Transcriptional immunoresponse of tissue-specific macrophages in swine after infection with African swine fever virus

Abstract

Macrophages and cytokines are important in the control of inflammation and regulation of the immune response. However, they can also contribute to immunopathology in the host after viral infection and the regulatory network can be subverted by infectious agents, including viruses, some of which produce cytokine analogues or have mechanisms that inhibit cytokine function. African swine fever virus (ASFV) encodes a number of proteins which modulate cytokine and chemokine induction, host transcription factor activation, stress responses, and apoptosis. The aim of this review is to elucidate the mechanisms of immune responses to ASFV in different subpopulations of porcine macrophages. A transcriptional immune response in different resident tissue macrophages following ASFV infection was presented in many publications. ASFV-susceptible porcine macrophages can be of several origins, such as peripheral blood, lungs, bone marrow, etc. blood monocytes, blood macrophages, and lung macrophages have demonstrated a modulation of phenotype. Monocyte-derived macrophages could express surface markers not found on their monocyte precursors. Moreover, they can undergo further differentiation after infection and during inflammation. When viruses infect such cells, immunological activity can be seriously impaired or modified.

African Swine Fever Virus Interaction with Host Innate Immune Factors

“…A few of the studied animals exhibited elevated TGF-β levels after immunization. Therefore, ASFV induces TGF-β synthesis in infected macrophages and inhibits the synthesis of IL-8, IFN-α, and TNF-α [ 62 ]. The clinical results, as well as hematological parameters of swine at 12 and 18 weeks old infected with the Netherland’86, an isolate with a mildly pathogenic strain, and their reactions, were compared.…”