Potato viruses cause enormous economic loss in agriculture production. Potatoes can be infected by a number of different viruses that affect negatively the harvest and the tuber quality. Direct and effective drugs against plant virus diseases are still not available and control is only applied as agricultural measures and pesticides against virus vectors. Potato virus Y (PVY) is transmitted by aphids in non-persistent manner and on that account using insecticides to prevent spread of the infection is useless. Breeding of resistant plant cultivars proved to be not always a solution of the problem because of the fast evolution of the virus strains and the constantly growing group of recombinants. In this study, we have proposed a new way of controlling the virus by blocking replication and transmission through the plant by RNAi-based vaccination of potato seedlings with specific to viral HC-Pro gene siRNAs. Thus, PVY replication is decreased without altering the valuable qualities of the sensitive to the virus potato cultivars like Agria.
27 June 2015 in European Journal of Plant Pathology
Potato virus Y (PVY) is the reason for significant losses in the potato crop yearly. The recent technologies in molecular biology have given insights on possibilities for control of viral infections at epigenetic level. In the present study, we obtained a DNA template complementary to a key sequence at the NIb genetic region of PVY. Potato leaves were inoculated with dsRNAs and siRNAs complementary to NIb 48 h before inoculation with PVY strain N/NTN. The treated plants did not develop any signs of disease. Double antibody sandwich еnzyme-linked immunosorbent assay (DAS-ELISA) of the plants treated with Nib-dsRNAs showed optical density values commensurate to the cut-off value. The Nib-siRNAs obtained in this study were twice as effective, with DAS-ELISA values which were below the cut-off and similar to the values of the healthy plants. Inducing posttranscriptional gene silencing in crops presents a promising utility for control of virus diseases and for prevention of crop losses, being non-inheritable, non-toxic and adaptable to a specific crop.
1 April 2006 in Antiviral Chemistry and Chemotherapy
In view of the potential menace of a terrorism attack with smallpox virus, an intensive search of chemotherapeutic agents active against orthopoxviruses is underway. We comparatively studied the antiviral activity of cidofovir (CDV) and idoxuridine (IUdR) against two vaccinia virus (VV) strains, Bratislava and RIIPD, in cell cultures of chick embryo fibroblasts (CEF). The investigations were carried out according to cytopathic effect (CPE) inhibition assay protocols. To determine the cytotoxicity of the compounds, maximal tolerated concentration (MTC) was calculated in CEF cell monolayers and 50% cell growth inhibitory concentration (CGIC50) was calculated in growing cell cultures. It was found that the antiviral effects were strongly dependent on virus inoculum size. There were no marked differences in the susceptibility to CDV and IUdR between the two VV strains. The individual half maximal inhibitory concentration (IC50) for CDV varied from 7.1–8.5 µM at 10/100 virus 50% infectious dose (ID50) to 13.6–26.5 µM at 10,000 ID50. The CDV selectivity index was also virus dose-dependent with MTC/IC50 and CGIC50/IC50 values ranging between 37.8–141.4 and 33.3–124.6, respectively. For IUdR, IC50 ranged from 0.58 to 0.85 µM, but the selectivity index for monolayer CEF and growing cell cultures produced substantial different results with MTC/IC50 and CGIC50/IC50 values between 117.7–172.4 and 20.4–33.3, respectively. The combination effects of CDV and IUdR against VV Bratislava strain in the CPE inhibition test were also determined. The test design of both combination antiviral effect and combined cytotoxicity followed a three-dimensional model. The combined effect of CDV and IUdR on VV replication in monolayer CEF cultures was characterized as a markedly synergistic one. In contrast, CDV and IUdR together reduced cytotoxicity in both monolayer and growing CEF cells.