Life as a virus is demanding. Tiny in size, and with limited genetic material, a virus must successfully take over comparatively gigantic cells or multicellular organisms. Unlike symbiotic invaders it will face a hostile reception, and it is no surprise that viruses have evolved to carry simplified, multifunctional conquest weapons, resembling the sophisticated equipment in the pocket of 007's dinner suit. A good example of such a weapon is the ‘helper component protease’ (HC-Pro), which is found in the group of potyviruses that infect, and cause severe disease in, a spectrum of plant species. Three papers published in Proceedings of the National Academy of Sciences1, EMBO Journal2 and Cell3 now tell us something about why HC-Pro makes these viruses so successful.

As indicated by its name, HC-Pro was identified as the protease that cleaves a viral polyprotein into its functional subunits. But, like a Swiss army knife, it packs in more than just a cutting blade. It binds RNA and is involved in amplification of the viral RNA genome, spreading the virus from the site of infection and transmitting it from plant to plant via sap-sucking insects4. Although almost all plant viruses have proteins to do these jobs (albeit in different combinations), the new work1,2,3 shows that HC-Pro has another function unknown in any other virus — it paralyses an important plant defence mechanism that normally acts against viruses.

The mechanism in question is based on ‘post-transcriptional gene silencing’ (PTGS), whereby specific transcripts are degraded before they can be translated5. The process was initially observed in transgenic plants when, instead of being overexpressed, transgenes (as well as homologous endogenous genes) became silent. Cytoplasmic viral templates can be degraded by the same mechanism, especially if parts of the virus have been integrated into the plant's nucleus as transgenes. Indeed, silencing of viral gene expression by PTGS can explain ‘recovery’ of virus-infected plants which, despite initial viral replication and spread throughout the plant, develop new, virus-free shoots and leaves6.

Because RNA viruses replicate through double-stranded RNA intermediates, and silenced transgenes are suspected to produce aberrant antisense RNA, double-stranded RNA could be the common signal for specific degradation, probably also related to the mechanism that operates in animal models7. PTGS is thought to have evolved either as an antiviral defence mechanism, or as a regulatory mechanism for endogenous plant genes that also affects viral genes8. In both cases, the potential to act against many viral sequences, combined with the high specificity of the response, seems to make PTGS part of a plant's ‘immune system’ based on particular RNA sequences. Therefore, it is not surprising that, like their animal counterparts, some plant viruses have developed strategies to attack this defence. The HC-Pro protein of tobacco etch virus and protein 2b of cucumber mosaic virus are part of this attack. Anandalakshmi et al.1, Brigneti et al.2 and Kasschau and Carrington3 now show that when these proteins are expressed in tobacco (Nicotiana tabacum) and N. benthamiana , the PTGS response is suppressed — existing silencing and virus resistance are removed, and silencing cannot be established during viral infection.

These results also bear on the concept of synergistic viral infection. When plants are infected with two different species of virus, the result is often more severe symptoms than inoculation with either virus alone. Potyviruses are successful partners in this double-attack strategy, allowing strong replication and spread of the other partner. HC-Pro is essential for double infection9, and it is probably its ability to suppress PTGS that limits the general plant defence response, allowing other viruses that do not encode HC-Pro to be amplified. Viral modulation of the plants’ gene-silencing system might also cause unexpected changes in gene expression if transgenic plants cannot be saved from uncontrolled infections.

We do not yet know how, at the molecular level, HC-Pro is involved in viral amplification, spread and transmission. Is it really a multifunctional tool, or are all of the functions that support infection simply consequences of suppressing PTGS? Whatever the answer, HC-Pro is a promising bait to fish for interacting plant components and to learn more about the molecular basis of PTGS. The newly discovered function of this viral Swiss army knife will make it a tool for plant geneticists, allowing gene silencing in transgenic plants to be increased or avoided. But because exaggerated euphoria about gene-transfer techniques has often been followed by unwanted gene silencing, we will probably also discover the limits to which we can manipulate gene silencing. Components such as HC-Pro are not the only factors involved, and they cannot provide a 100% effective control. Armed with the new information, it is amusing to note that the connection between gene silencing and viral resistance was first described for tobacco etch virus6, despite the fact that it carries HC-Pro and was the source of this protein for the new studies describing its PTGS-suppressing effect1,2,3. In any case, it will be exciting to learn how plants combat this viral super-weapon from their side.