Membrane leakiness after viral infection and a new approach to the development of antiviral agents.
Viral development induces changes in the permeability properties of the plasma membrane of the host cell. Here it is shown that, because of this leakiness, inhibitors of protein synthesis normally impermeable to uninfected cells are able to enter infected cells and thereby specifically inhibit viral protein synthesis.
D000255:Adenosine Triphosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D000998:Antiviral Agents / Q000138:chemical synthesis* / Q000494:pharmacology; D002460:Cell Line; D002462:Cell Membrane / Q000378:metabolism; D002463:Cell Membrane Permeability; D002472:Cell Transformation, Viral; D004686:Encephalomyocarditis virus / Q000187:drug effects / Q000378:metabolism; D006160:Guanosine Triphosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D006165:Guanylyl Imidodiphosphate / Q000494:pharmacology; D008565:Membrane Proteins / Q000096:biosynthesis; D008970:Molecular Weight; D014176:Protein Biosynthesis / Q000187:drug effects; D013997:Time Factors; D014764:Viral Proteins / Q000096:biosynthesis; D014777:Virus Diseases / Q000378:metabolism / Q000503:physiopathology*
D000998:Antiviral Agents; D008565:Membrane Proteins; D014764:Viral Proteins; D006165:Guanylyl Imidodiphosphate; D006160:Guanosine Triphosphate; D000255:Adenosine Triphosphate