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Biomedicines
Special Issues
Long COVID: Mechanisms, Biomarkers, and Treatment
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Long COVID: Mechanisms, Biomarkers, and Treatment

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 6490

Special Issue Editor

Dr. Frédérique Ponchel

E-Mail Website
Guest Editor
Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds LS2 9JT, UK
Interests: arthritis; T-cells; Treg; Th17; inflammation; IL6; IL7; epigenetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Prolonged symptoms post-SARS-CoV-2 infection are appearing at the alarming rate of 10–15% worldwide. These post-infection sequalae, widely termed long COVID (LC) or post-acute sequalae of COVID-19 (PACS), include a wide range of profiles of overlapping symptoms persisting for more than 12 weeks, with debilitating fatigue as the main one, associated with cognitive impairment, and many more, notably pain and postural orthostatic tachycardia (POTS)-like symptoms. An official definition of LC was released in 2021, but LC is perceived, diagnosed, and managed in many different ways across the world, with very few policies, consensus, or guidelines between the many disciplines involved.

Chronic fatigue does not ameliorate with time and, most importantly, if not resolved within the first 6 months, it may never resolveA wide range of biological disturbances have been associated with chronic fatigue and, as such, many hypotheses have been proposed, but the causative mechanisms remain unknown. Due to this lack of mechanistic insight into the causes and pathological events, no effective drug/intervention exists for LC. Furthermore, it is crucial to establish whether LC has a unique mechanism leading to chronic fatigue with potentially a universal treatment or if it represents a combination of symptoms with different mechanisms that culminate in fatigue but need alternative types of treatments. In fact, most of the proposed mechanisms for LC may not be mutually exclusive and they may overlap; alternatively, different mechanisms may develop in specific subgroups of patients. This will have a large impact on defining how rehabilitation, pharmaceutical, and lifestyle therapeutic strategies can reduce the personal/societal burden of this devastating condition.

The Special Issue invites manuscripts related to all aspects of long COVID research, including clinical, mechanistic, biomarkers, and treatment strategies.

Dr. Frédérique Ponchel
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • long-COVID
  • clinical observations
  • disease mechanism
  • biomarkers
  • treatment strategies
  • opinions

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Published Papers (3 papers)

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Research

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15 pages, 1488 KiB  
Article
Cross-Sectional Study Evaluating the Role of Autonomic Nervous System Functional Diagnostics in Differentiating Post-Infectious Syndromes: Post-COVID Syndrome, Chronic Fatigue Syndrome, and Lyme Disease
by Branislav Milovanovic, Nikola Markovic, Masa Petrovic, Vasko Zugic, Milijana Ostojic and Milovan Bojic
Biomedicines 2025, 13(2), 356; https://doi.org/10.3390/biomedicines13020356 - 4 Feb 2025
Viewed by 1512
Abstract
Background/Objectives: Post-infectious syndromes, including Post-COVID syndrome, Chronic Fatigue Syndrome, and late-stage Lyme disease, are associated with overlapping clinical features and autonomic dysfunction. Despite shared symptoms such as fatigue and orthostatic intolerance, the underlying pathophysiology and specific patterns of autonomic dysfunction may differ. [...] Read more.
Background/Objectives: Post-infectious syndromes, including Post-COVID syndrome, Chronic Fatigue Syndrome, and late-stage Lyme disease, are associated with overlapping clinical features and autonomic dysfunction. Despite shared symptoms such as fatigue and orthostatic intolerance, the underlying pathophysiology and specific patterns of autonomic dysfunction may differ. This study aimed to evaluate and compare autonomic nervous system function in these syndromes using multiple diagnostic modalities to identify unique characteristics and improve differentiation between these conditions. Methods: This cross-sectional study included 758 patients, which were divided into four groups: Post-COVID syndrome, Chronic Fatigue Syndrome following Post-COVID syndrome, Chronic Fatigue Syndrome unrelated to COVID-19, and late-stage Lyme disease. Autonomic nervous system function was assessed using cardiovascular reflex tests, the Head-Up Tilt Test, beat-to-beat analysis, five-minute electrocardiogram recordings, 24 h Holter electrocardiogram monitoring, and 24 h ambulatory blood pressure monitoring. Statistical analyses compared parameters across the groups, focusing on patterns of sympathetic and parasympathetic dysfunction. Results: The patients with Lyme disease showed distinct autonomic patterns, including a higher prevalence of orthostatic hypotension (53.4%) and changes in heart rate variability during the Head-Up Tilt Test suggestive of adrenergic failure. Compared to the other groups, patients with Lyme disease exhibited reduced baroreceptor sensitivity and diminished changes in frequency domain heart rate variability parameters during orthostatic stress. Parasympathetic dysfunction was less prevalent in the Lyme disease group, while the Post-COVID syndrome and Chronic Fatigue Syndrome groups showed more pronounced autonomic imbalances. Conclusions: The patients with Post-COVID syndrome, Chronic Fatigue Syndrome, and late-stage Lyme disease exhibited varying degrees and types of autonomic dysfunction. Late-stage Lyme disease is characterized by adrenergic failure and distinct hemodynamic responses, differentiating it from other syndromes. The functional assessment of autonomic nervous system function could aid in understanding and managing these conditions, offering insights for targeted therapeutic interventions. Full article
(This article belongs to the Special Issue Long COVID: Mechanisms, Biomarkers, and Treatment)
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Figure 1

