The comparative profile of lymphoid cells and the T and B cell spectratype of germ-free piglets infected with viruses SIV, PRRSV or PCV2

Abstract

Lymphocyte subsets isolated from germ-free piglets experimentally infected with swine influenza virus (SIV), porcine reproductive and respiratory syndrome virus (PRRSV) or porcine circovirus type 2 (PCV2) were studied and the profile of these subsets among these three infections was monitored. Germ-free piglets were used since their response could be directly correlated to the viral infection. Because SIV infections are resolved even by colostrum-deprived neonates whereas PRRSV and PCV2 infections are not, SIV was used as a benchmark for an effectively resolved viral infection. PRRSV caused a large increase in the proportion of lymphocytes at the site of infection and rapid differentiation of B cells leading to a high level of Ig-producing cells but a severe reduction in CD2 -CD21 + primed B cells. Unlike SIV and PCV2, PRRSV also caused an increase in terminally differentiated subset of CD2 + CD8α + γδ cells and polyclonal expansion of major Vβ families suggesting that non-specific helper T cells drive swift B cell activation. Distinct from infections with SIV and PRRSV, PCV2 infection led to the: (a) prevalence of MHC-II + T cytotoxic cells, (b) restriction of the T helper compartment in the respiratory tract, (c) generation of a high proportion of FoxP3 + T cells in the blood and (d) selective expansion of IgA and IgE suggesting this virus elicits a mucosal immune response. Our findings suggest that PRRSV and PCV2 may negatively modulate the host immune system by different mechanisms which may explain their persistence.

Porcine reproductive and respiratory syndrome (PRRS): an immune dysregulatory pandemic

“…CD8 ? c/d T cells was increased, which is the only subset is known to be cytotoxic [119]. The paucity of information at this point is insufficient to construct a meaningful hypotheses regarding the role of c/d T cells in PRRS.…”

“…It is known that pulmonary dendritic cells can induce tolerance through IL-10 [118]. However, in a three virus study using isolator piglets, an increase in CD4 cells with a suppressor phenotype was not associated with PRRS [119]. Few studies have experimentally tested whether PRRSV is functionally immunosuppressive while many show inhibition of type I interferons by PRRSV (''The innate immune response to PRRSV'' section).…”

“…Some of the lymphopenia that occurs shortly after birth may reflect the rapidly expanding blood volume but whatever the cause, it is not due to a selective depletion of T cells [119]. In young pigs, PRRSV induces a reduction in circulating lymphocytes early after infection, but not in age-matched controls (C. Loving, pers com).…”

“…Studies using PRRSV-infected isolator piglets [22,119,152,153] have revealed a number of features about the immune response to PRRSV that may provide clues as to how this virus modulates the host immune system. Immediately obvious is hypergammaglobulinemia, lymphoid adenopathy, and the appearance of autoantibodies [22] ( Fig.…”

“…Hydrophobic binding sites are incompatible with antibodies that recognize glycoproteins and are a feature of the pre-immune antibody repertoire [155]. In these animals, B cell differentiation is extremely rapid and cells representing the activated B cell stage are nearly undetectable indicating that B cells rapidly become plasma cells [119].…”