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Article ; Online: Platelets in HIV: A Guardian of Host Defence or Transient Reservoir of the Virus?

Pretorius, Etheresia

2021 Volume 12, Page(s) 649465

Abstract: The immune and inflammatory responses of platelets to human immunodeficiency virus 1 (HIV-1) and its envelope proteins are of great significance to both the treatment of the infection, and to the comorbidities related to systemic inflammation. Platelets ... ...

Abstract	The immune and inflammatory responses of platelets to human immunodeficiency virus 1 (HIV-1) and its envelope proteins are of great significance to both the treatment of the infection, and to the comorbidities related to systemic inflammation. Platelets can interact with the HIV-1 virus itself, or with viral membrane proteins, or with dysregulated inflammatory molecules in circulation, ensuing from HIV-1 infection. Platelets can facilitate the inhibition of HIV-1 infection
MeSH term(s)	Anti-Retroviral Agents/pharmacology ; Anti-Retroviral Agents/therapeutic use ; Blood Platelets/drug effects ; Blood Platelets/immunology ; Blood Platelets/virology ; CD4-Positive T-Lymphocytes/immunology ; Cell Communication/drug effects ; Cell Communication/immunology ; Drug Therapy, Combination ; Erythrocytes/immunology ; HIV Infections/blood ; HIV Infections/complications ; HIV Infections/drug therapy ; HIV Infections/immunology ; HIV-1/immunology ; HIV-1/metabolism ; Humans ; Platelet Aggregation/immunology ; Thrombocytopenia/blood ; Thrombocytopenia/immunology ; Thrombocytopenia/virology ; Thrombosis/blood ; Thrombosis/immunology ; Thrombosis/virology ; Viral Load ; Virus Replication/immunology ; env Gene Products, Human Immunodeficiency Virus/metabolism
Chemical Substances	Anti-Retroviral Agents ; env Gene Products, Human Immunodeficiency Virus
Language	English
Publishing date	2021-04-23
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.649465
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Article ; Online: Are fibrinaloid microclots a cause of autoimmunity in Long Covid and other post-infection diseases?

Kell, Douglas B / Pretorius, Etheresia

The Biochemical journal

2023 Volume 480, Issue 15, Page(s) 1217–1240

Abstract: It is now well established that the blood-clotting protein fibrinogen can polymerise into an anomalous form of fibrin that is amyloid in character; the resultant clots and microclots entrap many other molecules, stain with fluorogenic amyloid stains, are ...

Abstract	It is now well established that the blood-clotting protein fibrinogen can polymerise into an anomalous form of fibrin that is amyloid in character; the resultant clots and microclots entrap many other molecules, stain with fluorogenic amyloid stains, are rather resistant to fibrinolysis, can block up microcapillaries, are implicated in a variety of diseases including Long COVID, and have been referred to as fibrinaloids. A necessary corollary of this anomalous polymerisation is the generation of novel epitopes in proteins that would normally be seen as 'self', and otherwise immunologically silent. The precise conformation of the resulting fibrinaloid clots (that, as with prions and classical amyloid proteins, can adopt multiple, stable conformations) must depend on the existing small molecules and metal ions that the fibrinogen may (and is some cases is known to) have bound before polymerisation. Any such novel epitopes, however, are likely to lead to the generation of autoantibodies. A convergent phenomenology, including distinct conformations and seeding of the anomalous form for initiation and propagation, is emerging to link knowledge in prions, prionoids, amyloids and now fibrinaloids. We here summarise the evidence for the above reasoning, which has substantial implications for our understanding of the genesis of autoimmunity (and the possible prevention thereof) based on the primary process of fibrinaloid formation.
MeSH term(s)	Humans ; Post-Acute COVID-19 Syndrome ; Autoimmunity ; COVID-19 ; Amyloid/metabolism ; Prions ; Thrombosis ; Fibrinogen ; Amyloidogenic Proteins
Chemical Substances	Amyloid ; Prions ; Fibrinogen (9001-32-5) ; Amyloidogenic Proteins
Language	English
Publishing date	2023-08-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2969-5
ISSN	1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
ISSN (online)	1470-8728
ISSN	0006-2936 ; 0306-3275 ; 0264-6021
DOI	10.1042/BCJ20230241
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Article ; Online: A Perspective on How Fibrinaloid Microclots and Platelet Pathology May be Applied in Clinical Investigations.

Pretorius, Etheresia / Kell, Douglas B

Seminars in thrombosis and hemostasis

2023

Abstract: Microscopy imaging has enabled us to establish the presence of fibrin(ogen) amyloid (fibrinaloid) microclots in a range of chronic, inflammatory diseases. Microclots may also be induced by a variety of purified substances, often at very low ... ...