Figure 1
<p>Changes in diastolic blood pressure during HUTT. +—<span class="html-italic">p</span> value for comparing ΔDBP of 1st group with ΔDBP of groups 2, 3, and 4 (+—<span class="html-italic">p</span> &lt; 0.05; ++—<span class="html-italic">p</span> &lt; 0.01); #—<span class="html-italic">p</span> value for comparing ΔDBP 2nd group with ΔDBP of group 3 and group 4 (#—<span class="html-italic">p</span> &lt; 0.05; ##—<span class="html-italic">p</span> &lt; 0.01); *—<span class="html-italic">p</span> value for comparing ΔDBP of the 3rd group with ΔDBP of the 4th group (*—<span class="html-italic">p</span> &lt; 0.05; **—<span class="html-italic">p</span> &lt; 0.01); all <span class="html-italic">p</span>-values were adjusted for pairwise comparisons using the Bonferroni correction.</p> Full article ">Figure 2
<p>Changes in baroreflex sensitivity during HUTT. #—<span class="html-italic">p</span> value for comparing ΔBRS 2nd group with ΔBRS of groups 3 and 4 (#—<span class="html-italic">p</span> &lt; 0.05; ##—<span class="html-italic">p</span> &lt; 0.01); *—<span class="html-italic">p</span> value for comparing ΔBRS of 3rd group with ΔBRS of 4th group (*—<span class="html-italic">p</span> &lt; 0.05; **—<span class="html-italic">p</span> &lt; 0.01); all <span class="html-italic">p</span>-values were adjusted for pairwise comparisons using the Bonferroni correction.</p> Full article ">Figure 3
<p>VLF (ms<sup>2</sup>) in supine position. VLF—very-low-frequency component of HRV; +—<span class="html-italic">p</span> value for comparing the 1st group with groups 2, 3, and 4 (+—<span class="html-italic">p</span> &lt; 0.05; ++—<span class="html-italic">p</span> &lt; 0.01); #—<span class="html-italic">p</span> value for comparing the 2nd group with groups 3 and 4 (#—<span class="html-italic">p</span> &lt; 0.05; ##—<span class="html-italic">p</span> &lt; 0.01); *—<span class="html-italic">p</span> value for comparing the 3rd group with the 4th group (*—<span class="html-italic">p</span> &lt; 0.05; **—<span class="html-italic">p</span> &lt; 0.01); all <span class="html-italic">p</span>-values were adjusted for pairwise comparisons using the Bonferroni correction.</p> Full article ">Figure 4
<p>(<b>A</b>) Changes in SDSD, (<b>B</b>) total power, (<b>C</b>) very low frequency, (<b>D</b>) low frequency, (<b>E</b>) LF/HF (expressed in ms<sup>2</sup>) during HUTT between the groups. SDSD—the standard deviation of the successive differences between adjacent normal RR interval; total power of HRV; very-low-frequency component of HRV (0–0.05 Hz); low-frequency component of HRV (0.05–0.17 Hz); LF/HF—low-frequency/high-frequency ratio of HRV; +—<span class="html-italic">p</span> value for comparing Δ values of the 1st group with groups 2, 3, and 4 (+—<span class="html-italic">p</span> &lt; 0.05; ++—<span class="html-italic">p</span> &lt; 0.01); #—<span class="html-italic">p</span> value for comparing Δ values of 2nd group with groups 3 and 4 (#—<span class="html-italic">p</span> &lt; 0.05; ##—<span class="html-italic">p</span> &lt; 0.01); *—<span class="html-italic">p</span> value for comparing Δ values of the 3rd group with the 4th group (*—<span class="html-italic">p</span> &lt; 0.05; **—<span class="html-italic">p</span> &lt; 0.01); all <span class="html-italic">p</span>-values were adjusted for pairwise comparisons using the Bonferroni correction.</p> Full article ">Figure 5
<p>Changes in rMSSD and pNN50 during HUTT. rMSSD—the square root of the mean of the squares of the successive differences between adjacent normal RR intervals; pNN50—the percentage of intervals &gt; 50 ms different from preceding interval; +—<span class="html-italic">p</span> value for comparing the 1st group with groups 2, 3, and 4 (+—<span class="html-italic">p</span> &lt; 0.05; ++—<span class="html-italic">p</span> &lt;0.01); #—<span class="html-italic">p</span> value for comparing the 2nd group with groups 3 and 4 (#—<span class="html-italic">p</span> &lt; 0.05; ##—<span class="html-italic">p</span> &lt; 0.01); *—<span class="html-italic">p</span> value for comparing the 3rd group with the 4th group (*—<span class="html-italic">p</span> &lt; 0.05; **—<span class="html-italic">p</span> &lt; 0.01).</p> Full article ">
13 pages, 699 KiB  
Article
Pharmacotherapy from Pre-COVID to Post-COVID: Longitudinal Trends and Predictive Indicators for Long COVID Symptoms
by Nadia Baalbaki, Sien T. Verbeek, Harm Jan Bogaard, Jelle M. Blankestijn, Vera C. van den Brink, Merel E. B. Cornelissen, Jos W. R. Twisk, Korneliusz Golebski and Anke H. Maitland-van der Zee
Biomedicines 2024, 12(12), 2694; https://doi.org/10.3390/biomedicines12122694 - 26 Nov 2024
Viewed by 764
Abstract
Background/objectives: A significant number of COVID-19 cases experience persistent symptoms after the acute infection phase, a condition known as long COVID or post-acute sequelae of COVID-19. Approved prevention and treatment options for long COVID are currently lacking. Given the heterogeneous nature of long [...] Read more.
Background/objectives: A significant number of COVID-19 cases experience persistent symptoms after the acute infection phase, a condition known as long COVID or post-acute sequelae of COVID-19. Approved prevention and treatment options for long COVID are currently lacking. Given the heterogeneous nature of long COVID, a personalized medicine approach is essential for effective disease management. This study aimed to describe trends in pharmacotherapy from pre-COVID to post-COVID phases to gain insights into COVID-19 treatment strategies and assess whether pre-COVID pharmacotherapy can predict long COVID symptoms as a health status indicator. Methods: In the Precision Medicine for more Oxygen (P4O2) COVID-19 study, 95 long COVID patients were comprehensively evaluated through post-COVID outpatient clinics and study visits. This study focused on descriptive analysis of the pharmacotherapy patterns across different phases: pre-COVID-19, acute COVID, and post-COVID. Furthermore, associations between pre-COVID medication and long COVID outcomes were analyzed with regression analyses. Results: We observed peaks in the use of certain medications during the acute infection phase, including corticosteroids and antithrombotic agents, with a decrease in the use of renin–angiotensin system inhibitors. Consistently high use of alimentary tract medications was found across all phases. Pre-COVID respiratory medications were associated with fatigue symptoms, while antiinfectives and cardiovascular drugs were linked to fewer persisting long COVID symptom categories. Conclusion: Our findings provide longitudinal, descriptive pharmacotherapy insights and suggest that medication history can be a valuable health status indicator in characterizing patients for personalized disease management strategies, considering the heterogeneous nature of long COVID. Full article
(This article belongs to the Special Issue Long COVID: Mechanisms, Biomarkers, and Treatment)
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Figure 1

