Biomolecule Contributors to Long COVID Syndrome

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 December 2024) | Viewed by 9938

Special Issue Editor


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Guest Editor
Department of Cardiology, Medical University of Vienna, Vienna, Austria
Interests: long COVID-19; post-COVID-19; multiorgan disease; cardiac regeneration; cell-based and cell-free therapies; translational animal models of cardiac diseases; ischemic heart diseases
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Special Issue Information

Dear Colleagues,

Long COVID-19 syndrome is a new multiorgan manifestation of SARS-CoV-2 infection, with a prolonged post-viral phase lasting over months or even years in many patients. Depending on the SARS-CoV-2 variants, the prevalence of long COVID-19 syndrome ranges from 3% (newest omicron variant) to 37% (early alpha and beta variants), resulting in an unexpected huge socioeconomic and health burden worldwide. According to disease treatment priority to prevent COVID-19-related death, enormous effort is ongoing to elaborate circulating biomarkers predictive of acute COVID-19 disease severity and outcome and to search for effective treatment options. The mortality rates of long COVID-19 disease are low, even though morbidity rates are high; as such, long COVID-19 syndrome has attracted much less interest in the scientific medical community. However, as the number of patients with long-lasting post-viral syndromes (such as chronic fatigue syndrome, disability, diverse neurological and neuropsychiatric syndrome, leading to inability to work and to carry out daily activities) exponentially increases, research on long COVID-19 syndrome has also come to the front.  Several circulating biomarkers or clinical symptoms documented during acute illness have been related to developing long COVID-19 or post-COVID-19 syndrome. However, as over 90% of SARS-CoV-2-infected patients had no medical investigations during the acute phase, predicting the occurrence of long COVID-19 is difficult, if not impossible. Currently, no diagnostic biomolecules or circulating mediators have been identified to be present in patients with long COVID-19 syndrome, and none have been found to be predictive of severity, type, or longevity of long COVID-19 disease.

In this Special Issue of Biomolecules called “Biomolecule Contributors to Long COVID-19 Syndrome”, we invite original research articles or reviews reporting significant diagnostic or prognostic biomolecules, which are related to this new multiorgan disease and in association with the patient clinical presentation.

Prof. Dr. Mariann Gyöngyösi
Guest Editor

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Keywords

  • long COVID-19
  • post-COVID-19
  • post-viral
  • SARS-CoV-2
  • chronic fatigue syndrome
  • multiorgan disease

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Published Papers (3 papers)

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Research

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14 pages, 583 KiB  
Article
Circulating Autoantibodies Against Vasoactive Biomarkers Related to Orthostatic Intolerance in Long COVID Patients Compared to No-Long-COVID Populations: A Case-Control Study
by Emilie Han, Katrin Müller-Zlabinger, Ena Hasimbegovic, Laura Poschenreithner, Nina Kastner, Babette Maleiner, Kevin Hamzaraj, Andreas Spannbauer, Martin Riesenhuber, Anja Vavrikova, Antonia Domanig, Christian Nitsche, Dominika Lukovic, Thomas A. Zelniker and Mariann Gyöngyösi
Biomolecules 2025, 15(2), 300; https://doi.org/10.3390/biom15020300 - 18 Feb 2025
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Abstract
Endothelial dysfunction mediated by elevated levels of autoantibodies against vasoactive peptides occurring after COVID-19 infection is proposed as a possible pathomechanism for orthostatic intolerance in long COVID patients. This case-control study comprised 100 long COVID patients from our prospective POSTCOV registry and three [...] Read more.
Endothelial dysfunction mediated by elevated levels of autoantibodies against vasoactive peptides occurring after COVID-19 infection is proposed as a possible pathomechanism for orthostatic intolerance in long COVID patients. This case-control study comprised 100 long COVID patients from our prospective POSTCOV registry and three control groups, each consisting of 20 individuals (Asymptomatic post-COVID group; Healthy group = pan-negative for antispike protein of SARS-CoV-2; Vaccinated healthy group = no history of COVID-19 and vaccinated). Autoantibodies towards muscarinic acetylcholine receptor M3, endothelin type A receptor (ETAR), beta-2 adrenergic receptor (Beta-2 AR), angiotensin II receptor 1 and angiotensin 1-7 (Ang1-7) concentrations were measured by enzyme-linked immunosorbent assay in long COVID patients and controls. Orthostatic intolerance was defined as inappropriate sinus tachycardia, postural tachycardia, orthostatic hypotonia and other dysautonomia symptoms, such as dizziness or blurred vision (n = 38 long COVID patients). Autoantibody concentrations were compared with routine laboratory parameters and quality of life questionnaires (EQ-5D). The concentration of ETAR autoantibodies were significantly higher in long COVID, Asymptomatic and Vaccinated groups compared to the antispike protein pan-negative Healthy group. A trend towards higher plasma levels of Beta-2 AR and Ang1-7 was measured in long COVID patients, not related to presence of orthostatic intolerance. ETAR autoantibody concentration showed significant positive correlation with the EQ-5D item “Problems in performing usual activities”. Full article
(This article belongs to the Special Issue Biomolecule Contributors to Long COVID Syndrome)
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Review

