Cyclopentenone prostaglandins inhibit the replication of several DNA and RNA viruses, including retroviruses. The antiviral activity has been associated with the induction of a 70-kDa heat-shock protein (HSP70), via activation of the heat-shock transcription factor (HSF) in infected cells. In the present study we investigated the effect of prostaglandin A1 (PGA1) on the regulation of HSP70 gene expression as well as on viral RNA and protein synthesis in CEM-SS cells during acute infection with human immunodeficiency virus type 1 (HIV-1). We report that HIV-1 infection does not alter HSF activation by PGA1, whereas it causes an increase in intracellular HSP70 mRNA levels, as a result of enhanced HSP70 mRNA stability. We also show that, as reported in studies of different virus/host cell models, PGA1 inhibits HIV-1 replication by acting at multiple levels during HIV-1 infection. In addition to the previously reported block of HIV-1 mRNA transcription, PGA, was also found to inhibit viral protein synthesis. These results, together with the fact that prostaglandins are used clinically in the treatment of several diseases, open new perspectives in the search for novel antiretroviral drugs.

Induction of the heat-shock response by antiviral prostaglandins in human cells infected with human immunodeficiency virus type 1 / De Marco, A; Carattoli, A; Rozera, C; Fortini, D; Giorgi, C; Belardo, G; Amici, C; Santoro, M. G.. - In: EUROPEAN JOURNAL OF BIOCHEMISTRY. - ISSN 0014-2956. - 256:2(1998), pp. 334-341. [10.1046/j.1432-1327.1998.2560334.x]

Induction of the heat-shock response by antiviral prostaglandins in human cells infected with human immunodeficiency virus type 1

Carattoli A;
1998

Abstract

Cyclopentenone prostaglandins inhibit the replication of several DNA and RNA viruses, including retroviruses. The antiviral activity has been associated with the induction of a 70-kDa heat-shock protein (HSP70), via activation of the heat-shock transcription factor (HSF) in infected cells. In the present study we investigated the effect of prostaglandin A1 (PGA1) on the regulation of HSP70 gene expression as well as on viral RNA and protein synthesis in CEM-SS cells during acute infection with human immunodeficiency virus type 1 (HIV-1). We report that HIV-1 infection does not alter HSF activation by PGA1, whereas it causes an increase in intracellular HSP70 mRNA levels, as a result of enhanced HSP70 mRNA stability. We also show that, as reported in studies of different virus/host cell models, PGA1 inhibits HIV-1 replication by acting at multiple levels during HIV-1 infection. In addition to the previously reported block of HIV-1 mRNA transcription, PGA, was also found to inhibit viral protein synthesis. These results, together with the fact that prostaglandins are used clinically in the treatment of several diseases, open new perspectives in the search for novel antiretroviral drugs.
1998
heat shock protein; heat shock protein 70; messenger rna; prostaglandin a1; transcription factor; virus rna, antiviral activity; article; cell line; controlled study; heat shock response; human; human cell; human immunodeficiency virus 1; human immunodeficiency virus infection; in vitro study; priority journal; protein synthesis; rna synthesis, Antiviral Agents; Cell Line; DNA-Binding Proteins; Gene Expression Regulation, Viral; HIV Infections; HSP70 Heat-Shock Proteins; Humans; Prostaglandins A; Protein Synthesis Inhibitors; Retroviridae Proteins, Oncogenic; RNA, Messenger; RNA, Viral; Trans-Activation (Genetics); Transcription Factors; Viral Proteins, Human immunodeficiency virus; Human immunodeficiency virus 1; RNA viruses
01 Pubblicazione su rivista::01a Articolo in rivista
Induction of the heat-shock response by antiviral prostaglandins in human cells infected with human immunodeficiency virus type 1 / De Marco, A; Carattoli, A; Rozera, C; Fortini, D; Giorgi, C; Belardo, G; Amici, C; Santoro, M. G.. - In: EUROPEAN JOURNAL OF BIOCHEMISTRY. - ISSN 0014-2956. - 256:2(1998), pp. 334-341. [10.1046/j.1432-1327.1998.2560334.x]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1284804
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