COVID-19: Study Warns Lung Damage Continues In The Recovered

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A new study shows that the persistent breathing issues that plague some COVID-19 survivors, known as “long COVID,” may be due to microscopic processes that continue to damage lungs even after the acute infection is over! https://www.medrxiv.org/content/10.1101/2021.08.10.21261834v1

The scientists studied blood and bronchoalveolar fluid samples from 38 patients who still had breathing problems at least three months after they were discharged from hospital.

Shockingly when compared to healthy volunteers, the airways of these COVID-19 survivors had higher numbers of cytotoxic lymphocytes (especially tissue resident CD8+ T cells), lactate dehydrogenase and albumin (biomarkers of cell death and barrier integrity).

Study co-author, Dr James Harker of Imperial College London, told Thailand Medical News, “Interestingly, similar changes were not found when comparing blood samples, where the composition of immune cells and proteins was similar to those of the healthy controls.”

The study findings, which still need confirmation in larger studies, suggest some patients have ongoing disturbances in their immune cells and damage to cells that line the airways, even several months after their initial infection and discharge from hospital.

Dr Harker added, “In a small group of patients, we were able to show that the abnormalities may in fact resolve with more time.”

A news Irish study shows that recovered COVID-19 patients will suffer persistent endotheliopathy and is one of the contributors to the so-called Long COVID Syndrome. https://onlinelibrary.wiley.com/doi/abs/10.1111/jth.15490
To date, constant symptoms including breathlessness, fatigue and decreased exercise tolerance have been reported in patients after acute SARS-CoV-2 infection.

The biological mechanisms underlying this ‘Long COVID’ syndrome remain unknown. However, autopsy studies have highlighted the key roles played by pulmonary endotheliopathy and microvascular immunothrombosis in acute COVID-19.

The study team hypothesized that endothelial cell activation may be sustained in convalescent COVID-19 patients and contribute to Long COVID pathogenesis.

A total of fifty patients were reviewed at a median of 68 days following SARS-CoV-2 infection. In addition to clinical workup, acute phase markers, EC activation and NETosis parameters and thrombin generation were assessed.

Interestingly, thrombin generation assays revealed significantly shorter lag times (p<0.0001, 95% CI -2.57– -1.02min), increased endogenous thrombin potential (ETP) (p=0.04, 95% CI 15–416nM/min) and peak thrombin (p<0.0001, 95% CI 39–93nM) in convalescent COVID-19 patients. These pro-thrombotic changes were independent of ongoing acute phase response or active NETosis.

Significantly, EC biomarkers including VWF:Ag, VWF propeptide (VWFpp) and Factor VIII (FVIII:C) were significantly elevated in convalescent COVID-19 compared to controls (p=0.004, 95% CI 0.09–0.57IU/ml; p=0.009, 95% CI 0.06–0.5IU/ml; p=0.04, 95% CI 0.03–0.44IU/ml, respectively). In addition, plasma soluble thrombomodulin (sTM) levels were significantly elevated in convalescent COVID-19 (p=0.02, 95% CI 0.01–2.7ng/ml).

It was found that sustained endotheliopathy was more frequent in older, comorbid patients and those requiring hospitalization. Also, both plasma VWF:Ag and VWFpp levels correlated inversely with 6-minute walk tests.

The study findings demonstrated that sustained endotheliopathy is common in convalescent COVID-19 and raise the intriguing possibility that this may contribute to Long COVID pathogenesis.


Reditus Laboratories, a genomic sequencing lab in Pekin, Illinois-USA is warning that the Delta variant is mutating rapidly. Reditus CEO Dr. Aaron Rossi said on Friday night, “The Delta variant (B.1.617.2) is currently the most predominate SARS-CoV-2 circulating within the U.S. and are supported by these data within our testing area. However, we are also seeing a large number of Delta sub-variants with some only beginning to be mentioned elsewhere.

Specifically, the AY.12 subvariant is not as common in U.S. circulation. However, within our testing population, AY.12 is nearly equivalent in prevalence as the original B.1.617.2. These data suggest that the Delta variant is mutating as quickly as it has risen to the predominate strain.”

The lab identified 361 additional cases of the B.1.617.2 variant and its sub-variants during a sequencing run on Aug. 12. These encompassed 99% of the entire sequenced positives. Most were just from Illinois. https://www.redituslabs.com/press-releases/

Alarming study findings of a new research by the University of Wisconsin have shown that in the case of breakthrough infections, the Delta variant is able to grow in the noses of vaccinated people to the same degree as if they were not vaccinated at all. The virus that grows is just as infectious as that in unvaccinated people, meaning vaccinated people can transmit the virus and infect others. https://www.medrxiv.org/content/10.1101/2021.07.31.21261387v4

Dr Kasen Riemersma, a virologist at University of Wisconsin who is one of the authors of the study said, “We’re the first to demonstrate, as far as I’m aware, that infectious virus can be cultured from the fully vaccinated infections.”

Dr Ravindra Gupta, a microbiologist at University of Cambridge whose lab was one of the first to document that fully vaccinated healthcare workers could get infected with Delta and had high levels of virus in their noses commented, “Delta is breaking through more preferentially after vaccines as compared to the non-Delta variants because it’s extremely infectious and evades the immune response.”