Abstract	Microscopy imaging has enabled us to establish the presence of fibrin(ogen) amyloid (fibrinaloid) microclots in a range of chronic, inflammatory diseases. Microclots may also be induced by a variety of purified substances, often at very low concentrations. These molecules include bacterial inflammagens, serum amyloid A, and the S1 spike protein of severe acute respiratory syndrome coronavirus 2. Here, we explore which of the properties of these microclots might be used to contribute to differential clinical diagnoses and prognoses of the various diseases with which they may be associated. Such properties include distributions in their size and number before and after the addition of exogenous thrombin, their spectral properties, the diameter of the fibers of which they are made, their resistance to proteolysis by various proteases, their cross-seeding ability, and the concentration dependence of their ability to bind small molecules including fluorogenic amyloid stains. Measuring these microclot parameters, together with microscopy imaging itself, along with methodologies like proteomics and imaging flow cytometry, as well as more conventional assays such as those for cytokines, might open up the possibility of a much finer use of these microclot properties in generative methods for a future where personalized medicine will be standard procedures in all clotting pathology disease diagnoses.
Language	English
Publishing date	2023-09-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	196901-8
ISSN	1098-9064 ; 0094-6176
ISSN (online)	1098-9064
ISSN	0094-6176
DOI	10.1055/s-0043-1774796
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Article ; Online: Platelets as Potent Signaling Entities in Type 2 Diabetes Mellitus.

Pretorius, Etheresia

Trends in endocrinology and metabolism: TEM

2019 Volume 30, Issue 8, Page(s) 532–545

Abstract: Type 2 diabetes mellitus (T2DM) is a multifactorial disease with a dysregulated circulating inflammatory molecule tendency. T2DM is closely associated with systemic inflammation, endothelial dysfunction, cardiovascular risk, and increased clotting ... ...

Abstract	Type 2 diabetes mellitus (T2DM) is a multifactorial disease with a dysregulated circulating inflammatory molecule tendency. T2DM is closely associated with systemic inflammation, endothelial dysfunction, cardiovascular risk, and increased clotting susceptibility. Platelets have fundamental roles in the development and propagation of inflammation and cardiovascular risk. They signal through membrane receptors, resulting in (hyper)activation and release of inflammatory molecules from platelet compartments. This review highlights how circulating inflammatory molecules, acting as platelet receptor ligands, interact with platelets, causing platelets to be potent drivers of systemic inflammation. We conclude by suggesting that focused platelet research in T2DM is an important avenue to pursue to identify novel therapeutic targets, and that platelets could be used as cellular activity sensors themselves.
MeSH term(s)	Animals ; Biomarkers/blood ; Blood Platelets/metabolism ; Blood Platelets/physiology ; Diabetes Mellitus, Type 2/blood ; Diabetes Mellitus, Type 2/metabolism ; Humans ; Signal Transduction/physiology
Chemical Substances	Biomarkers
Language	English
Publishing date	2019-06-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1042384-9
ISSN	1879-3061 ; 1043-2760
ISSN (online)	1879-3061
ISSN	1043-2760
DOI	10.1016/j.tem.2019.05.003
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Article: Fibrinaloid Microclots and Atrial Fibrillation.

Kell, Douglas B / Lip, Gregory Y H / Pretorius, Etheresia

Biomedicines

2024 Volume 12, Issue 4

Abstract: Atrial fibrillation (AF) is a comorbidity of a variety of other chronic, inflammatory diseases for which fibrinaloid microclots are a known accompaniment (and in some cases, a cause, with a mechanistic basis). Clots are, of course, a well- ... ...

Abstract	Atrial fibrillation (AF) is a comorbidity of a variety of other chronic, inflammatory diseases for which fibrinaloid microclots are a known accompaniment (and in some cases, a cause, with a mechanistic basis). Clots are, of course, a well-known
Language	English
Publishing date	2024-04-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines12040891
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Article ; Online: Herpesvirus Infection of Endothelial Cells as a Systemic Pathological Axis in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.

Nunes, Jean M / Kell, Douglas B / Pretorius, Etheresia

Viruses

2024 Volume 16, Issue 4

Abstract: Understanding the pathophysiology of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is critical for advancing treatment options. This review explores the novel hypothesis that a herpesvirus infection of endothelial cells (ECs) may underlie ... ...

