Differential inhibitory action of two azoic compounds against arenaviruses

C. C. GARCÍA; NÉLIDA A. CANDURRA; E. B. DAMONTE

The International Journal of Antimicrobial Agents

Año: 2003 vol. 21 p. 319 - 324

<!-- /* Style Definitions */ p.MsoNormal, li.MsoNormal, div.MsoNormal {mso-style-parent:""; margin:0cm; margin-bottom:.0001pt; mso-pagination:widow-orphan; mso-layout-grid-align:none; punctuation-wrap:simple; text-autospace:none; font-size:12.0pt; mso-bidi-font-size:10.0pt; font-family:"Times New Roman"; mso-fareast-font-family:"Times New Roman"; mso-ansi-language:ES-AR;} @page Section1 {size:612.0pt 792.0pt; margin:70.85pt 3.0cm 70.85pt 3.0cm; mso-header-margin:36.0pt; mso-footer-margin:36.0pt; mso-paper-source:0;} div.Section1 {page:Section1;} --> The action of five azo-based compounds against the arenaviruses Junin (JUNV) and Tacaribe (TCRV) was evaluated in vitro by a virus yield inhibition assay in Vero cells and a cell-free virion inactivation assay. The compound 2-azo-(1’-(2’nitroso)naphthyl)-benzoate (ANNB) was the most effective inhibitor of arenavirus production in Vero cells with EC50 (effective concentration 50%) values in the range 6.5-26.2 µM and without inactivating properties. By contrast, the azodicarbonamide (ADA) was very effective to inactivate both arenaviruses with IC50 (inactivating concentration 50%) values of 7.6 and 5.3 µM against JUNV and TCRV, respectively. The virucidal activity of ADA was time- and temperature-dependent. ANNB had no inhibitory action on virus binding and penetration to target cells neither affected the synthesis of viral proteins. The most likely event susceptible to ANNB would be the process of intracellular virion assembly.