Effect of adoptive transfer of CD4, CD8 and B cells on recovery from MHV3‐induced immunodeficiencies

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Abstract
A chronic viral infection can occur when the host fails to mount an effective immune response to clear the virus. Mouse hepatitis virus type 3 (MHV3) appears to be an excellent model for the study of the relationship between viral‐induced immunodeficiency and chronic disease development. (C57BL/6 x A/J)F1 mice surviving acute hepatitis develop a chronic disease characterized by T‐and B‐cell immunodeficiencies, viral persistence in various organs including the brain, spleen and thymus, and death within 3 months postinfection (p.i.). We have reported that T‐ or B‐cell deficiencies, observed in MHV3 chronically infected (C57BL/6 x A/J)F1 mice, can be partially or totally thwarted by adoptive transfer of CD4+, CD8+ and/or B cells, at 15 days p.i. in mice surviving the acute phase of the disease. Adoptive transfer of syngeneic CD4+ and/or CD8+ allowed a partial restoration of the T‐cell deficiencies, as characterized by thymic atrophy, decrease in splenic T cells, and in all thymocyte subpopulations. B‐cell immunodeficiency, as defined by a decrease in splenic B cells, as well as in the bone marrow pre‐B‐ and B‐cell compartments, and the occurrence of abnormally larger forms of bone marrow pre‐B and B cells, were partially thwarted by B‐cell treatment only. Splenic B cells and the bone marrow B‐cell compartment, respectively, returned partially or totally to normal values, whereas the pre‐B‐cell compartment remained depleted in infected mice treated with B cells. Levels of all immunoglobulin classes returned to normal values in MHV3 chronically infected mice when treated with CD4+ in combination with CD8+ cells. All T‐ and/or B‐cell treatments, however, were sufficient to thwart the process of the chronic disease, and favoured the survival of mice for up to 6 months p.i.