Abstract	Understanding the pathophysiology of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is critical for advancing treatment options. This review explores the novel hypothesis that a herpesvirus infection of endothelial cells (ECs) may underlie ME/CFS symptomatology. We review evidence linking herpesviruses to persistent EC infection and the implications for endothelial dysfunction, encompassing blood flow regulation, coagulation, and cognitive impairment-symptoms consistent with ME/CFS and Long COVID. This paper provides a synthesis of current research on herpesvirus latency and reactivation, detailing the impact on ECs and subsequent systemic complications, including latent modulation and long-term maladaptation. We suggest that the chronicity of ME/CFS symptoms and the multisystemic nature of the disease may be partly attributable to herpesvirus-induced endothelial maladaptation. Our conclusions underscore the necessity for further investigation into the prevalence and load of herpesvirus infection within the ECs of ME/CFS patients. This review offers conceptual advances by proposing an endothelial infection model as a systemic mechanism contributing to ME/CFS, steering future research toward potentially unexplored avenues in understanding and treating this complex syndrome.
MeSH term(s)	Humans ; Fatigue Syndrome, Chronic/virology ; Fatigue Syndrome, Chronic/physiopathology ; Endothelial Cells/virology ; Herpesviridae Infections/virology ; Virus Latency ; Herpesviridae/physiology ; COVID-19/virology ; COVID-19/physiopathology ; COVID-19/pathology
Language	English
Publishing date	2024-04-08
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v16040572
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Article ; Online: The potential role of ischaemia-reperfusion injury in chronic, relapsing diseases such as rheumatoid arthritis, Long COVID, and ME/CFS: evidence, mechanisms, and therapeutic implications.

Kell, Douglas B / Pretorius, Etheresia

The Biochemical journal

2022 Volume 479, Issue 16, Page(s) 1653–1708

Abstract: Ischaemia-reperfusion (I-R) injury, initiated via bursts of reactive oxygen species produced during the reoxygenation phase following hypoxia, is well known in a variety of acute circumstances. We argue here that I-R injury also underpins elements of the ...

Abstract	Ischaemia-reperfusion (I-R) injury, initiated via bursts of reactive oxygen species produced during the reoxygenation phase following hypoxia, is well known in a variety of acute circumstances. We argue here that I-R injury also underpins elements of the pathology of a variety of chronic, inflammatory diseases, including rheumatoid arthritis, ME/CFS and, our chief focus and most proximally, Long COVID. Ischaemia may be initiated via fibrin amyloid microclot blockage of capillaries, for instance as exercise is started; reperfusion is a necessary corollary when it finishes. We rehearse the mechanistic evidence for these occurrences here, in terms of their manifestation as oxidative stress, hyperinflammation, mast cell activation, the production of marker metabolites and related activities. Such microclot-based phenomena can explain both the breathlessness/fatigue and the post-exertional malaise that may be observed in these conditions, as well as many other observables. The recognition of these processes implies, mechanistically, that therapeutic benefit is potentially to be had from antioxidants, from anti-inflammatories, from iron chelators, and via suitable, safe fibrinolytics, and/or anti-clotting agents. We review the considerable existing evidence that is consistent with this, and with the biochemical mechanisms involved.
MeSH term(s)	Arthritis, Rheumatoid/therapy ; COVID-19/complications ; Fatigue Syndrome, Chronic/metabolism ; Humans ; Oxidative Stress/physiology ; Reperfusion Injury/therapy
Language	English
Publishing date	2022-08-28
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2969-5
ISSN	1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
ISSN (online)	1470-8728
ISSN	0006-2936 ; 0306-3275 ; 0264-6021
DOI	10.1042/BCJ20220154
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Article ; Online: Editorial: The immunological role of platelet activation in the pathophysiology of COVID-19.

Rossouw, Theresa Marie / Pretorius, Etheresia / Wool, Geoffrey D

Frontiers in immunology

2023 Volume 14, Page(s) 1285355

MeSH term(s)	Humans ; COVID-19 ; Platelet Activation
Language	English
Publishing date	2023-09-25
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1285355
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Article ; Online: Precision Medicine and a Patient-Orientated Approach: Is this the Future for Tracking Cardiovascular Disorders?

Pretorius, Etheresia

Current pharmaceutical design

2017 Volume 23, Issue 6, Page(s) 889–893

Abstract: The latest statistics from the 2016 heart disease and stroke statistics update shows that cardiovascular disease is the leading global cause of death, currently accounting for more than 17.3 million deaths per year. Type II diabetes is also on the rise ... ...

