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Review
. 2021 Feb 20;10(4):877.
doi: 10.3390/jcm10040877.

Thrombocytopenia in Virus Infections

Matthijs Raadsen  1 , Justin Du Toit  2 , Thomas Langerak  1 , Bas van Bussel  3   4 , Eric van Gorp  1   5 , Marco Goeijenbier  1   5
Affiliations
Review

Thrombocytopenia in Virus Infections

Matthijs Raadsen et al. J Clin Med. .

Abstract

Thrombocytopenia, which signifies a low platelet count usually below 150 × 109/L, is a common finding following or during many viral infections. In clinical medicine, mild thrombocytopenia, combined with lymphopenia in a patient with signs and symptoms of an infectious disease, raises the suspicion of a viral infection. This phenomenon is classically attributed to platelet consumption due to inflammation-induced coagulation, sequestration from the circulation by phagocytosis and hypersplenism, and impaired platelet production due to defective megakaryopoiesis or cytokine-induced myelosuppression. All these mechanisms, while plausible and supported by substantial evidence, regard platelets as passive bystanders during viral infection. However, platelets are increasingly recognized as active players in the (antiviral) immune response and have been shown to interact with cells of the innate and adaptive immune system as well as directly with viruses. These findings can be of interest both for understanding the pathogenesis of viral infectious diseases and predicting outcome. In this review, we will summarize and discuss the literature currently available on various mechanisms within the relationship between thrombocytopenia and virus infections.

Keywords: HIV; SARS-CoV-2; aggregation; coronavirus; hantavirus; influenza; thrombocytopathy; thrombocytopenia; virus infection.

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Conflict of interest statement

The authors declare no conflict of interest.

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