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28 pages, 1855 KiB  
Review
Insights into COVID-19: Perspectives on Drug Remedies and Host Cell Responses
by Ahmed M. Awad, Kamryn Hansen, Diana Del Rio, Derek Flores, Reham F. Barghash, Laura Kakkola, Ilkka Julkunen and Kareem Awad
Biomolecules 2023, 13(10), 1452; https://doi.org/10.3390/biom13101452 - 26 Sep 2023
Cited by 3 | Viewed by 3568
Abstract
In light of the COVID-19 global pandemic caused by SARS-CoV-2, ongoing research has centered on minimizing viral spread either by stopping viral entry or inhibiting viral replication. Repurposing antiviral drugs, typically nucleoside analogs, has proven successful at inhibiting virus replication. This review summarizes [...] Read more.
In light of the COVID-19 global pandemic caused by SARS-CoV-2, ongoing research has centered on minimizing viral spread either by stopping viral entry or inhibiting viral replication. Repurposing antiviral drugs, typically nucleoside analogs, has proven successful at inhibiting virus replication. This review summarizes current information regarding coronavirus classification and characterization and presents the broad clinical consequences of SARS-CoV-2 activation of the angiotensin-converting enzyme 2 (ACE2) receptor expressed in different human cell types. It provides publicly available knowledge on the chemical nature of proposed therapeutics and their target biomolecules to assist in the identification of potentially new drugs for the treatment of SARS-CoV-2 infection. Full article
(This article belongs to the Special Issue Biomolecule Contributors to Long COVID Syndrome)
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16 pages, 3076 KiB  
Review
Pathogenetic Mechanisms of Liver-Associated Injuries, Management, and Current Challenges in COVID-19 Patients
by Muhammad Naeem, Naheed Bano, Saba Manzoor, Aftab Ahmad, Nayla Munawar, Saiful Izwan Abd Razak, Tze Yan Lee, Sutha Devaraj and Abu Hazafa
Biomolecules 2023, 13(1), 99; https://doi.org/10.3390/biom13010099 - 3 Jan 2023
Cited by 6 | Viewed by 4414
Abstract
The global outbreak of COVID-19 possesses serious challenges and adverse impacts for patients with progression of chronic liver disease and has become a major threat to public health. COVID-19 patients have a high risk of lung injury and multiorgan dysfunction that remains a [...] Read more.
The global outbreak of COVID-19 possesses serious challenges and adverse impacts for patients with progression of chronic liver disease and has become a major threat to public health. COVID-19 patients have a high risk of lung injury and multiorgan dysfunction that remains a major challenge to hepatology. COVID-19 patients and those with liver injury exhibit clinical manifestations, including elevation in ALT, AST, GGT, bilirubin, TNF-α, and IL-6 and reduction in the levels of CD4 and CD8. Liver injury in COVID-19 patients is induced through multiple factors, including a direct attack of SARS-CoV-2 on liver hepatocytes, hypoxia reperfusion dysfunction, cytokine release syndrome, drug-induced hepatotoxicity caused by lopinavir and ritonavir, immune-mediated inflammation, renin-angiotensin system, and coagulopathy. Cellular and molecular mechanisms underlying liver dysfunction are not fully understood in severe COVID-19 attacks. High mortality and the development of chronic liver diseases such as cirrhosis, alcoholic liver disease, autoimmune hepatitis, nonalcoholic fatty liver disease, and hepatocellular carcinoma are also associated with patients with liver damage. COVID-19 patients with preexisting or developing liver disease should be managed. They often need hospitalization and medication, especially in conjunction with liver transplants. In the present review, we highlight the attack of SARS-CoV-2 on liver hepatocytes by exploring the cellular and molecular events underlying the pathophysiological mechanisms in COVID-19 patients with liver injury. We also discuss the development of chronic liver diseases during the progression of SARS-CoV-2 replication. Lastly, we explore management principles in COVID-19 patients with liver injury and liver transplantation. Full article
(This article belongs to the Special Issue Biomolecule Contributors to Long COVID Syndrome)
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