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Control of Virus Diseases of Plants 161and cGMP for the <strong>in</strong>duction of active AVF <strong>in</strong> leaves and callus cultures ofN. glut<strong>in</strong>osa.Inhibitor of virus replicationLoebenste<strong>in</strong> and Gera (1981) reported, for the first time, an <strong>in</strong>hibitor of virusreplication (IVR). IVR is released <strong>in</strong>to the medium from TMV-<strong>in</strong>fected cells ofSamsun NN <strong>plant</strong>s and <strong>in</strong>hibits replication <strong>in</strong> protoplasts from local-lesionrespond<strong>in</strong>gSamsun <strong>plant</strong>s. IVR is detected as soon as 24 h after <strong>in</strong>oculationof protoplasts and it is effective when applied up to 18 h after <strong>in</strong>oculation.IVR is neither host nor virus specific. It <strong>in</strong>hibits TMV, CMV and also PVX(Gera and Loebenste<strong>in</strong>, 1983). Gera and Loebenste<strong>in</strong> (1983) reported that IVRalso <strong>in</strong>hibited TMV replication <strong>in</strong> <strong>in</strong>tact leaves when applied to cut stems orwhen used as a spray.Plant-extract-<strong>in</strong>duced virus <strong>in</strong>hibitory agentIt would be <strong>in</strong>terest<strong>in</strong>g to study the entire cascade of events and properties ofthe virus <strong>in</strong>hibitory agent (VIA) <strong>in</strong>duced by antiviral agents. Treatment oflower / upper leaves of hypersensitive or systemic hosts of virus withantiviral agents results <strong>in</strong> the development of resistance throughout the <strong>plant</strong>a few hours later. This is detectable by challenge <strong>in</strong>oculation with virusesproduc<strong>in</strong>g local lesions or systemic symptoms. The lesions are either reducedor totally absent and systemic symptoms are either milder or totally suppressed.Plant extracts or the semi-purified prote<strong>in</strong>s from these <strong>plant</strong>s stimulatethe hosts to produce VIAs that spread to surround<strong>in</strong>g tissues and other<strong>plant</strong> parts (Verma et al., 1996). The VIAs have been isolated from leaves of<strong>plant</strong>s treated with phytoprote<strong>in</strong>s and they have been shown to <strong>in</strong>activatethe viruses <strong>in</strong> vitro (Verma and Awasthi, 1980; Verma and Dwivedi, 1984;Verma et al., 1996). The production of VIA lead<strong>in</strong>g to resistance seems to bean activation of a pre-exist<strong>in</strong>g system and hence is easily stimulated. VIA isable to move from one leaf to another through the vascular system of the<strong>plant</strong>.Therefore, the antiviral agents from <strong>plant</strong>s can be broadly grouped <strong>in</strong>totwo categories based on their mode of action: (i) those affect<strong>in</strong>g virus <strong>in</strong> vitro;and (ii) those affect<strong>in</strong>g via host <strong>plant</strong>s.Amongst the latter, we can dist<strong>in</strong>guish (1) those that act by affect<strong>in</strong>g hostsusceptibility and which need to be applied <strong>in</strong> leaf tissue before or at the timeof virus <strong>in</strong>oculation, e.g. prote<strong>in</strong> <strong>in</strong>hibitors from Phytolacca spp., Dianthusspp., Chenopodium spp. and so on, and (2) those act<strong>in</strong>g by <strong>in</strong>duc<strong>in</strong>g the hostresistance mechanism, which can truly be called antiviral agents, and act byobstruct<strong>in</strong>g the establishment of virus. They exert their effect when applied afew hours before virus <strong>in</strong>oculation. Their effect is visible even on non-treatedparts of susceptible <strong>plant</strong>s (Verma and Mukherjee, 1975; Verma and Awasthi,1979; Verma et al., 1979, 1980, 1982, 1985, 1995, 1996; Kumar et al., 1997).

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