The study of viral proteases is crucial to understand the mechanism used by animal viruses to replicate their genomes and to translate viral mRNAs at the molecular level. In addition, we wish to draw attention to the concept that viral proteases can be used as tools to reveal the exact functioning of their target cellular proteins. In this regard, PV 2A pro has been very useful for examining the requirements for eIF4G to translate different cellular or viral mRNAs. In addition to this, in this paper, we have highlighted the role of PV 2A pro not only in the processing of the poliovirus polyprotein but also in the interaction with the host-cell. Interestingly, a single viral protein is able to modulate many steps of gene expression in order to generate an optimal intracellular environment for the viral biological cycle. In particular, PV 2A pro cleaves cell proteins involved in transcription, pre-mRNA splicing, nucleus/cytoplasm transport and translation, in order to hijack those host functions and to concentrate the cellular resources on the production of the viral progeny. For example, PV 2A pro inactivates host translational machinery for capped cellular mRNAs by cleaving eIF4G, whereas viral protein synthesis takes place under those conditions by IRES-driven translation [14] . Because of the decrease of cellular mRNA translatability in PV-infected cells, host ribosomes are available for viral protein synthesis. Probably, the inhibition of host protein synthesis may prevent the production of antiviral proteins. Similarly, the blockade of nucleus/cytoplasm transport of macromolecules might isolate nuclear processes from cytoplasmic cellular ones, hampering the arrival of specific proinflammatory transcription factors to the nucleus and of mRNAs encoding proinflammatory, antiviral or proapoptotic proteins to the cytoplasm of infected cells. Finally, transcription and pre-mRNA splicing could be also modulated by PV 2A pro and might reduce the availability of mature mRNAs. Nevertheless, very little is known about the potential role of PV 2A pro in transcription and pre-mRNA splicing, and further studies of these steps of gene expression in PV-infected and 2A-expressing cells should be carried out. Making use of the "omics" technologies it would be possible to identify changes in the host transcriptome in those cells, allowing us to understand the readjustment of host gene expression to viral infection and to the cytotoxic effect of PV 2A pro . Gene ontology tools can be used to cluster the pathways (KEGG), molecular activities and biological functions of the genes which are transcriptionally up-or downregulated or not affected after these unfavourable stimuli. In silico analysis could be carried out in order to identify whether these gene clusters belong to particular networks controlled by specific transcription factors. This approach will give us additional information about potential host targets for PV 2A pro . Complementarily, deep sequence (RNAseq), specific microarrays types and conventional RT-PCR could be used to screen for nonspliced or abnormal spliced mRNA variants in PV-infected and 2A pro -expressing cells. Finally, microarrays can be employed to identify the cytoplasmic and nuclear transcriptome in those cells to determine whether mRNA nuclear export inhibition induced by PV 2A pro impacts on the distribution of the entire host mRNA bulk or in specific mRNA pools. Taken together, all this information may provide us with a general and deep vision of the modification induced by PV 2A pro on the different steps of mRNA metabolism. Additionally, the physiological role of Nups and Gemin-3 cleavage might be studied using different models. One possible and interesting approach is to engineer stable cell lines expressing noncleavable versions of Nup98, Nup62, Nup153 and/or Gemin-3 and then to analyze the fitness of PV in the different cell types, especially in presence of extracellular antiviral stimuli such as IFNs or interleukins, which will activate different epigenetic programs. These studies will provide essential information to help us understand the specific role that those host factors play in PV infection. The total number of cellular proteins targeted by PV 2A pro (degradome) remains unknown, but it can be anticipated that with the expanding use of proteomic methodologies, this analysis will be known soon not only for PV 2A pro , but also for other viral proteases of interest. Furthermore, the analysis of the PV 2A pro -induced degradome in human cells will be of general interest for many researchers, including virologists and cellular biologists. This goal could be achieved combining in silico prediction of 2A pro cleavage sites and experimental tools such as proteomics. In the first case, Blom and collaborators developed a bioinformatics tool using