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Antimicrobial Agents and Chemotherapy, April 1999, p. 822-829, Vol. 43, No. 4
0066-4804/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Antiviral Effect of Hyperthermic Treatment in Rhinovirus Infection

C. Conti,¹ A. de Marco,² P. Mastromarino,¹ P. Tomao,¹ and M. G. Santoro^2,3,*

Institute of Microbiology, School of Medicine, University "La Sapienza," 00185, Rome,¹ and Department of Biology, University of Rome Tor Vergata,² and Institute of Experimental Medicine, CNR,³ 00133 Rome, Italy

Received 31 July 1998/Returned for modification 19 October 1998/Accepted 4 February 1999

Human rhinoviruses (HRV) are recognized as the major etiologic agents of the common cold. Starting from the observation that local hyperthermic treatment is beneficial in patients with natural and experimental common colds, we have studied the effect of brief hyperthermic treatment (HT) on HRV replication in HeLa cells. We report that a 20-min HT at 45°C is effective in suppressing HRV multiplication by more than 90% when applied at specific stages of the virus replication cycle. Synthesis of virus proteins is not affected by HT, indicating that the target for treatment is a posttranslational event. The antiviral effect is a transient cell-mediated event and is associated with the synthesis of the 70-kDa heat shock protein hsp70. Unlike poliovirus, rhinovirus infection does not inhibit the expression of hsp70 induced by heat. The possibility that hsp70 could play a role in the control of rhinovirus replication is suggested by the fact that a different class of HSP inducers, the cyclopentenone prostaglandins PGA₁ and ¹²-PGJ₂, were also effective in inhibiting HRV replication in HeLa cells. Inhibition of hsp70 expression by actinomycin D prevented the antiviral activity of prostaglandins in HRV-infected cells. These results indicate that the beneficial effect of respiratory hyperthermia may be mediated by the induction of a cytoprotective heat shock response in rhinovirus-infected cells.

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^* Corresponding author. Mailing address: Department of Biology, University of Rome Tor Vergata, Via della Ricerca Scientifica, 00133 Rome, Italy. Phone: 39-06-7259-4822. Fax: 39-06-7259-4821. E-mail: santoro{at}bio.uniroma2.it.

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Antimicrobial Agents and Chemotherapy, April 1999, p. 822-829, Vol. 43, No. 4
0066-4804/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

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