Long Covid Land Toolbox

LONG COVID WEB

A network supporting and conducting research into the Post-COVID Condition (PCC)

Nearly 15% of long-COVID patients have cardiovascular symptoms, most often chest pain

A meta-analysis of 37 studies involving 3 million people suggests that those with long COVID are much more likely to experience chest pain, heart palpitations, and high blood pressure than their uninfected counterparts.

For the analysis, published late last week in BMC Medicine, researchers from Central South University in Hunan, China, systematically reviewed literature on high blood pressure, palpitations, and chest pain published up to March 17, 2024. Study sample sizes ranged from 60 to 2.4 million, with follow-up periods of 3 to 12 months.

“Emerging evidence indicates that COVID-19 may lead to post-acute COVID-19 syndrome (PACS) with cardiovascular implications, potentially driven by factors such as ACE2 interaction with viruses, systemic inflammation, and endothelial dysfunction,” the researchers wrote. “However, there remains a limited amount of research on the cardiovascular manifestations of PACS, which may delay the development of optimal treatment strategies for affected patients.”

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Targeting the SARS-CoV-2 reservoir in long COVID

There are no approved treatments for post-COVID-19 condition (also known as long COVID), a debilitating disease state following SARS-CoV-2 infection that is estimated to affect tens of millions of people. A growing body of evidence shows that SARS-CoV-2 can persist for months or years following COVID-19 in a subset of individuals, with this reservoir potentially driving long-COVID symptoms or sequelae. There is, therefore, an urgent need for clinical trials targeting persistent SARS-CoV-2, and several trials of antivirals or monoclonal antibodies for long COVID are underway. However, because mechanisms of SARS-CoV-2 persistence are not yet fully understood, such studies require important considerations related to the mechanism of action of candidate therapeutics, participant selection, duration of treatment, standardisation of reservoir-associated biomarkers and measurables, optimal outcome assessments, and potential combination approaches. In addition, patient subgroups might respond to some interventions or combinations of interventions, making post-hoc analyses crucial. Here, we outline these and other key considerations, with the goal of informing the design, implementation, and interpretation of trials in this rapidly growing field. Our recommendations are informed by knowledge gained from trials targeting the HIV reservoir, hepatitis C, and other RNA viruses, as well as precision oncology, which share many of the same hurdles facing long-COVID trials.

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Welcome to the Long COVID Resource

The COVID-19 pandemic has led to a widespread occurrence of Long COVID, a condition that significantly impacts health, daily life, and overall well-being. Long COVID, also referred to as post-acute sequelae of SARS-CoV-2 infection (PASC), affects a broad spectrum of people, irrespective of the initial severity of their COVID-19 infection.

The Long COVID Resource is dedicated to providing information and resources on Long COVID. We are committed to ensuring that individuals who are experiencing prolonged symptoms following a COVID-19 infection have access to the information and support they need. We recognize the profound challenges faced by individuals living with ongoing symptoms after recovering from the initial infection.

Beyond a simple list of facts, we strive to empower you with knowledge and tools to navigate this complex condition. Whether you’re recently diagnosed, struggling with persistent symptoms, or seeking support for a loved one, our website offers a safe harbor and a wealth of resources.

At Long Covid Resource, we’re committed to:

  • Providing accurate and up-to-date information based on the latest scientific findings.
  • Continuously expanding our resources to reflect the evolving landscape of research and support.
  • Empowering you with the knowledge and tools to manage your Long COVID journey with confidence.

