Abstract
C observations suggested that an antiviral effect of propranolol has confirmed at an observational level for influenza infections, as well as for other viral infections like herpes simplex I and herpes zoster virus infections. A theory of the mechanism of this antiviral effect has been developed, and examples of published observations apparently confirming the antiviral effect of propranolol have been analyzed based on the assumed mechanism. The proposed mechanism is an increased activity of most cells of the immune system via an activation of the cAMP-PKA pathway, reducing the inhibitory impact of some stress-related influences on the immune system. In contrast, in tissues activated by stress the cAMP-PKA pathway is activated by beta-receptor agonists. A larger view concerning the impact of stress on tissues inactivated versus tissues activated by stress is proposed and the potential consequences concerning treatment strategies are presented.
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