[en] Gammaherpesvirus (ɣ-HVs) infections are highly prevalent in both human and animals. They persist in their host by establishing and maintaining latent infections. Murid herpesvirus 4 (MuHV-4) is a wild rodent pathogen that can be used as a model of ɣ-HV infection in the laboratory mouse. Like other ɣ-HVs, MuHV-4 profoundly imprints the host immune system to allow completion of its biological cycle. In particular, MuHV-4-induced modulations have been shown to confer bystander protection against heterologous secondary infections. Type 2 respiratory immunopathologies are of major interest in public health, specifically in developped countries. Notably, allergic asthma affects more than 300 million people worldwide and hSRV (human respiratory syncytial virus) inactivated vaccine-induced Th2 immunopathology substantially delays the development of vaccines against this virus which is yet the main infectious agent of bronchopneumopathies in children and olders. According to the hygiene hypothesis, epidemiological studies suggest that late primoinfections to human ɣ-HVs are correlated to an increased risk of allergic sensitization later in life. Using the MuHV-4 model, the in vivo impact of a ɣ-HV infection was tested against the development of on one hand, allergic airway inflammation induced by house dust mites (HDM) allergens (study 1) and on the other hand, anti-pneumovirus Th2 immunopathology, using Pneumonia virus of mice (PVM) to faithfully mimic the original hRSV disease in homologous host-virus model (study 2). Our results have shown that MuHV-4-infected mice are protected from the development of both allergic and vaccine-induced type 2 immune disorders. Moreover, MuHV-4-infected mice were also clinically protected from the subsequent heterologous infection with PVM. Finally, the protective mechanism against HDM allergic asthma was deciphered; pulmonary MuHV-4 lytic infection causes the severe depletion of the alveolar niche which is repopulated by bone marrow-derived monocytes. These latter cells then differentiate into alveolar macrophages (AMs) that are both phenotypically and functionally distinct from resident AMs. Indeed, in previously MuHV-4 infected mice, these monocyte-derived AMs express regulatory functions to block the activation of dendritic cells involved in allergic sensitization, therefore, conferring protection against allergic airway inflammation. In conclusion, the present thesis has unambiguously unraveled that ɣ-HV infection can protect the host against the development of main public health-related respiratory type 2 immune disorders. Replacement of embryonic AMs by regulatory monocytes is thus a major feature underlying the long-term training of the lung immunity after infections, and could provide a possible mechanistic explanation for the hygiene hypothesis. Altogether, this work opens interesting perspectives for the prevention of respiratory type 2 immunopathologies.