neural network algorithms to predict cellular targets for picornavirus proteases [219] . This approach has been successfully used to predict the cleavage of dystrophin by coxsackievirus 2A pro [220] although most of the predicted human targets for rhinovirus and enterovirus 2A pro have not been proved yet. In addition, the algorithm did not predict the cleavage of cellular targets that have been later demonstrated to be proteolyzed by picornaviral 2A pro such as Nup98 and cytokeratin 8 [16, 17, 221] . Thus, it would be necessary to develop an improved algorithm able to find optimal cleavage sequences in the host proteome by implementing the proteolytic sites known for newly described 2A pro targets. Many parameters have to be taken into account, including the protein localization (cytoplasmic and nuclear protein will be considered, but not proteins resident in the lumen of other organelles such as RE or peroxisomes), the exposure of the cleavage site to the solvent (the sequence must be accessible to the protease), and the secondary structure in which the proteolytic site is included (optimally, unstructured regions). Potential targets could be ordered by their degree of homology with optimal cleavage sequences, as well as with the degree in which they fulfill the above prerequisites. On the other hand, novel PV 2A pro targets can be identified by proteomic tools such as two-dimensional differential gel electrophoresis (DIGE) or quantitative proteomics such as stable isotope labeling by amino acids in cell culture (SILAC) coupled to monodimensional electrophoresis. Following these two methods, it will be feasible to identify proteins with reduced levels on 2A pro expression and, in addition, to detect the cleavage products that will appear as lower size peptides. By the uncovering of novel 2A pro targets we will be able to map the cellular networks impacted by PV 2A pro and to integrate them in the context of PV infection. In fact, the role of 2A pro hijacking host processes could be potentially expanded to other cellular pathways with direct impact on control of viral infection. Such knowledge will provide more insight into our understanding of the cytopathogenicity of viral proteases at the molecular level. Transmission Potential of Chikungunya Virus and Control Measures: The Case of Italy During summer 2007 Italy has experienced an epidemic caused by Chikungunya virus – the first large outbreak documented in a temperate climate country – with approximately 161 laboratory confirmed cases concentrated in two bordering villages in North–Eastern Italy comprising 3,968 inhabitants. The seroprevalence was recently estimated to be 10.2%. In this work we provide estimates of the transmission potential of the virus and we assess the efficacy of the measures undertaken by public health authorities to control the epidemic spread. To such aim, we developed a model describing the temporal dynamics of the competent vector, known as Aedes albopictus, explicitly depending on climatic factors, coupled to an epidemic transmission model describing the spread of the epidemic in both humans and mosquitoes. The cumulative number of notified cases predicted by the model was 185 on average (95% CI 117–278), in good agreement with observed data. The probability of observing a major outbreak after the introduction of an infective human case was estimated to be in the range of 32%–76%. We found that the basic reproduction number was in the range of 1.8–6 but it could have been even larger, depending on the density of mosquitoes, which in turn depends on seasonal meteorological effects, besides other local abiotic factors. These results confirm the increasing risk of tropical vector–borne diseases in temperate climate countries, as a consequence of globalization. However, our results show that an epidemic can be controlled by performing a timely intervention, even if the transmission potential of Chikungunya virus is sensibly high. During summer 2007 Italy has experienced the first large outbreak caused by Chikungunya virus (CHIKV) documented in a temperate climate country [1] . CHIKV is an arthropod-borne virus which can be transmitted to humans by Aedes mosquitoes [2] , widespread in some tropical regions [3] [4] [5] [6] [7] [8] . Aedes albopictus is highly competent for CHIKV [9, 10] . In Italy, the presence of this mosquito was first documented in Genoa and Padua (Northern Italy) in the earliest 1990's [11, 12] . Over the following years, Aedes albopictus expanded its distribution and is now well established in Northern and Central Italy [13, 14] . Having the potential to colonize the Mediterranean basin [15] , the species has been reported from most Mediterranean European countries [16] . Samples of Aedes albopictus from the two villages were found to be positive for CHIKV sequences [1] .