung pathology in a murine model of COVID-19.
The findings suggest that DCLK1 is a promising target for therapeutic intervention in COVID-19.
My Take:
Really interesting article, I learned a lot.
Inhibiting DCLK1 with a small molecule kinase inhibitor could be a potential therapeutic approach to block viral replication, reduce inflammation, and improve lung pathology.
SUMMARY:
Several reports have documented a specific effect of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on blood pressure.
Clinical studies have shown that COVID-19 is associated with an increased risk of a persistent increase in blood pressure.
A pooled analysis of four studies found that COVID-19 was associated with a 65% increased risk of new-onset hypertension compared to controls.
The interaction between spike proteins of SARS-CoV-2 and angiotensin converting enzyme 2 (ACE2) remains a plausible mechanism underlying the raise in blood pressure.
My Take:
The findings suggest that new-onset hypertension is a significant cardiovascular sequelae of COVID-19.
Understanding the mechanisms underlying this association, such as the interaction between spike proteins and ACE2, can help guide further research and inform treatment strategies for patients with COVID-19.
DEFINITIONS:
CD8+ T Cells: a type of T cell that plays a critical role in the adaptive immune response by recognizing and killing virus-infected cells or tumor cells.
Phenotypic Signatures: specific combinations of surface markers or gene expression patterns that define the phenotype or characteristics of a cell population.
Machine Learning: a subset of artificial intelligence that uses algorithms to enable computer systems to learn from data and make predictions or decisions without being explicitly programmed.
SUMMARY:
The study aimed to analyze human virus-specific CD8+ T cells and identify unique phenotypic signatures associated with T cell specificity prediction.
The researchers used in-depth profiling techniques, such as mass cytometry and single-cell RNA sequencing, to characterize CD8+ T cells specific for viruses like CMV, EBV, influenza, and SARS-CoV-2.
The study found that virus-specific CD8+ T cells displayed distinct phenotypic profiles and differentiation states, indicating a unique progressive differentiation profile for cells specific to different virus antigens.
Machine learning models were utilized to extract phenotypic markers associated with viral specificity, and the models accurately predicted the antigen specificity of CD8+ T cells in independent validation cohorts.
SUMMARY:
The study examined the postacute risk and burden of new-incident cardiovascular, cerebrovascular, and other thrombotic complications after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.
In this multiethnic Southeast Asian population, study authors reported 1.45–2.04 times higher risk of various cardiovascular complications, including IHD, dysrhythmias, and other cardiac disorders in the unvaccinated, infected group.
However, they did not observe elevated thrombotic risk, in contrast to other studies demonstrating increased risk of thrombotic complications in the United States (US) and United Kingdom.
In this study, the risk of cardiovascular complications postacute infection was evident even in mild cases who were not hospitalized.
Boris Johnson is a numbskull, with the haircut to match.
Appreciate the insurance article - gonna dig into that now. Thanks!
And OMG we do need a moonshot! That article was fantastic. And spot on.