Swine leukocyte antigen and macrophage marker expression on both African swine fever virus-infected and non-infected primary porcine macrophage cultures

Abstract

Swine leukocyte antigens (SLA) and a macrophage specific marker were monitored on porcine macrophages cultured with or without macrophage colony stimulatory factor (M-CSF) and on cells infected with African swine fever virus (ASFV). SLA expression was maximal either in the total cell extract or on the cell surface at 3-4 days of culture; after 4 days these values began to decrease. Fluorescence analyses of immunostained macrophages cultured with or without M-CSF indicated a major upward shift in the number of SLA Class I molecules on individual macrophages whereas for SLA Class II both a novel expression of Class II and an upward shift in the number of molecules per cell were evident. Infection of 3-day-old macrophage cultures with three different isolates of ASFV resulted in minor changes in surface expression of SLA Class I, SLA Class II, and macrophage markers. No differences in infection with ASFV was observed whether macrophages were SLA Class II positive or negative, nor was there blocking by anti-SLA Class I or Class II monoclonal antibodies of ASFV infection of cultured macrophages.

Transcription analysis of the porcine alveolar macrophage response to porcine circovirus type 2

“…These molecules include DOA, DOB, DQA1, DQB1, DRA, and DRB1, and their molecule chaperone CD74; all of which were up-regulated in PCV2-infected PAMs. This expression pattern contradicts the host response observed for other viruses, such as African swine fever virus (CSFV) [33], classical swine fever virus [34] and influenza A virus [35], and that was observed in follicles and PAMs of PMWS piglets [36,37]. Increased expression of MHC class II molecular have been shown to be correlated to increased interferon production in pigs infection infected with hog cholera virus [38].…”

African swine fever: A re-emerging viral disease threatening the global pig industry

“…Under experimental conditions, older pigs appear to have better survival than younger pigs after infection with a moderately virulent isolate of ASFV, regardless of the inoculation dose ( Post et al, 2017 ). ASFV mainly replicates in myeloid lineage cells, especially antigen presenting cells (APCs) such as monocytes/macrophages and dendritic cells ( Malmquist and Hay, 1960 , Wardley and Wilkinson, 1977 , Gonzalez-Juarrero et al, 1992b , Carrillo et al, 1994 , Gregg et al, 1995a , Gregg et al, 1995b , Sánchez-Cordón et al, 2008 ). There is evidence of modulation of major histocompatibility class II expression in the spleen of pigs infected with a virulent strain of ASFV ( Gonzalez-Juarrero et al, 1992a ).…”

The low-virulent African swine fever virus (ASFV/NH/P68) induces enhanced expression and production of relevant regulatory cytokines (IFNα, TNFα and IL12p40) on porcine macrophages in comparison to the highly virulent ASFV/L60

“…Previous studies have shown that ASFV inhibits phagocytosis, antibody-mediated phagocytosis and chemotaxis in porcine macrophages cultivated in vitro, although no changes were observed in the expression of Fc receptors, nor in the capacity to induce antibody-dependent cytotoxicity (ADCC) [ 21 ]. In identical circumstances, the expression of SLA antigens was not changed on those cells [ 13 ].…”