Hi everyone,
In this edition, we delve into a myriad of topics, shedding light on the distinct hormonal and immune differences found in individuals with Long Covid, as well as the heightened risk of heart attack and stroke associated with COVID-19. Additionally, we explore the long-term neurological and gastrointestinal effects of the virus, occupational differences in its prevalence and severity, and intriguing findings on the interplay between viral load, inflammatory markers, and lymphocyte subpopulations in the development of Long Covid. With contributions from leading institutions such as Mount Sinai, NYU Langone, and Wiley Online Library, this newsletter aims to raise awareness and foster support for the ever-growing Long Covid community.
Media
[Paywalled]
SUMMARY:
Amanda Twinam’s dogged efforts led to a new scientific discovery at the National Institutes of Health and a promising new line of research that may end up helping many other people with chronically fatiguing illnesses, possibly including long covid.
The red flags that Twinam had an unrecognized chronic illness began after her suspected case of mono in high school. She says she feels she never fully recovered.
“Amanda showed up and she challenged us,” says Hwang during an interview in his office. “So we dug.”
He found that skin cells taken from Twinam appeared to be churning out an excess of a protein called WASF3.
For Hwang, developing a treatment for the illness is now “what keeps me going.” His small laboratory, just four scientists, is planning a clinical trial with a drug that recently came onto the market for another disease.
SUMMARY:
Long Covid patients have clear differences in immune and hormone function from patients without the condition, according to a new study led by the Icahn School of Medicine at Mount Sinai and Yale School of Medicine.
“These findings are important—they can inform more sensitive testing for Long Covid patients and personalized treatments for Long Covid that have, until now, not had a proven scientific rationale,” says Principal Investigator David Putrino
Overall, the algorithm was able to differentiate between people with and without Long Covid with 96 percent accuracy and detect the condition based on distinctive features detected in the blood of participants in the Long Covid group.
Some of the most pronounced differences between the Long Covid group and the two control groups were related to immune and hormonal dysfunction.
This was characterized by biomarkers indicating abnormal T cell activity, reactivation of multiple latent viruses (including the Epstein-Barr virus and other herpesviruses) and significant reductions in cortisol levels.
Article: Study Helps Explain How COVID-19 Heightens Risk of Heart Attack & Stroke | NYU Langone News
DEFINITIONS:
Atherosclerosis: a disease in which plaque collects in major arteries and prompts chronic inflammation.
Macrophages: local immune cells in the body that protect the heart by "swallowing" and disposing of excess fat molecules in arteries.
SUMMARY:
In some patients, infection with the pandemic virus SARS-CoV-2 can trigger a dangerous immune response in hardened fatty deposits (plaques) lining the heart’s largest blood vessels, a new study shows.
The experiments further showed that in response to the infection, the macrophages released inflammatory signaling proteins called cytokines that promote a chronic immune response.
For the analysis, the research team collected 27 artery tissue samples from autopsies of patients who had died of severe COVID-19 between May 2020 and May 2021.
All had been previously diagnosed with heart disease.
Together the experimental findings revealed that macrophages rich in engulfed fat were invaded more frequently and for longer periods than those containing less fat.
The research team next plans to more closely explore this potential link between the coronavirus’s behavior during atherosclerosis and Long Covid, which includes heart palpitations, chest pain, and fatigue, among other issues.
My Take:
The virus can trigger an immune response in hardened fatty deposits, leading to inflammation and potentially the breaking up of plaques, which leads to blocked arteries and a myocardial infarction (heart attack).
One of my main takeaways from running this newsletter is that it appears one of Covid’s main vectors of attack is through our blood.
Article: Long Covid: When Doctors Become Patients
SUMMARY:
The elephant in the room of this pandemic is Long Covid, and doctors aren't immune to it.
A report conducted by the British Medical Association (BMA) and published in The BMJ is a worrying read: 60% of doctors with this diagnosis said that they get tired when going about their day-to-day activities.
Just under 20% admit to fatigue so debilitating that they can no longer work.
Yet, just 31% currently have a full-time job, 46% less than before being diagnosed with the disease.
My Take:
Brandon
The high rates of Long Covid among healthcare workers, including doctors, raise concerns about the impact of this chronic condition on healthcare systems around the world.
Doctors are integral to a functional society, another large reason why we need some Long Covid treatments ASAP.
AJE (contributing editor)
in my case I worked full time as an OB/GYN with severe fatigue before my condition became much worse and I could no longer work. I’ve been out of the workforce for 2 years.
Article: Long Covid isolates sick people and their loved ones - Wisconsin Examiner
SUMMARY:
“It’s been two years since I fell ill with what seemed at first like a mild Covid infection.
My illness grew into a chronic condition that left me disabled for more than a year.
Estimates of how many people develop Long Covid vary widely, but it’s at least millions of people in the United States alone.
For most of the past two years, I could not have composed the words you’re reading now.
My health has improved dramatically in the past several months thanks largely to an active Long Covid community on social media.”
My Take:
The author shares their personal experience of having Long Covid, I think it is always a good idea to highlight pieces like these.
Research
DEFINITIONS:
Viral load: the amount of viral genetic material present in a sample, which can indicate the level of viral replication and infection severity.
Lymphocyte subpopulations: different types of lymphocytes (a type of white blood cell) that play a role in immune response, including natural killer (NK) cells.
SUMMARY:
There is limited information on how inflammatory markers, viral load, and lymphocyte subpopulations during acute infection relate to the development of Long Covid.
This study aimed to explore the association between Long Covid and these factors in hospitalized patients.
Although previous studies have indicated that the amount of SARS-CoV-2 viral load correlates with the presence of long COVID and the extent of its symptoms, the current study did not find this correlation.