Abstract	The latest statistics from the 2016 heart disease and stroke statistics update shows that cardiovascular disease is the leading global cause of death, currently accounting for more than 17.3 million deaths per year. Type II diabetes is also on the rise with out-of-control numbers. To address these pandemics, we need to treat patients using an individualized patient care approach, but simultaneously gather data to support the precision medicine initiative. Last year the NIH announced the precision medicine initiative to generate novel knowledge regarding diseases, with a near-term focus on cancers, followed by a longer-term aim, applicable to a whole range of health applications and diseases. The focus of this paper is to suggest a combined effort between the latest precision medicine initiative, researchers and clinicians; whereby novel techniques could immediately make a difference in patient care, but long-term add to knowledge for use in precision medicine. We discuss the intricate relationship between individualized patient care and precision medicine and the current thoughts regarding which data is actually suitable for the precision medicine data gathering. The uses of viscoelastic techniques in precision medicine are discussed and how these techniques might give novel perspectives on the success of treatment regimes of cardiovascular patients are explored. Thrombo-embolic stroke, rheumathoid arthritis and type II diabetes are used as examples of diseases where precision medicine and a patient-orientated approach can possibly be implemented. In conclusion it is suggested that if all role players work together by embracing a new way of thought in treating and managing cardiovascular disease and diabetes will we be able to adequately address these out-ofcontrol conditions.
Language	English
Publishing date	2017
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1304236-1
ISSN	1873-4286 ; 1381-6128
ISSN (online)	1873-4286
ISSN	1381-6128
DOI	10.2174/1381612822666161006124400
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Zs.A 4714: Show issues

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Article ; Online: Cardiovascular and haematological pathology in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS): A role for viruses.

Nunes, Jean M / Kell, Douglas B / Pretorius, Etheresia

Blood reviews

2023 Volume 60, Page(s) 101075

Abstract: ME/CFS is a debilitating chronic condition that often develops after viral or bacterial infection. Insight from the study of Long COVID/Post Acute Sequelae of COVID-19 (PASC), the post-viral syndrome associated with SARS-CoV-2 infection, might prove to ... ...

Abstract	ME/CFS is a debilitating chronic condition that often develops after viral or bacterial infection. Insight from the study of Long COVID/Post Acute Sequelae of COVID-19 (PASC), the post-viral syndrome associated with SARS-CoV-2 infection, might prove to be useful for understanding pathophysiological mechanisms of ME/CFS. Disease presentation is similar between the two conditions, and a subset of Long COVID patients meet the diagnostic criteria for ME/CFS. Since Long COVID is characterized by significant vascular pathology - including endothelial dysfunction, coagulopathy, and vascular dysregulation - the question of whether or not the same biological abnormalities are of significance in ME/CFS arises. Cardiac abnormalities have for a while now been documented in ME/CFS cohorts, with recent studies demonstrating major deficits in cerebral blood flow, and hence vascular dysregulation. A growing body of research is demonstrating that ME/CFS is accompanied by platelet hyperactivation, anomalous clotting, a procoagulant phenotype, and endothelial dysfunction. Endothelial damage and dysregulated clotting can impair substance exchange between blood and tissues, and result in hypoperfusion, which may contribute to the manifestation of certain ME/CFS symptoms. Here we review the ME/CFS literature to summarize cardiovascular and haematological findings documented in patients with the condition, and, in this context, briefly discuss the potential role of previously-implicated pathogens. Overall, cardiac and haematological abnormalities are present within ME/CFS cohorts. While atherosclerotic heart disease is not significantly associated with ME/CFS, suboptimal cardiovascular function defined by reduced cardiac output, impaired cerebral blood flow, and vascular dysregulation are, and these abnormalities do not appear to be influenced by deconditioning. Rather, these cardiac abnormalities may result from dysfunction in the (autonomic) nervous system. Plenty of recently published studies are demonstrating significant platelet hyperactivity and endothelial dysfunction in ME/CFS, as well as anomalous clotting processes. It is of particular importance to determine to what extent these cardiovascular and haematological abnormalities contribute to symptom severity, and if these two systems can be targeted for therapeutic purposes. Viral reservoirs of herpesviruses exist in ME/CFS, and most likely contribute to cardiovascular and haematological dysfunction directly or indirectly. This review highlights the potential of studying cardiac functioning, the vasculature, and coagulation system in ME/CFS.
MeSH term(s)	Humans ; Fatigue Syndrome, Chronic/etiology ; Fatigue Syndrome, Chronic/diagnosis ; Post-Acute COVID-19 Syndrome ; COVID-19/complications ; SARS-CoV-2
Language	English
Publishing date	2023-03-20
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	639015-8
ISSN	1532-1681 ; 0268-960X
ISSN (online)	1532-1681
ISSN	0268-960X
DOI	10.1016/j.blre.2023.101075
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