Blood clots in COVID-19 patients: Simplifying the curious mystery
Open accessAbstract
The universal phenomenon of blood clotting is well known to be protective in external cellular/ tissue injury. However, the emergence of unusual thrombotic presentations in COVID-19 patients is the real concern. Interaction of the spike glycoprotein with ACE2 receptor present in the host cell surface mediates the entry of SARS-CoV-2 causing COVID-19 infection. New clinical findings of SARS-CoV-2 pathogenesis are coming out every day, and one such mystery is the formation of mysterious blood clots in the various tissues and organs of COVID-19 patients, which needs critical attention. To address this issue, we hypothesis that, high ACE2 expression in the endothelium of blood vessels facilitates the high-affinity binding of SARS-CoV-2 using spike protein, causing infection and internal injury inside the vascular wall of blood vessels. This viral associated injury may directly/indirectly initiate activation of coagulation and clotting cascades forming internal blood clots. However, the presence of these clots is undesirable as they are responsible for thrombosis and need to be treated with anti-thrombotic intervention.
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The widespread presence of ACE-2 receptors in different organs facilitates extrapulmonary SARS-CoV-2 infection and associated complications such as ARDS, cytokine storm, blood clots, and possibly psychological and neurological problems.
“The widespread presence of ACE-2 receptors in different organs facilitates the extrapulmonary infection by SARS-CoV-2, causing associated complications such as acute respiratory distress syndrome (ARDS), cytokine storm, blood clots [6, 9], and possibly psychological and neurological problems [10].”
From Waves and variants of SARS-CoV-2: understanding the causes and effect of the COVID-19 catastrophe (2022) · cites this paper as [6]
The Background (page unavailable) describes ACE2 expression in multiple organs and lists extrapulmonary manifestations of COVID-19. The Discussion & conclusion (page unavailable) proposes that SARS-CoV-2 binding to ACE2 in blood-vessel endothelium may cause blood clots; it presents that mechanism as a hypothesis, not an established cause. The psychological and neurological problems are separately attributed to reference [10], so they are not judged against this source. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe S gene encodes a homotrimeric type I fusion transmembrane glycoprotein that enables viral entry through the ACE-2 receptor.
“The S gene encodes for the prominent homotrimeric, type I fusion and transmembrane glycoprotein which enables viral entry into the host target cell through the angiotensin-converting enzyme-2 (ACE-2) receptor [5, 6].”
From Waves and variants of SARS-CoV-2: understanding the causes and effect of the COVID-19 catastrophe (2022) · cites this paper as [6]
The Background (page not provided) says that the viral spike protein binds the host ACE2 receptor to mediate entry. It does not state that the S gene encodes the protein or describe it as homotrimeric, type I fusion, or transmembrane. (LLM, conf=0.87)
Experimental — accuracy not yet measuredThe spike protein enables viral entry into host cells through the ACE-2 receptor.
“The S gene encodes for the prominent homotrimeric, type I fusion and transmembrane glycoprotein which enables viral entry into the host target cell through the angiotensin-converting enzyme-2 (ACE-2) receptor [5, 6].”
From Waves and variants of SARS-CoV-2: understanding the causes and effect of the COVID-19 catastrophe (2022) · cites this paper as [6]
The spike protein mediates entry into host cells by binding the ACE-2 receptor.
“The S gene encodes for the prominent homotrimeric, type I fusion and transmembrane glycoprotein which enables viral entry into the host target cell through the angiotensin-converting enzyme-2 (ACE-2) receptor [5, 6].”
From Waves and variants of SARS-CoV-2: understanding the causes and effect of the COVID-19 catastrophe (2022) · cites this paper as [6]
Widespread ACE-2 expression in multiple organs is described as a reason SARS-CoV-2 can infect tissues beyond the lungs.
“The widespread presence of ACE-2 receptors in different organs facilitates the extrapulmonary infection by SARS-CoV-2, causing associated complications such as acute respiratory distress syndrome (ARDS), cytokine storm, blood clots [6, 9], and possibly psychological and neurological problems [10].”
From Waves and variants of SARS-CoV-2: understanding the causes and effect of the COVID-19 catastrophe (2022) · cites this paper as [6]
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References 34 · Cited by 74
Research works printed but not linked: 1
- [2]Worldometer (2020) ‘Coronavirus Cases’, Worldometer, pp. 1–22. doi: 10.1101/2020.01.23.20018549V2. · DOI
- Authors
- Biswas, S., Thakur, V., Kaur, P., Khan, A., Kulshrestha, S., & Kumar, P.
- Affiliations
- Shoolini University (IN)
- Post Graduate Institute of Medical Education and Research (IN)
- Corresponding author
- Kumar, Pradeep
- Venue
- Medical Hypotheses
- Publisher
- Elsevier BV
- Published
- 2021-01
- Volume
- 146
- Pages
- 110371
- ISSN
- 0306-9877 (ISSN-L)
- PMC
- PMC7644431
- OpenAlex
- W3095312542
- Cited by
- 74
- References
- 34
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 12 · 2023: 16 · 2022: 20 · 2021: 20
- FWCI
- 1.83
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Medical Hypotheses (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Shoolini University of Biotechnology and Management Sciences
- Topics
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Blood properties and coagulation
- Keywords
- COVID-19 pandemic, SARS-CoV-2, blood clots, thrombosis, coagulation activation, ACE2 receptor, spike protein, endothelial cell infection, vascular injury, antithrombotic therapy
- MeSH terms
- Host Microbial Interactions, Angiotensin-Converting Enzyme 2, COVID-19, SARS-CoV-2, Blood Coagulation, Endothelium, Vascular, Humans, Models, Cardiovascular, Receptors, Virus, Thrombosis, Pandemics, Spike Glycoprotein, Coronavirus
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