The study demonstrates that different viruses within the Picornaviridae family utilize distinct mechanisms, including caveolae formation, local lysis, and macropinocytosis, to enter resident macrophages.
Distinct picornavirus entry routes in macrophages should not alter clinical practice; leaves open targeted antiviral research in viral myocarditis.
For viruses, the following mechanisms of penetration into cells are typical: clathrin- or dinaminmediated endocytosis, the formation of caveolae, local lysis of cell membranes, and macropinocytosis. It is accepted that (those nonenveloped viruses in the Picornaviridae family) enter cells mostly through the local lysis of their membranes. The purpose of the present study is to research the mechanisms of penetration into resident macrophages of viruses of the indicated family, including poliovirus, Echol1 and Coxsackie B1 viruses, and Type 71 enterovirus. It has been detected that, at the adhesion sites of the Coxsackie B1 virus and Type 71 enterovirus on a macrophage surface, invaginations of the plasma membranes of cells appear, followed by the consequent formation of endocytoplasmatic vesicles, i.e., caveolae. The penetration of poliovirus into macrophages occurs both through the formation of caveolae and the local lysis of the plasmolemma of cells; during the later terms (after 45 min), macropinocytosis is observed in the viral particles during the first 15 min after the Echol1 virus penetrated the cytoplasm of macrophages through the local lysis of their plasmolemma. Thereafter, the formation of endocytic vacuolae including viral particles was observed in the cytoplasm of infected macrophages. The exit of the Echol1 virus from endocytic vacuoles was performed by the local lysis of cell membrane.
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Плехова et al. (2008) studied this question.
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