David it Up! Profile picture
Sep 29 1 tweets 1 min read Read on X
Inflamed from Within: How COVID-19 Ignites Heart Damage

Here is a version non-medical language terms.

Scientists recently uncovered something unsettling in a study of 54 heart tissue samples. The virus behind COVID-19 can creep into heart cells too, stirring up a storm of inflammation. These heart cells, called *cardiomyocytes*, are meant to keep our hearts beating strong, but this virus has found a way in, using the *TNF-NF-κB* pathway—a process that, when pushed too far, spells trouble.

Once inside, the virus seems to change the very way these heart cells function, flipping genetic switches that can lead to chaos. One gene, called *CXCL2*, kicks into high gear, summoning immune cells to the heart like soldiers to a battlefield. But sometimes, too many soldiers can cause more damage than they fix.

The protein at the center of this, *NF-κB*, is like the conductor of this chaotic orchestra, fueling inflammation that, if left unchecked, can weaken the heart. It’s as if the body, in trying to defend itself, starts tearing at its own foundation.

This study adds to a growing concern—COVID-19 is leaving its mark on the heart, and some of that damage may linger long after the virus has left. Scientists are sounding the alarm, and they’re urging us to take this more seriously than ever before.

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More from @Dave_it_up

Jun 23
Is their evidence for viral persistence in COVID-19?

From the meticulous work of the PolyBio Research Foundation, in collaboration with the esteemed halls of UC San Francisco and Harvard Medical School, to the robust findings published in Nature and The Lancet, we are presented with compelling evidence of the virus’s tenacity. 

These studies not only confirm the presence of viral proteins and RNA months after the acute phase of infection but also suggest a troubling link to the chronic, debilitating symptoms known as long COVID.

Let’s delve into some of the evidence for the evidence pointing to viral persistence of SARS-CoV-2, 

1. PolyBio Research Foundation Study
A study published by the PolyBio Research Foundation, supported by UC San Francisco and Harvard Medical School, found that viral proteins from SARS-CoV-2 could persist in the body for up to 14 months post-infection. This study used an ultra-sensitive blood test to detect viral proteins in 25% of the 171 participants, indicating that the virus can linger in tissues and organs long after recovery from the acute phase of the infection. The likelihood of detecting these proteins was higher among those who were hospitalized or reported severe symptoms during their initial infection[1].

2. Nature Study on Persistent SARS-CoV-2 RNA Shedding
A cohort study published in *Nature* identified persistent SARS-CoV-2 RNA shedding in individuals for at least 30 days, with some cases extending to 60 days. The study found that individuals with persistent infections had more than 50% higher odds of reporting long COVID symptoms compared to those with non-persistent infections. This suggests that persistent infections could contribute to the pathophysiology of long COVID, although the exact mechanisms remain to be fully understood[3].

3. NCBI Study on Long COVID and Viral Persistence
Research published on NCBI proposed a hypothesis-driven model for long COVID, suggesting that the persistence of SARS-CoV-2 or its components (such as the spike protein) could lead to chronic inflammation and a dysregulated immune response. This model is supported by evidence of viral RNA and antigens being detected in various tissues, including the cerebrospinal fluid and feces, months after the initial infection. The study highlights the potential for viral persistence to trigger long-term health issues[2].

4. Lancet Study on Viral Persistence in Tissues
A study published in *The Lancet* examined the persistence of SARS-CoV-2 in various tissues, including blood, gastrointestinal, and surgical samples. The research found that viral RNA and proteins could be detected in these tissues long after the acute phase of infection, suggesting that the virus can persist in different parts of the body and potentially contribute to ongoing symptoms and health complications[5].

5. NCBI Study on Viral Persistence and Reactivation
Another study on NCBI explored the persistence of viral RNA and antigens in patients with long COVID. It found that viral components could be detected in blood, stool, and urine, and that the presence of these components was associated with persistent symptoms. The study also noted that viral persistence might involve either active replication or the presence of non-replicating viral RNA, which could still trigger immune responses and inflammation[4].

The evidence from these studies collectively supports the notion that SARS-CoV-2 can persist in the body for extended periods, potentially leading to long-term health issues such as long COVID. This persistence can involve both active viral replication and the presence of viral components that continue to stimulate the immune system, leading to chronic inflammation and other symptoms. 

Further research should be done to put to rest this question of viral persistence and to develop effective treatments for long-term COVID.Image
Sources
[1] COVID-19 Virus Can Persist in the Body More Than a Year after ...
[2] Long COVID: A proposed hypothesis-driven model of viral ... - NCBI
[3] Prevalence of persistent SARS-CoV-2 in a large community ... - Nature
[4] Viral persistence, reactivation, and mechanisms of long COVID - NCBI
[5] The persistence of SARS-CoV-2 in tissues and its association with ... biospace.com/article/releas…
ncbi.nlm.nih.gov/pmc/articles/P…
nature.com/articles/s4158…
ncbi.nlm.nih.gov/pmc/articles/P…
thelancet.com/journals/lanin…
Someone just let me know that there are actually two more studies that are important. I will post them as soon as I get a hold of them.
Read 6 tweets
Dec 24, 2023
Similarities of HIV and Covid.

A study reveals that SARS-CoV-2 can infect human CD4+ T helper cells, impacting the immune response in severe COVID-19 cases. The virus uses the CD4 molecule to enter these cells, leading to functional impairment and cell death. This infection results in increased IL-10 production in T cells, associated with viral persistence and severe disease. The findings suggest that SARS-CoV-2 infection of CD4+ T cells contributes to immune dysfunction in COVID-19.

elifesciences.org/articles/84790
From Merk manual for healthcare professionals.
Image
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Also thanks for graphic @dbdugger
Read 4 tweets

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