What is the impact of monkeypox infection on the hemostatic system?

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The scientific community’s understanding of the framework associating viral infection with endothelial inflammation, prothrombotic transformation, and barrier failure has been considerably enhanced by the analysis of the pathogenetic mechanisms underlying COVID-19-associated coagulopathy (CAC). Additionally, the population was made aware of the potential thrombotic and hemorrhagic risks associated with adenovirus as vectors for vaccines and gene therapies due to the Vaccine-Induced Thrombosis and Thrombocytopenia (VITT) syndrome reported in some recipients of ChAdOx1 nCoV-19 and Ad26.

Pathology of monkeypox infection

The predominant pathological manifestation of MPX virus infection is epithelial cell damage, which manifests as ballooning degeneration, intracytoplasmic eosinophilic inclusion, hyperplasia, and keratinocyte necrosis. Vasculitis and lymphocytic inflammation of the dermis are also present. It should be noted that there is no data on the histology of persons who have succumbed to MPX infection.

Fever is frequently the first sign of illness, followed by the appearance of many papular, ulcerative, and vesiculopustular lesions on the face and body, along with lymphadenopathy. Most of the time, monkeypox infection was self-limited and lasted for two to four weeks. However, complications such as encephalitis, keratitis, pneumonitis, and secondary bacterial infections can occur, which can result in a fatality rate between 1% to 11%, mostly in low-income nations. It is noteworthy that the viral genome sequenced from several nations closely resembled the strain indigenous to Western Africa, which has a mortality rate of 1%, which is roughly ten times lower as compared to the rate observed for the Central African clade.

Impact of MPX infection

Due to their capacity to avoid detection and targeting by the host immune system, phleboviruses are predicted to have a less significant effect on the thrombo-inflammation process. MPX virus infection of primary fibroblasts in vitro results in the inhibition of the expression of the interferon-stimulated gene (ISG) and the C-C motif chemokine ligand 5 (CCL-5), tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 alpha and beta, and IL-6, all of which are factors that are implicated in the cytokine storm experienced in COVID-19.

Given these clinical and pathophysiological considerations, it is expected that the hemostatic system will play a little or insignificant role in the monkeypox infection, as evidenced by the absence of thrombotic or hemorrhagic consequences in these patients. Since the deoxyribonucleic acid (DNA) virus Variola major, the causal pathogen of smallpox (SPX), and the monkeypox virus are relatively distant relatives, the minor consequences of monkeypox infections may be short-lived.

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