Viruses are considered the best cellular biologists; with little genetic information they take control of the cell for self-perpetuation and spread worldwide. Learning how this occurs is extremely difficult because of the large number of cellular factors involved and the multifunctional nature of viral components. Alphaviruses (such as Chikungunya virus) have four non structural proteins which have been studied for decades accumulating loads of information on host interactors, enzymatic and structural data on single domains or partial complexes. However, the functional units of replication and host interactions are macromolecular complexes gathering viral RNA, cell membranes and viral and host proteins. I will present the architecture of in vitro reconstituted full replication complexes showing how the complexes can change protein nsPs composition and stoichiometry in order to form evolving membrane associated replication complexes within replication organelles. I will also present how nsP3, a major interactor with the host, forms tubular scaffolds structuring cytoplasmic Alphagranules which gather host and viral factors into a massif interaction hub. Overall, these data depict the mode of action of Chikungunya nsPs explaining with unprecedented detail how only four four viral proteins manage to deploy multiple functions at different times of the infection and reconfigures the cell cytoplasm landscape.