Mechanisms of entry of nonenveloped viruses

Nonenveloped virus particles must be incorporated into the cell via a process called translocation across the lipid bilayer. This process is one in which the capsid or a cell-modified capsid physically crosses the cell plasma membrane. There are at least four mechanisms that result in virus translocation across the membrane: clathrin-mediated endocytosis, caveolae-mediated

Virion

Clathrin coated pit forms-triggered by virion-receptor interaction

ICAM receptors

Virion

Clathrin coated pit forms-triggered by virion-receptor interaction

ICAM receptors

Endocytotic vesicle forms and becomes acidified

Clathrin released virion partially "opened"

Partial degradation of virion and potential expression of processed antigen

Endocytotic vesicle forms and becomes acidified

Clathrin released virion partially "opened"

Partial degradation of virion and potential expression of processed antigen

Viral genome (mRNA) released in cytoplasm

Viral genome (mRNA) released in cytoplasm

Fig. 6.2 Schematic of receptor-mediated endocytosis utilized by rhinovirus for entry into the host cell. The endocytotic vesicle forms as a consequence of close association between the rhinovirus—receptor complex and the plasma membrane.

endocytosis, lipid-raft-mediated endocytosis, and macropinocytosis. Each of these processes is endocytotic, in that they result in the formation of endosomal vesicles containing extracellular material (including the attached virus particles) that move into the cytoplasm of the cell. They are differentiated by the nature of the cellular components that line the endocytotic vesicle and mediate its formation. The clathrin-mediated pathway involving receptor binding is illustrated for rhinovirus in Fig. 6.2. The acidic environment of the endocytotic vesicle causes specific changes to the rhinovirus capsid so that the internal genome (positive-sense RNA) is released into the cytoplasm where it can be translated and begin gene expression.

A nuclear replicating nonenveloped virus, such as the papovavirus, SV40, begins entry in a similar fashion, but the interaction between viral capsid proteins and the vesicle, along with other intracellular trafficking proteins, allows the modified virion to be transported to the nuclear membrane. Once there, the viral genome is released and viral DNA interacts with cellular transcription factors to begin gene expression. Because specific genetic alterations (mutations) in the SV40 capsid protein will interfere with this transport, it is known that the virus controls the process.

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