This paper shows that morphine increases Sendai virus replication in cultured epithelial cells. The effect was maximal when it was added before viral infection. Morphine also reduced the intracellular level of glutathione, namely, the oxidative and most abundant cell thiol. Altered intracellular redox status has recently been proposed as a factor influencing viral infection. Support for this view was provided by our data showing that inhibition of de novo glutathione synthesis, using L-buthionine sulfoximine, increased virus replication. These findings provide the first evidence that morphine increases the susceptibility to virus infection by altering the intracellular levels of glutathione. Copyright (C) 1998 Elsevier Science B.V.
Increased replication of sendai virus in morphine-treated epithelial cells: Evidence for the involvement of the intracellular levels of glutathione / Iole, Macchia; Palamara, ANNA TERESA; Cristina, Bue; Patrizia, Savini; Maria, Ciriolo; Roberta, Gaziano; P., Di Francesco. - In: INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY. - ISSN 0192-0561. - 21:3(1999), pp. 185-193. [10.1016/s0192-0561(98)00080-0]
Increased replication of sendai virus in morphine-treated epithelial cells: Evidence for the involvement of the intracellular levels of glutathione
PALAMARA, ANNA TERESA;
1999
Abstract
This paper shows that morphine increases Sendai virus replication in cultured epithelial cells. The effect was maximal when it was added before viral infection. Morphine also reduced the intracellular level of glutathione, namely, the oxidative and most abundant cell thiol. Altered intracellular redox status has recently been proposed as a factor influencing viral infection. Support for this view was provided by our data showing that inhibition of de novo glutathione synthesis, using L-buthionine sulfoximine, increased virus replication. These findings provide the first evidence that morphine increases the susceptibility to virus infection by altering the intracellular levels of glutathione. Copyright (C) 1998 Elsevier Science B.V.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.