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Postacute COVID-19 is Characterized by Gut Viral Antigen Persistence in Inflammatory Bowel Diseases

Background & Aims
The coronavirus disease 2019 (COVID-19) pandemic has affected populations, societies, and lives for more than 2 years. Long-term sequelae of COVID-19, collectively termed the postacute COVID-19 syndrome, are rapidly emerging across the globe. Here, we investigated whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) antigen persistence underlies the postacute COVID-19 syndrome.
Results
We report expression of SARS-CoV-2 RNA in the gut mucosa ∼7 months after mild acute COVID-19 in 32 of 46 patients with IBD. Viral nucleocapsid protein persisted in 24 of 46 patients in gut epithelium and CD8+ T cells. Expression of SARS-CoV-2 antigens was not detectable in stool and viral antigen persistence was unrelated to severity of acute COVID-19, immunosuppressive therapy, and gut inflammation. We were unable to culture SARS-CoV-2 from gut tissue of patients with viral antigen persistence. Postacute sequelae of COVID-19 were reported from the majority of patients with viral antigen persistence, but not from patients without viral antigen persistence.
Conclusion
Our results indicate that SARS-CoV-2 antigen persistence in infected tissues serves as a basis for postacute COVID-19. The concept that viral antigen persistence instigates immune perturbation and postacute COVID-19 requires validation in controlled clinical trials.

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Neurological sequelae of long COVID: a comprehensive review of diagnostic imaging, underlying mechanisms, and potential therapeutics

One lingering effect of the COVID-19 pandemic created by SARS-CoV-2 is the emergence of Long COVID (LC), characterized by enduring neurological sequelae affecting a significant portion of survivors. This review provides a thorough analysis of these neurological disruptions with respect to cognitive dysfunction, which broadly manifest as chronic insomnia, fatigue, mood dysregulation, and cognitive impairments with respect to cognitive dysfunction. Furthermore, we characterize how diagnostic tools such as PET, MRI, EEG, and ultrasonography provide critical insight into subtle neurological anomalies that may mechanistically explain the Long COVID disease phenotype. In this review, we explore the mechanistic hypotheses of these neurological changes, which describe CNS invasion, neuroinflammation, blood-brain barrier disruption, and gut-brain axis dysregulation, along with the novel vascular disruption hypothesis that highlights endothelial dysfunction and hypoperfusion as a core underlying mechanism. We lastly evaluate the clinical treatment landscape, scrutinizing the efficacy of various therapeutic strategies ranging from antivirals to anti-inflammatory agents in mitigating the multifaceted symptoms of LC.

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What is Long COVID?

A Beginner's Guide

Like many people with Long COVID, I spend a good amount of time learning about my disease. I spend an additional large chunk of time educating friends, family, the audience of my newsletter, and even my own doctors about Long COVID.

Without the help of clear, frequent, and reliable public health communications about what we’ve learned, the public remains ignorant about Long COVID. And that isn’t likely to change with Trump in the White House, Elon’s minions skulking around federal agencies like the NIH, and RFK Jr eyeing HHS; it’s likely to get much, much worse.

With that in mind, this article aims to outline the basics of Long COVID. What the term refers to scientifically and colloquially, how it can present, hypotheses as to its pathogenesis/es, and where we go from here. It presents some broad definitions, explores some subcategories, and leaves you with the open questions and debates researchers and patients are asking, exploring and living out. There are still many things we don’t know yet. But what we do know, should be shared.

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Doctors Warn COVID-19 Could Be a Hidden Trigger for Heart Attacks Long After Recovery

COVID-19 isn’t just a respiratory illness — it can silently attack the heart. New research reveals that the virus accelerates plaque buildup in arteries, increasing the risk of heart attacks and strokes long after recovery.

A new study has found that COVID-19, caused by the SARS-CoV-2 virus, is linked to accelerated plaque buildup in the coronary arteries, increasing the risk of heart-related complications. The findings were published today (February 4)  in Radiology, the journal of the Radiological Society of North America (RSNA).

“COVID-19, caused by SARS-CoV-2, is initially characterized by acute lung injury and respiratory failure,” explained the study’s senior author, Junbo Ge, M.D., professor and director of the Cardiology Department at Zhongshan Hospital, Fudan University in Shanghai, China. “However, emerging evidence indicates COVID-19 also involves an extreme inflammatory response that can affect the cardiovascular system.”

Inflammation’s Lasting Consequences

Dr. Ge noted that this inflammation continues beyond the first month of infection, raising the risk of severe cardiovascular issues and even death.

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