Suppressed mucosal lymphocyte populations by LP-BM5 murine leukemia virus infection producing murine AIDS.

LP-BM5 murine leukemia virus (MuLV) infection induces an immunodeficient state in susceptible strains of mice. It has been previously characterized at the level of spleen and peripheral lymph nodes. We recently demonstrated that LP-BM5 MuLV-infected mice lost intestinal host resistance to common opportunistic pathogens. In this article we investigated how murine retroviral infection alters the differentiation of IgA B cell precursors in Peyer's patches (PP), mesenteric lymph nodes (MLN), and the intestinal lamina propria (ILP). After 4 months of LP-BM5 MuLV infection, there was a significant decrease in the absolute numbers of Thy1+, CD4+, and CD8+ cells in PP with a concomitant decrease in the percentage and in the absolute numbers of surface IgA+--(sIgA+) and surface IgM+--bearing (sIgM+) cells. Infection also produced an enlarged MLN with a six-fold increase in cell numbers and a decrease in the relative percentage of sIgA+, cytoplasmic IgA+, and cytoplasmic IgM+ cells. However, murine retrovirus infection caused no significant changes in the percentages of Thyl+, CD4+, CD8+, and CD5+ cells in the MLN. After 4 months of murine retrovirus infection cIgA+ cells from MLN were not able to populate the intestinal lamina propria as the number of IgA plasma cells was significantly decreased. Moreover, there was a concomitant decrease in the number of CD4+ cells per field in the ILP. These results suggest that murine retrovirus infection favors the expansion of IgA B cell precursors at the level of MLN, while simultaneously interfering with the terminal differentiation step and thus preventing IgA plasma cell precursors from seeding the ILP.(ABSTRACT TRUNCATED AT 250 WORDS)