ntroduction: below: Vaccination is the main control strategy against the Porcine Respiratory and Reproductive Syndrome virus (PRRSv), a major concern of the swine industry. However, none commercial vaccine is efficient to eradicate the infection mainly because they only confer a partial protection of the host. Moreover, PRRSv exhibits a high virulence variability among strains and current vaccines provide only a partial cross-protection. Consequently, improving vaccine efficiency at the host level is still a major challenge for PRRS control. The immune mechanisms involved in vaccination and determining the host protection are not yet fully identified and seem variable among PRRSv strains. Considering this variability context and the complexity of immune mechanisms, we chose a modelling approach to tackle this issue. We focused on modified-live vaccines, as they are assumed to be the more efficient against PRRSv. Materials and Methods: From the literature review of PRRSv immune dynamics, we developed an original model of the PRRSv within-host dynamics representing the immune mechanisms at the between-cell scale. This model describes the evolution over time of (i) the within-host viral load and (ii) the major immune components (involved in the PRRSv-target cell interactions, the innate response, the adaptive response orientation and the cytokine regulations). We used this model to simulate a PRRSv infection of a vaccinated pig (i.e. starting with memory response, 2 levels of memory activation has been tested) considering both PRRSv virulence (3 levels: low, reference and high) and exposure (3 intensities x 2 durations) variabilities. Results: Our results exhibited a clear vaccination efficiency to reduce the infection duration, whatever the strain virulence and the exposure, but no efficiency on either the infection severity (characterised by the area under the curve of the viral titer) or the viral peak. The higher the memory activation level and the virulence level, the higher the vaccine efficiency. The innate mechanisms (phagocytosis, cell infection, viral replication) were not involved in the vaccination efficiency. The adaptive response orientation associated with the infection duration decreases exhibited a high variability depending on virulence and exposure level. High vaccine efficiency was globally associated with high levels of regulatory response. Finally, the higher the cytolysis and neutralisation activities the higher the infection duration decreases due to vaccination. Conclusion: We proposed an original and adapted method to explore the efficiency of vaccination strategies. Our results provide insights to improve the vaccination efficiency, in particular regrading the adaptive response orientation towards the regulatory. As we here considered a full cross-protection between viral strains, this model has to be adapted to take into account the genetic heterogeneity observed in the field.