Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several antitumor substances extracted from cones of various pine trees inhibited the plaque formation of Herpes simplex virus types 1 and 2 (HSV-1, HSV-2) strains in African green monkey kidney cells and human adenocarcinoma cells. The 50% effective dose of the most active fraction, Fr. VI (0.3 micrograms/ml) was 0.001 times its 50% cytotoxic dose (greater than 300 micrograms/ml). The anti-HSV activity of various pine cone extracts increased with their acidity. Identification of the polyphenol groups as donors of the acidity was further supported by the observation that the anti-HSV activity of the natural polyphenolic products, such as tannin and lignin, significantly exceeded that of other natural or chemically modified antitumor polysaccharides. An experiment using radiolabeled virus particles indicated that the anti-HSV effect of both Fr. VI and lignin was attributable to interference with virus adsorption to these cells rather than to inhibition of virus penetration into the cells.
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PMID:Inhibition of herpes simplex virus infection by pine cone antitumor substances. 254 81

Mature virions of herpes simplex virus type 1 contain an activating factor that primes transcription from the five virally encoded immediate early (IE) genes. This activator is specified by a 65-kD polypeptide termed VP16. The action of VP16 is mediated through cis-regulatory elements located in regions adjacent to each IE gene. Although VP16 is normally introduced into cells by infecting virions, its trans-activating function can also be observed by cotransfecting cells with a plasmid that encodes VP16 along with a reporter gene driven by IE cis-regulatory sequences. We have used such an assay to examine the function of mutant forms of VP16. Our results provide tentative identification of two domains of VP16 that are crucial to its role in the induction of IE gene expression. One domain is located within the carboxy-terminal 78 amino acids of VP16 and is characterized by its acidity. Another domain, located in a more amino-terminal region of the protein, appears to tailor the specificity of VP16 for IE genes. According to the results presented in this and the accompanying paper, we predict that VP16 achieves IE gene specificity via protein: protein, rather than protein: DNA, interaction.
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PMID:Functional dissection of VP16, the trans-activator of herpes simplex virus immediate early gene expression. 284 25

The mode of entry of herpes simplex virus type 1 (HSV-1) into Vero cells was investigated quantitatively with biological techniques. The entry of virus occurred rapidly when the virus-adsorbed cells were incubated at 37 C. The kinetics of virus entry was found to be similar to that of the process of uncoating, indicating that the uncoating of HSV-1 occurs simultaneously with the entry of virus into the cell. Experiments with ammonium chloride revealed that acidity in endosomes is not necessary for the entry or uncoating of HSV-1, in contrast with the cases of enveloped RNA viruses. In addition, endocytosis of the virus seems to be one of the processes of entry for HSV-1. However, the kinetics of endocytosis showed that the cell-bound virus is endocytosed gradually and suggested that the endocytosis of HSV-1 does not lead the virus to an uncoating process. These results are most consistent with a mechanism of entry for HSV-1 involving fusion of the viral envelope with the plasma membrane of the host cell.
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PMID:The mode of entry of herpes simplex virus type 1 into Vero cells. 303 81