At least one long-term symptom seen in 37% of COVID-19 patients -study

by Reuters Wednesday, 29 September 2021 11:06 GMT

Sept 29 (Reuters) – At least one long-term COVID-19 symptom was found in 37% of patients three to six months after they were infected by the virus, a large study from Oxford University and the National Institute for Health Research showed on Wednesday.

The most common symptoms included breathing problems, fatigue, pain and anxiety, Oxford University said, after investigating symptoms in over 270,000 people recovering from COVID-19.

The symptoms were more frequent among people who had been previously hospitalised with COVID-19 and were slightly more common among women, according to the study.

The study did not provide any detailed causes of long-COVID symptoms, their severity, or how long they could last.

It, however, said older people and men had more breathing difficulties and cognitive problems, whereas young people and women had more headaches, abdominal symptoms and anxiety or depression.

“We need to identify the mechanisms underlying the diverse symptoms that can affect survivors,” said Oxford University professor Paul Harrison, who headed the study.

“This information will be essential if the long-term health consequences of COVID-19 are to be prevented or treated effectively,” Harrison added. (

The OC43 human coronavirus envelope protein is critical for infectious virus production and propagation in neuronal cells and is a determinant of neurovirulence and CNS pathology

Authors:Jenny K.Stodola1GuillaumeDubois1AlainLe CoupanecMarcDesforgesPierre J.Talbot

Highlights

Coronavirus structural envelope (E) protein specific motifs involved in protein-protein interaction or in homo-oligomeric ion channel formation are needed for optimal production of recombinant infectious virus.•

Fully functional E protein of HCoV-OC43 is crucial for viral propagation in the CNS and neurovirulence.•

Fully functional E protein of HCoV-OC43 is crucial for efficient viral propagation in the central nervous system and thereby for neurovirulence.

Abstract

The OC43 strain of human coronavirus (HCoV-OC43) is an ubiquitous respiratory tract pathogen possessing neurotropic capacities. Coronavirus structural envelope (E) protein possesses specific motifs involved in protein-protein interaction or in homo-oligomeric ion channel formation, which are known to play various roles including in virion morphology/assembly and in cell response to infection and/or virulence. Making use of recombinant viruses either devoid of the E protein or harboring mutations either in putative transmembrane domain or PDZ-binding motif, we demonstrated that a fully functional HCoV-OC43 E protein is first needed for optimal production of recombinant infectious viruses. Furthermore, HCoV-OC43 infection of human epithelial and neuronal cell lines, of mixed murine primary cultures from the central nervous system and of mouse central nervous system showed that the E protein is critical for efficient and optimal virus replication and propagation, and thereby for neurovirulence.

For More Information: https://www.sciencedirect.com/science/article/pii/S0042682217304361

Inflammatory brain injury higher in men with acute COVID-19, finds study

Authors: By Dr. Liji Thomas, MD

The coronavirus disease 2019 (COVID-19) pandemic has been associated with both short- and long-term neurologic complications, including stroke, brain fog and persistent tiredness.

A new study concludes that the effects of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on the central nervous system are due to the endothelial injury and inflammation that this produces in the brain.Study: Markers of brain and endothelial Injury and inflammation are acutely and sex specifically regulated in SARS-CoV-2 infection. Image Credit: Ralwell / ShutterstockStudy: Markers of brain and endothelial Injury and inflammation are acutely and sex specifically regulated in SARS-CoV-2 infection. Image Credit: Ralwell / Shutterstock

A preprint version of the study is available on the medRxiv* server, while the article undergoes peer review.

Study aims

Since the beginning of the pandemic, it has become clear that men are often more affected by COVID-19, with a higher likelihood of severe illness and a greater chance of death.

The current study focused on assessing brain injury markers (BIM) within 48 hours of hospitalization and at three months later.

BIMs are recognized as being valid indicators of injury to nerve cells and astrocytes, in human immunodeficiency virus (HIV) infection, sepsis and cardiac arrest. The current study focused on six, namely, glial fibrillary acidic protein (GFAP), neuron-specific enolase (NSE), S100B, ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCHL1), Syndecan-1 and microtubule-associated protein 2 (MAP 2).

The scientists also examined levels of two markers of endothelial injury (Intercellular Adhesion Molecule 1, ICAM-1 and Vascular Cell Adhesion Molecule 1, VCAM-1) and of inflammation, in the form of cytokines or chemokines.

These were measured in hospitalized patients and in controls in a single hospital in Houston, Texas, USA. None of them had chronic lung, heart, neurological or psychiatric disease, cancer, or any disabling condition.

Increased markers of endothelial and brain injury

The researchers found that within 48 hours of hospitalization, that is, during the acute phase, patients had higher markers of brain injury like MAP2 and NSE than controls. The mean levels showed an increase of 60% to 145%, depending on the individual marker, relative to the controls.

Of these markers, MAP2 is a sign of dendritic injury, and was high at both acute and chronic time points. It has previously been shown to be high after traumatic brain injury and predicts long-term outcomes.

NSE is found in nerve cells and indicates damage. S100B is found in astrocytes and is high in traumatic brain injury and in strokes. Thus, this combination of BIMs shows combined nerve cell and astrocytic injury in COVID-19, worse in men than in women.

However, all markers had returned to normal at three months from hospitalization.

Markers of endothelial injury were also higher with acute infection, with the mean levels being two and three times higher than in controls, for ICAM1 and VCAM1, respectively. These were not assessed at three months.

The endothelial marker ICAM1 is released in response to IL-1b and TNFα. The effects are increased leukocyte adhesion, which reduces the barrier’s integrity and promotes leakage from the blood vessels.

Cytokines and chemokines were also much higher, in some cases, in acute infection, but others showed a decrease. Of 38 chemokines and cytokines evaluated, seven were high, while two were low. Again, these reverted to normal levels at three months.  

TNFα is a potent inflammatory mediator. Its elevation in this context indicates that the vascular injury is probably inflammatory in origin and not due to viral injury.

For More Information: https://www.news-medical.net/news/20210531/Inflammatory-brain-injury-higher-in-men-with-acute-COVID-19-finds-study.aspx