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COVID-19 News - SARS-CoV-2 Viral Persistence  Dec 02, 2022  1 year, 2 months, 4 weeks, 2 days, 6 hours, 1 minute ago

COVID News: New York Scientists Find SARS-CoV-2 Viral Presence In The Lung Up To 359 Days After Acute Phase Of Disease Even In The Negative Tested!

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COVID News: New York Scientists Find SARS-CoV-2 Viral Presence In The Lung Up To 359 Days After Acute Phase Of Disease Even In The Negative Tested!
COVID-19 News - SARS-CoV-2 Viral Persistence  Dec 02, 2022  1 year, 2 months, 4 weeks, 2 days, 6 hours, 1 minute ago
COVID News: A new study conducted by researchers from Weill Cornell Medicine, New York - USA has found SARS-CoV-2 viral presence in the lung up to 359 days after acute phase of disease, even in patients with negative nasopharyngeal swab tests!

The study findings validate that SARS-CoV-2 viral persistence is a major health issues that needs to be addressed immediately as it is not only a contributing factor to Long COVID issues but is also a major driving force behind a variety of mid to long term medical conditions that can also have fatal outcomes, leading to the rise of excess deaths that we are now witnessing globally.
Despite Thailand Medical News issuing warnings about the dangers of SARS-CoV-2 viral persistence in our various past COVID-19 News coverages, till date…no research groups or physicians have come up with solutions to address the problem let alone acknowledge that it is a major problem and that current guidelines and protocols of handling the disease are all wrong!
Current diagnostics to ascertain as to whether a person has recovered using nasal or saliva swabs are totally ridiculous as we know that the SARS-CoV-2 virus can hide in various reservoirs in the body including various tissues and organs and that viremia is also a common occurrence. At presence, we do not have any effective antivirals that can thoroughly clear the virus from the body.,-infections-pass-71-8-million-why-are-authorities-downplaying-viral-persistence
SARS-CoV-2 infection can manifest as a wide range of respiratory and systemic symptoms well after the acute phase of infection in over 50% of patients.
However, key questions remain on the long-term effects of infection on tissue pathology in recovered COVID-19 patients.
In order to address these questions, the study team from Weil Medicine performed multiplexed imaging of post-mortem lung tissue from 12 individuals who died post-acute COVID-19 (PC) and compared them to lung tissue from patients who died during the acute phase of COVID-19, or patients who died with idiopathic pulmonary fibrosis (IPF), and otherwise healthy lung tissue.
Shockingly, the study findings showed evidence of viral presence in the lung up to 359 days after the acute phase of disease, including in patients with negative nasopharyngeal swab tests.
The lung of post-acute COVID-19 (PC) patients were characterized by the accumulation of senescent alveolar type 2 cells, fibrosis with hypervascularization of peribronchial areas and alveolar septa, as the most pronounced pathophysiological features.
At the cellular level, lung disease of PC patients, while distinct, shares pathological features with the chronic pulmonary disease of IPF. which may help rationalize interventions for PC patients.
The study findings provide an important foundation for the understanding of the long-term effects of SARS-CoV-2 pulmonary infection at the microanatomical, cellular, and molecular level.
The study findings were published on a preprint server and are currently being peer reviewed.
One of the important key findings of the study is that persistent SARS-CoV-2 presence is associated with AT-2 cell senescence that plays a role in AT-2 dysfunction driving fibrosis in UIP/IPF (usual interstitial pneumonia associated with idiopathic pulmonary fibrosis)
During the study involving post-acute COVID-19 (PC) patients followed for a period of up to 399 days, the study team identified surprisingly persistent loss of lung lacunarity (as a proxy for pulmonary capacity), fibrosis, and perturbed immune and structural cellular components of the lung.
Importantly, the study team identified persistent presence of SARS-CoV-2 epitopes in the lung of PC patients, which did not necessarily agree with the status of the last nasopharyngeal test of the patients.
The findings however agree with recent reports showing viral factors present in circulation and in the gut of long COVID patients.
The study team also observed that SARS-CoV-2 presence is linked with the activation of senescence in AT-2, mesenchymal, endothelial, and fibroblast cells as detected by the upregulation of p16INK4A, uPAR, and IL-6 which is part of the senescence associated secretory profile (SASP).
Interestingly, SARS-CoV-2 induction of senescence in AT-2 cells had been suggested in acute disease, but its long-term persistence after the acute disease raises the question of whether AT-2 senescence provides a reservoir for SARS-CoV-2 - something that would require future validation using viral replication assays.
The fact that mesenchymal cells in addition to AT-2s display increased senescence suggests a “double-hit” for the maintenance of epithelial cells in the lung since they can promote AT-2 self-renewal and relieve AT-2 senescence.
On the whole, the study findings found that PC cases showed distinct features in comparison to healthy lung or acute COVID-19, with extensive derangement of the vascular network characterized by increased microvascularization and NET-induced vascular damage.
Thrombosis as well as intussusceptive and sprouting angiogenesis have been found in acute COVID-19 at higher levels than in Influenza patients.
The fact that the study findings found the level of vascular derangement higher in post-acute than in acute COVID-19 suggests that vascular remodeling is a continuously acting process during post-acute COVID disease.
Although UIP/IPF and sequelae of SARS-CoV-2 infection develop at largely different time scales (years and months respectively), the study team identified several common aspects between the diseases such as increased fibrosis and fibroblast abundance, vascular remodeling, increase of Mast cells, and upregulation of CC16/SCGB1A1 secretion.
It must be noted that mast cells play a pivotal role in IPF, with particular importance to the establishment of the fibrotic phenotype. Mast cell involvement in PASC has been suggested based on comparative analysis of symptomatic questionnaires and molecular analysis of circulatory factors.
The secreted Club cell marker CC16/SCGB1A1 is overexpressed in IPF42 but it was recently linked to negative regulation of the microbial response of alveolar macrophages.
However, this feedback may not function similarly in the host response to COVID-19 which is characterized by high influx of interstitial macrophages to the lung and may not be responsive to CC16 inhibition.
The study findings suggests that while pathologically distinct entities, prolonged lung disease after acute COVID-19 may depend on the use of common features as IPF.
The study’s use of tissue from fatal cases of post-acute COVID-19 patients may not allow complete extrapolation to the full diversity of the PASC syndrome. It does however represent an extremely timely and valuable resource to study lung pathology of acute and post-acute COVID-19 from the microanatomical to single cell level and highlights persistent pathological derangement of lung structure in patients with prolonged lung disease post-acute COVID-19.
Most importantly the study findings add to the growing evidence that SARS-CoV-2 viral persistence is a major issue that needs to addressed urgently and also that current diagnostic protocols to assess recovery is simply ineffective!
For the latest COVID-19 News, keep on logging to Thailand Medical News.
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