Viral sepsis - pathophysiology and disease manifestation

Viral infection is found in approximately 30% of all sepsis cases and may be followed by bacterial infection in organs such as the lungs. Sepsis manifests as fever, hemorrhagic lesions and cell death. Organ dysfunction caused by sepsis, such as meningitis and encephalitis, can lead to organ damage. Sepsis is induced by various viral components, host cells and cellular mediators, such as cytokines and chemokines. Cytokines are secreted from stimulated macrophages, monocytes, dendritic cells and T lymphocytes.Further contributors to sepsis are the cleavage products after activation of the complement cascade with anaphylatoxin generation and peptides of the activated clotting cascade, thrombocytopenia and thrombocyte function alteration, intravasal clotting and/or endothelial leakage. The cells involved in viral sepsis are neutrophil granulocytes, monocytes and macrophages, dendritic cells and thrombocytes, and finally, endothelial cells and epithelial cells.Prolonged cytokine release leads to cell damage, immune cell dysfunction and exhaustion, and either impairs or hyperactivates immune cells. The course of viral sepsis may be enhanced by some patient conditions including age, underlying diseases such as diabetes, obesity; and immunodeficiency. Viral sepsis, similar to bacterial sepsis, is an extremely complex disorder, and the involvement of the abovementioned cellular and humoral components can present quite divergent biological and clinical patterns.Examples of viral sepsis discussed in the manuscript include three viruses causing Dengue fever - an emerging infection, COVID-19 - a disease with a prolonged course, Ebola disease - a disease with typically complete viral clearance, while rabies virus - induces a disease that causes coma and death before signs of viral sepsis are apparent.