Figure 1
<p>Methods visualization. Data were collected from 95 P4O2 COVID-19 study participants at 3–6 months post-infection. Pharmacotherapy was reported at four time points (pre-COVID-19, during COVID-19, post-COVID, and at 3–6 months post-infection or long COVID). Self-reported symptom data at 3–6 months were categorized into fatigue, respiratory, neurological, cardiovascular, gastrointestinal, and other complaints.</p> Full article ">Figure 2
<p>Pharmacotherapy from pre-COVID to LC. A longitudinal visualization of the percentages of pharmacotherapy use among P4O2 COVID-19 study participants, categorized according to the first-level ATC medication groups.</p> Full article ">

Other

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7 pages, 684 KiB  
Perspective
Neuroinflammation at the Dorsolateral Inferior Medulla: A Possible Central Nervous System Localization for POTS and Long COVID
by Svetlana Blitshteyn
Biomedicines 2025, 13(1), 166; https://doi.org/10.3390/biomedicines13010166 - 12 Jan 2025
Viewed by 3789
Abstract
Both postural orthostatic tachycardia syndrome (POTS) and Long COVID are currently viewed as heterogeneous disorders with complex, multi-factorial and multi-systemic pathophysiology. POTS, one of the most common autonomic disorders, is a frequent sequela of SARS-CoV-2 infection. Both POTS and autonomic dysfunction, in general, [...] Read more.
Both postural orthostatic tachycardia syndrome (POTS) and Long COVID are currently viewed as heterogeneous disorders with complex, multi-factorial and multi-systemic pathophysiology. POTS, one of the most common autonomic disorders, is a frequent sequela of SARS-CoV-2 infection. Both POTS and autonomic dysfunction, in general, are major pathophysiologic mechanisms of Long COVID. There is emerging evidence that neuroinflammation of the brainstem may be one of the mechanisms of POTS and Long COVID. This commentary argues that neuroinflammation at the dorsolateral inferior medulla is a possible central nervous system localization for POTS and Long COVID based on the limited scientific literature available to date and the neurologic manifestations of both disorders. Further studies involving advanced neuroimaging techniques and animal models with immunohistochemical brainstem tissue assessments are needed to understand how and why possible neuroinflammation at the dorsolateral inferior medulla may occur in patients with Long COVID, POTS and other disorders involving autonomic dysfunction. Full article
(This article belongs to the Special Issue Long COVID: Mechanisms, Biomarkers, and Treatment)
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Figure 1

Figure 1
<p>Cross-section of the inferior medulla with highlighted structures that may form the central nervous system localization of POTS and Long COVID.</p> Full article ">Figure 2
<p>Mechanisms that may lead to neuroinflammation at the dorsolateral inferior medulla.</p> Full article ">
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