Patients with severe COVID-19 have shown a significant reduction in levels of lymphocytes, monocytes, CD4+T cells, CD8+T cells, CD3 cells, CD19 cells, and natural killer cells. These alterations were also observed in patients with long COVID
In this study, we found that the patients who developed long COVID had higher levels of NK cells during their hospitalization. This could be due to the persistent immune response required to control the viral infection. However, over time, these persistent immune responses may lead to dysfunction and exhaustion of NK cells.
Pentraxin 3 (PTX3): a highly conserved innate immunity protein that may serve as a valuable biochemical marker in COVID-19.
SUMMARY:
The study aimed to compare serum levels of Pentraxin 3 (PTX3) and other immune-inflammatory mediators in healthcare workers who were previously infected with SARS-CoV-2 and those who were never infected.
No other comorbidity or long COVID-19 symptoms were described by the subjects of this study.
Elevated levels of PTX3 and other inflammatory proteins were found in previously infected COVID-19-positive subjects.
PTX3 expression was more pronounced in previously COVID-19-positive males compared to females, indicating a degree of severity influenced by gender.
The results suggest that PTX3 may serve as a systemic biomarker in prolonged systemic inflammatory responses in the context of COVID-19.
My Take:
This is the first time I have ever heard of PTX3, so I found this to be very interesting!
I am not aware of Long Covid studies looking into this one but could be wrong.
This study provides evidence that PTX3 levels are elevated in individuals previously infected with COVID-19, indicating a prolonged systemic inflammatory response.
[Locked]
SUMMARY:
The study investigates the long-term dynamic shifts in genomic base content and evolutionary trajectories of SARS-CoV-2 variants.
It highlights the mechanisms and concepts in RNA virus population dynamics and evolution.
The authors collated all data from publicly available data sources for their analyses.
The study reveals the biased mutation and selection in RNA viruses, including SARS-CoV-2.
My Take:
This research provides valuable insights into the long-term evolutionary changes in SARS-CoV-2 variants, shedding light on the mechanisms and concepts in RNA virus evolution.
By analyzing publicly available data, the authors were able to identify biased mutation and selection in RNA viruses, emphasizing the importance of understanding viral evolution for effective control and mitigation strategies.
DEFINITIONS:
Angiotensin converting enzyme (ACE2): The receptor on human cells that SARS-CoV-2 uses to enter the body.
Post-viral syndromes: A group of symptoms that occur after an infection, which can include fatigue, pain, and cognitive difficulties.
SUMMARY:
COVID-19 can lead to long-term neurological and gastrointestinal effects, known as post-acute sequelae of SARS-CoV-2 infection or Long Covid (LC).
The main neurological symptoms observed in LC patients include anxiety, depression, dysphagia, headache, myalgia, and fatigue.
GI symptoms commonly reported in LC patients include dysphagia, nausea, vomiting, gastroesophageal reflux, abdominal pain, and constipation.
The GI sequelae of SARS-CoV-2 can affect any part of the digestive system, not only in the acute infection phase but also in the post-acute phase, leaving long-term sequelae to manifest frequently or sporadically.
The severity of COVID-19 symptoms can be influenced by genetic factors such as variations in the expression of the ACE2 receptor in the body, as well as differences in the virulence and transmissibility of the virus strains.
SUMMARY:
The prevalence of self-reported long COVID increased throughout the study period, with the highest prevalence observed in industries such as social care and education.
Public-facing industries and occupations, including teaching and education, social care, healthcare, civil service, retail, and transport, had the highest likelihood of long COVID.
The likelihood of reporting long COVID symptoms generally followed the trend of risk of SARS-CoV-2 infection, except for professional occupations where the odds of long-COVID were higher than that of infections.
Long COVID symptoms had a significant impact on participants' ability to carry out daily activities, particularly in healthcare and social care industries and occupations.
My Take:
The findings of this study highlight the variations in the prevalence and severity of long COVID across different industries and occupations.
Industries and occupations that involve more public-facing roles, such as teaching and education, social care, healthcare, retail, and transport, appear to have a higher risk of long COVID.
DEFINITIONS:
SUMMARY:
After the acute phase of COVID-19, some patients develop Long Covid, a condition with a complex etiology including prolonged viral persistence and progression to lung fibrosis.
This case report presents an autopsy case of a patient with severe COVID-19 who developed interstitial lung fibrosis complicated by a fatal combination of cytomegalovirus and Aspergillus infection.
SARS-CoV-2 virus was detected in the lungs more than two months after the acute infection, despite negative tests from the nasopharynx.
Immune dysregulation after COVID-19 and the administration of corticoid therapy created favorable conditions for opportunistic infections such as CMV and Aspergillus.
My Take:
CMV (along with EBV) has been implicated in other post-viral syndromes.
14 minutes into this week’s TWIV #1049 (https://youtu.be/Tx-oa0F_SJMl) the panel reviews a new Nature article (https://www.nature.com/articles/s41586-023-06651-y) you may have already covered--apologies if I missed It--but at the 14:44 mark, Brianne Barker points out the importance of these vast numbers of L-C/ME/CFS people with the same Sx occurring NOW at the same time that we have immune profiling capabilities. Because of this timing, scientists can dive in and make some serious headway--which I like to think is what I see here. ☺️ thank you!
So thinking about the HCP article you shared here, as horrifying as the numbers of health care workers who’ve contracted Long-COVID are, there’s a tiny (probably snarky) voice in my head thinking, “perhaps that’s why we’re finally seeing some real research into ME/CFS and other Post Acute Infection Syndromes.”
Now the medical and scientific community believe us.