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Immediately after internalization of the particle, the viral RNA is released. Thus the genome enclosed within the viral particle can be used as messenger RNA and immediately translated by the host cell.On entry, the virus hijacks the cell's translation machinery, causing inhibition of cellular protein synthesis in favor of virus–specific protein production.
The newly synthesized positive-sense RNA molecules can serve as templates for translation of more viral proteins (7) or can be enclosed in a capsid (8), which ultimately generates progeny virions.Lysis of the infected cell results in release of infectious progeny virions (9).Attached to the host cell membrane, entry of the viral nucleic acid was thought to occur one of two ways: via the formation of a pore in the plasma membrane through which the RNA is then “injected” into the host cell cytoplasm, or that the virus is taken up by receptor-mediated endocytosis.Recent experimental evidence supports the latter hypothesis and suggests that poliovirus binds to CD155 and is taken up via endocytosis.The viral particle is about 30 nanometres in diameter with icosahedral symmetry.Because of its short genome and its simple composition—only RNA and a non-enveloped icosahedral protein coat that encapsulates it—poliovirus is widely regarded as the simplest significant virus.
The replication cycle of poliovirus is initiated (1) by binding to the cell surface receptor CD155.
The virion is taken up via endocytosis, and the viral RNA is released (2).
Translation of the viral RNA occurs by an IRES-mediated mechanism (3).
The polyprotein is cleaved, yielding mature viral proteins (4).
The positive-sense RNA serves as template for complementary negative-strand synthesis, producing double-stranded replicative form (RF) RNA(5).
Many positive strand RNA copies are produced from the single negative strand (6).