ReviewThrombosis research2014
The procoagulant envelope virus surface: contribution to enhanced infection.
Review in Thrombosis research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Tissue factor in COVID-19-associated coagulopathy.Thrombosis research · 2022Pooled it
- Article
- COVID-19 associated coagulopathy: Mechanisms and host-directed treatment.The American journal of the medical sciences · 2022Review
- Advocacy of targeting protease-activated receptors in severe coronavirus disease 2019.British journal of pharmacology · 2022Article
- Clinical use of thrombin generation assays.Journal of thrombosis and haemostasis : JTH · 2021Review
- Acute Viral Illnesses and Ischemic Stroke: Pathophysiological Considerations in the Era of the COVID-19 Pandemic.Stroke · 2021Review
- Is the COVID-19 thrombotic catastrophe complement-connected?Journal of thrombosis and haemostasis : JTH · 2020Review
- Antiviral anticoagulation.Research and practice in thrombosis and haemostasis · 2020Review
- Cerebral venous thrombosis: a rare complication of herpes simplex encephalitis.Journal of neurovirology · 2020Article
- Virus envelope tissue factor promotes infection in mice.Journal of thrombosis and haemostasis : JTH · 2019Article
- In silico thrombin generation: Plasma composition imbalance and mortality in human immunodeficiency virus.Research and practice in thrombosis and haemostasis · 2018Article
- Subcutaneous Administration of Low-Molecular-Weight Heparin to Horses Inhibits Ex Vivo Equine Herpesvirus Type 1-Induced Platelet Activation.Frontiers in veterinary science · 2018Article
- Evasion and interactions of the humoral innate immune response in pathogen invasion, autoimmune disease, and cancer.Clinical immunology (Orlando, Fla.) · 2015Review
- Effect of Puumala hantavirus infection on human umbilical vein endothelial cell hemostatic function: platelet interactions, increased tissue factor expression and fibrinolysis regulator release.Frontiers in microbiology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Many virus types are covered by a lipid bilayer. This structure called an envelope, is derived from the host cell and includes host- and virus-encoded proteins. Because envelope components first interact with the host, it is the trigger for infection, immunity and pathology. The roles of especially host-derived constituents are poorly understood. Focusing on herpes simplex type 1 (HSV1) as a model, we have shown that the envelope acquires the physiological initiators of coagulation from the host cell; tissue factor (TF) and procoagulant phospholipid (proPL). Unlike resting cells, where TF and proPL accessibility is carefully restricted, their expression is constitutive on the purified virus enabling factor VIIa (FVIIa)-dependant factor Xa (FXa) and thrombin generation. Interestingly, HSV1-encoded glycoprotein C (gC) on the virus enhances FXa production. In addition to coagulation proteases, HSV1 also facilitates fibrinolytic plasmin generation. HSV1 TF and gC combine to optimally enhance cultured cell infection when both FVIIa and FXa are available through protease activated receptor (PAR) 2. Plasmin also increases infection through PAR2, whereas thrombin provides an additive effect via PAR1. Thus, depending on the host cell, TF and proPL may be a general feature of enveloped viruses, enabling coagulation protease activation and PAR-mediated effects on infection.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.