guanosine-triphosphate and Virus-Diseases

Antiviral compounds have been developed for use in chemoprophylaxis and chemotherapy of a variety of infections in humans, including those caused by influenza viruses, respiratory syncytial virus, and herpesviruses. The efficacy of several of these compounds has been demonstrated in rigorously controlled trials. Advances in molecular virology have led to the identification of biochemically defined, virus-specific functions that serve as appropriate targets for the future development of antiviral compounds. Clinical investigators and practicing physicians are now confronting questions previously raised with the use of antibacterial antibiotics. These questions concern appropriate routes of administration for antiviral compounds, optimal dosage regimens, risks of long-term prophylaxis, and the emergence of resistant organisms.

Topics: Acyclovir; Adult; Aged; Amantadine; Antiviral Agents; Chickenpox; Clinical Trials as Topic; Cytomegalovirus; Encephalitis; Foscarnet; Guanosine Triphosphate; Herpes Simplex; Herpes Zoster; Herpesviridae Infections; Humans; Infant, Newborn; Infant, Newborn, Diseases; Influenza A virus; Influenza, Human; Phosphonoacetic Acid; Respiratory Tract Infections; Ribavirin; Rimantadine; Vidarabine; Virus Diseases

The effect of certain antiviral compounds said to act because of an increased permeability of virally infected cells has been tested in SFV-infected BHK cells. The time at which SFV-infected BHK cells become sensitive to the action of GppCH2p is more than an hour later than the time at which protein synthesis in such cells becomes depressed. The uptake of [3H]GppCH2p is the same in infected and uninfected cells, whether measured at 19 or 37 degrees C. We conclude that GppCH2p, and probably other 'impermeant' inhibitors of protein synthesis also, affect virally-infected cells selectively not because of an increased permeability, but because of a general impairment of protein synthesis in such cells.

Topics: Animals; Antiviral Agents; Cell Line; Cell Membrane Permeability; Cricetinae; Diphosphonates; Guanine Nucleotides; Guanosine Monophosphate; Guanosine Triphosphate; Kidney; Protein Biosynthesis; Semliki forest virus; Togaviridae Infections; Virus Diseases

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.

Topics: Adenosine Triphosphate; Animals; Antiviral Agents; Cell Line; Cell Membrane; Cell Membrane Permeability; Cell Transformation, Viral; Encephalomyocarditis virus; Guanosine Triphosphate; Guanylyl Imidodiphosphate; Membrane Proteins; Molecular Weight; Protein Biosynthesis; Time Factors; Viral Proteins; Virus Diseases