Long Covid Land Toolbox
Postacute COVID-19 is Characterized by Gut Viral Antigen Persistence in Inflammatory Bowel Diseases
Background & Aims
Results
Conclusion
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.
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.
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.
How the virus behind COVID-19 can harm your blood vessels and your heart
By Laura Williamson, American Heart Association News
It started as a respiratory illness – or so everyone thought. But it quickly became apparent that SARS-CoV-2, the virus that causes COVID-19, was so much more.
“Since the beginning, the virus showed a very dramatic ability to affect different organs and systems beyond the respiratory system,” said Dr. Chiara Giannarelli, an associate professor in the departments of medicine and pathology at NYU Grossman School of Medicine. “Early on, there was some evidence the virus was damaging the heart, causing an increased risk of heart attacks and strokes in these patients. But no one was looking at the vasculature,” the blood vessels that carry the virus throughout the body and in and out of the heart.
From her lab in New York City, Giannarelli had front-row seats in the spring of 2020 to the epicenter of COVID-19 infections in the U.S. Because her research already focused on the complex relationship between inflammatory and immune cells in the arteries and their role in atherosclerosis – the root of cardiovascular disease – she felt well positioned to investigate.
Meanwhile, other research teams were looking into what the virus was doing to the heart muscle. Cases of myocarditis, an inflammation of the heart muscle, were being identified as the cause of death in some people with COVID-19.
Choroid plexus volume is enlarged in long COVID and associated with cognitive and brain changes
Patients with post-COVID condition (PCC) present with diverse symptoms which persist at long-term after SARS-CoV-2 infection. Among these symptoms, cognitive impairment is one of the most prevalent and has been related to brain structural and functional changes. The underlying mechanisms of these cognitive and brain alterations remain elusive but neuroinflammation and immune mechanisms have been majorly considered. In this sense, the choroid plexus (ChP) volume has been proposed as a marker of neuroinflammation in immune-mediated conditions and the ChP epithelium has been found particularly susceptible to the effects of SARS-CoV-2. The objective was to investigate the ChP in PCC and evaluate its relationships with cognition, brain, and immunological alterations. One-hundred and twenty-nine patients with PCC after a mean of 14.79 ± 7.17 months of evolution since the infection and 36 healthy controls were recruited. Participants underwent a neuropsychological, and neuroimaging assessment and immunological markers evaluation. Results revealed ChP volume enlargement in PCC compared to healthy controls. The ChP enlargement was associated with cognitive dysfunction, grey matter volume reduction in frontal and subcortical areas, white matter integrity and diffusivity changes and functional connectivity changes. These ChP changes were also related to intermediate monocytes levels. Findings suggest that the ChP integrity may play a relevant role in the pathophysiology of cognitive deficits and the observed brain changes in PCC. The previously documented function of the ChP in maintaining brain homeostasis and regulating the entry of immune cells into the brain supports the presence of neuroinflammatory mechanisms in this disorder.
Neurological post-COVID syndrome is associated with substantial impairment of verbal short-term and working memory
In 2020, severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) triggered one of the most severe pandemics in human history. The World Health Organization (WHO) estimates that by the end of 2023, approximately 773 million people had contracted acute SARS-CoV-2 infection, resulting in the multi-organ coronavirus disease 19 (COVID-19). Many of these affected patients continue to suffer from persistent or new symptoms, even 12 weeks after acute infection. This condition, in which symptoms persist or new symptoms develop at least three months after the acute infection and persist for at least two months without the finding of any causal relationship, is subsumed under the terms post COVID-19 condition or post-COVID syndrome (PCS). In the following, the term PCS refers to COVID-19 symptoms or new symptoms that cannot be attributed to any other etiology and persist more than 12 weeks after the acute COVID-19 infection. Symptoms commonly found and included in the symptom complex of PCS are hair loss, chronic kidney disease, thromboembolism, palpitations and chest pain, headache, cognitive impairment, post-traumatic stress disorder, sleep disturbances, anxiety and depressive symptoms, cough, shortness of breath, arthralgias, myalgias, and frequently and most importantly, chronic fatigue.
Total long COVID symptoms scores, prior to COVID (Pre COVID), during the long COVID phase (Post COVID), after vaccination (Post Vaccine), and after infusion of monoclonal antibodies (Post MCA) for Patient 1, Patient 2 and Patient 3, respectively. Note: Patient 3 did not receive a vaccine.