Dr Katarina Grande, a public health supervisor and the COVID-19 Data Team Lead of Madison & Dane County, who led the study added, “This is an alarming finding! People with breakthrough infections many of whom do not develop COVID symptoms can unknowingly spread the virus.”


By early January, 2021, COVID-19, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), had resulted in more than 83 million confirmed cases and more than 1·8 million deaths. The clinical spectrum of SARS-CoV-2 infection is wide, encompassing asymptomatic infection, fever, fatigue, myalgias, mild upper respiratory tract illness, severe life-threatening viral pneumonia requiring admission to hospital, and death.1

Physicians are observing persisting symptoms and unexpected, substantial organ dysfunction after SARS-CoV-2 infection in an increasing number of patients who have recovered, as previously observed in the SARS outbreak.2 However, COVID-19 is a new disease and uncertainty remains regarding the possible long-term health sequelae.

This is particularly relevant for patients with severe symptoms, including those who required mechanical ventilation during their hospital stay, for whom long-term complications and incomplete recovery after discharge would be expected. Unfortunately, few reports exist on the clinical picture of the aftermath of COVID-19.

The study by Chaolin Huang and colleagues3 in The Lancet is relevant and timely. They describe the clinical follow-up of a cohort of 1733 adult patients (48% women, 52% men; median age 57·0 years, IQR 47·0–65·0) with COVID-19 who were discharged from Jin Yin-tan Hospital (Wuhan, China). 6 months after illness onset, 76% (1265 of 1655) of the patients reported at least one symptom that persisted, with fatigue or muscle weakness being the most frequently reported symptom (63%, 1038 of 1655). More than 50% of patients presented with residual chest imaging abnormalities.

Disease severity during the acute phase was independently associated with the extent of lung diffusion impairment at follow-up (odds ratio 4·60, 95% CI 1·85–11·48), with 56% (48 of 86) of patients requiring high-flow nasal cannula, non-invasive ventilation, and invasive mechanical ventilation during their hospital stay having impaired pulmonary diffusion capacity.3

These findings are consistent with those from earlier small studies that reported lingering radiological and pulmonary diffusion abnormalities in a sizeable proportion of COVID-19 patients up to 3 months after hospital discharge.4, 5 Evidence from previous coronavirus outbreaks suggests that some degree of lung damage could persist, as shown in patients who recovered from SARS, 38% of whom had reduced lung diffusion capacity 15 years after infection.2

Although SARS-CoV-2 primarily affects the lungs, several other organs, including the kidney, can also be affected.6 Therefore, Huang and colleagues assessed the sequelae of extrapulmonary manifestations of COVID-19. Unexpectedly, 13% (107 of 822) of the patients who did not develop acute kidney injury during their hospital stay and presented with normal renal function, based on estimated glomerular filtration rate (eGFR) during the acute phase, exhibited a decline in eGFR (<90 mL/min per 1·73 m2) at follow-up.3 However, this finding must be interpreted with caution.

Because repeated GFR measurement using a gold-standard technique—such as plasma clearance of iohexol or iothalamate—would presumably have been unfeasible in such a large cohort of patients, GFR-estimating equations, such as that used in the present study, do not enable a sound assessment of renal function, which can be overestimated or underestimated compared with measured GFR.7 Importantly, deep venous thrombosis was not diagnosed in any of the patients who underwent ultrasonography at follow-up.3 This is an encouraging finding, in light of the frequent development of venous thromboembolism in patients with COVID-19 who are critically ill while in hospital.6

Even though the study offers a comprehensive clinical picture of the aftermath of COVID-19 in patients who have been admitted to hospital, only 4% (76 of 1733) were admitted to an intensive care unit (ICU),3 rendering the information about the long-term consequences in this particular cohort inconclusive. However, previous research on patient outcomes after ICU stays suggests that several patients with COVID-19 who were critically ill during their hospital stay will subsequently face impairments regarding their cognitive and mental health or physical function far beyond their hospital discharge.8

Outpatient clinics that are dedicated to following up on lasting disabilities in the large number of patients who previously had COVID-19 are opening in many hospitals, especially in areas where large SARS-CoV-2 outbreaks have occurred. However, this initiative implies a further burden on the health-care system in terms of human and economic resources, in addition to conventional health-care services.

Unfortunately, these clinics are largely unaffordable in most low-income or middle-income countries that have also been severely affected by the COVID-19 pandemic. However, the success of this approach to monitoring and treating patients with COVID-19 who have recovered creates an opportunity to concomitantly conduct integrated multidisciplinary research studies during 1–2 years of follow-up, as is currently happening in the UK and USA.9

These studies will improve our understanding of the natural history of COVID-19 sequelae and the factors or mediators involved, and enable us to assess the efficacy of therapeutic interventions to mitigate the long-term consequences of COVID-19 on multiple organs and tissues.

This is consistent with the syndemic nature of the COVID-19 pandemic,10 and has implications for the long-term follow-up of COVID-19 sequelae, which in most instances should be interpreted against a background of an array of non-communicable diseases and social and income inequalities that exacerbate the adverse effects of each of these diseases in many communities.

reference link : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7833833/

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