Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Agents that perturb endocytosis or that alter the pH of endosomes were shown to have little or no effect on plaque formation by herpes simplex virus (HSV), whereas plaque formation by vesicular stomatitis virus was inhibited as expected. A number of agents were tested for their ability to inhibit early events in HSV infection. Amantadine, chloroquine and trifluoperazine, whose actions are known to alter the endocytic pathway, showed no selective inhibitory effects on early events in HSV infection. Wheat germ agglutinin and heparin, known inhibitors of HSV infection, blocked the adsorption of virus to cells, as expected. Succinylated concanavalin A blocked plaque formation without inhibiting virus adsorption but could enhance the elution of bound virus. To a greater or lesser extent, succinylated concanavalin A, dithiothreitol, colchicine, monensin and cytochalasin B all inhibited or reduced the rate of events subsequent to adsorption and prior to early viral protein synthesis. Evidence is presented to suggest that each of these agents has a different mode of action. On the basis of these results and others, we conclude that endocytosis is probably not required for infection by HSV (at least not the low pH-dependent endocytic pathway) and that events occurring at the cell surface trigger virion-cell fusion leading to infection.
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PMID:Penetration of cells by herpes simplex virus does not require a low pH-dependent endocytic pathway. 164 8

Enveloped viruses enter host cells by fusion or viropexis. The latter mechanism is the prevalent entry pathway of rhabdoviruses into susceptible cells. Amantadine, a lysosomotropic agent, inhibits the multiplication of various groups of viruses. The effect of this drug was investigated on vesicular stomatitis virus and rabies fixed virus strain replication in fibroblasts. Amantadine was added to cells before, during and after infection to detect the phase of viral replication affected by the drug. Cells were inoculated with viruses at 4 degrees C and the incubation temperature was progressively raised to 37 degrees C in order to observe the effect of amantadine on attachment and early stages of viral replication. Experimental results indicated that the compound inhibited rhabdovirus infection in CER cells. Viral attachment and penetration did not appear to be affected by the drug, while later steps were inhibited, probably at the level of uncoating when the virus is released from the lysosomes into the intracytoplasmic compartment.
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PMID:Effect of amantadine on rhabdovirus infection. 301 59