Herpes simplex virus type 1 pathogenicity in mice expressed by lytic infection in pre-B and B cells

The outcome of herpes simplex virus type 1 (HSV-1) infection in human or in the murine model can be influenced by host immunocompetency. We postulate in this work that HSV-1 infection alters bone marrow B lymphopoiesis in genetically determined susceptible mice. To verify this hypothesis, resistant C57BL/6 or susceptible A/J adult mice were intraperitoneally infected with HSV-1 (McIntyre strain). At various postinfection times, spleen and bone marrow were collected from both infected mouse strains. B lineage cell subpopulations were identified by double immunofluorescence assays using mAbs to terminal deoxynucleotidyl transferase (TdT), 220-kDa surface membrane glycoprotein (detected by mAb 14.8), and cytoplasmic (c mu) or surface (s mu) IgM chains. Results revealed a decrease in both percentage and absolute number of splenic B (c mu+, s mu+) cells and bone marrow pre-B (c mu+, s mu-) and B cells isolated only from susceptible A/J mice. No effect was observed on pro-B (14.8+, c mu-) or TdT+ precursor cells from both mouse strains. Intracellular viral proteins were detected in pre-B and B cells in in vivo-infected susceptible A/J mice. In vitro studies also revealed that virus-induced cell lysis occurred in purified splenic and bone marrow pre-B or B cells derived only from susceptible A/J mice. Viral tropism for pre-B and B cells represents another immunodeficiency mechanism involved in the genetic sensitivity to HSV-1.