LAURIC ACID INHIBITS THE MATURATION OF VESICULAR STOMATITIS-VIRUS

In the presence of lauric acid (C12), the production of infectious ves icular stomatitis virus (VSV) was inhibited in a dose-dependent manner . The inhibitory effect was reversible: after removal of C12 the antiv iral effect disappeared. In addition, the chain length of the monocarb oxylic acids proved to be crucial, as those with shorter or longer cha ins were less effective or had no antiviral activity. Concomitant with the C12-induced inhibition was the stimulation of triacylglycerol syn thesis, increasing the amount up to ninefold. Analysis of the antivira l mechanism of C12 revealed that the correct assembly of the viral com ponents was disturbed, but viral RNA and protein synthesis remained un impaired. By cell fractionation and Western blot analysis the amount o f viral M protein located in the plasma membrane was found to be marke dly reduced after treatment with C12, whereas in the cytoplasm the qua ntity of M protein was similar to that in untreated cells. C12 did not influence M protein synthesis, but prevented the binding of M protein to the host cell membrane, where the protein plays an essential role in virus assembly. Thus, treatment of VSV-infected cells with C12 resu lted in inhibition of virus release. It is suggested that the newly sy nthesized triacylglycerols might interact with the host cell plasma me mbrane and interfere with virus maturation.