Concept

Endothelial cell tropism

Endothelial cell tropism or endotheliotropism is a type of tissue tropism or host tropism that characterizes an pathogen's ability to recognize and infect an endothelial cell. Pathogens, such as viruses, can target a specific tissue type or multiple tissue types. Like other cells, the endothelial cell possesses several features that supports a productive viral infection a cell including, cell surface receptors, immune responses, and other virulence factors. Endothelial cells are found in various tissue types such as in the capillaries, veins, and arteries in the human body. As endothelial cells line these blood vessels and critical networks that extend access to various human organ systems, the virus entry into these cells can be detrimental to virus spread across the host system and affect clinical course of disease. Understanding the mechanisms of how viruses attach, enter, and control endothelial functions and host responses inform infectious disease understanding and medical countermeasures. There are a multitude of endothelial cell features that influence cell tropism and ultimately, contribute to endothelial cell activation and dysfunction as well as the continuation of the virus life cycle. Viral pathogens capitalize on cell surface receptors that are ubiquitous and can recognize many diverse ligands for attachment and ultimately, entry into the cell. These ligands not only consist of endogenous proteins but also bacterial and viral products. Once the virus is anchored to the cell surface, virus uptake typically occurs using host mechanisms such as endocytosis. One method of viral uptake is through clathrin-mediated endocytosis (CME). The cell surface receptors provide a binding pocket for attachment and entry into the cell, and therefore, affects a cell's susceptibility to infection. In addition, the receptor density on the surface of the endothelial cell also affects how efficiently the virus enters the host cell. For instance, a lower cell surface receptor density may render an endothelial cell less susceptible for virus infection than an endothelial with a higher cell surface receptor density.

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