Pattern of infection and selective loss of Ia positive cells in suckling and adult mice inoculated with lactic dehydrogenase virus

Abstract

Lactic dehydrogenase virus (LDV) infected cells were localised in cryostat sections of infected adult and suckling mice by fluorescent antibody staining. In almost every organ except brain and spinal cord, LDV infected cells were present in interstitial connective tissue, including dermis and submucosa of gastrointestinal and urinogenital tracts. They were also present in liver sinusoids and red pulp of spleen. The tissue distribution, shape, and fluorescence staining pattern of infected cells were similar in adult and suckling mice. The reactivity with monoclonal antibody to mouse macrophages (F4/80) and to Ia antigens indicated that infected cells were Ia antigen positive macrophages, and this was confirmed in double labelling experiments. Peak numbers of LDV infected cells were seen in every organ 12-18 hours post infection (p.i.), disappearing rapidly thereafter until at 48 hours p.i. they could no longer be detected. At the same time Ia positive cells fell to undetectable levels, although macrophages were still present in reduced numbers. At 7 days p.i. the total number of macrophages in sections had returned to normal, but the number of Ia positive cells remained at low levels. Macrophages recovered from peritoneal cavity and spleen of intraperitoneally infected mice were also studied. Ia positive cells had virtually disappeared from peritoneal cavity at 24-48 hours, and from spleen at 24-72 hours. Three weeks after infection the proportion of Ia positive cells was still low when compared with that of normal mice suggesting selective loss of these cells.

Neonatal Infection of Mice With Lactate Dehydrogenase-elevating Virus Results in Suppression of Humoral Antiviral Immune Response but does not Alter the Course of Viraemia or the Polyclonal Activation of B Cells and Immune Complex Formation

“…(Porter & Porter, 1971 ;Inada & Mims, 1985;Chan et al, 1989), these findings being consistent with the cytocidal nature of LDV replication in macrophages (Plagemann & Moennig, 1992). Similarly, LDV-infected cells have been detected in sections of the spleen by in situ hybridization and by electron microscopy at 1 day p.i., but not at later times (Stueckemann et al, 1982a;Chan et al, 1989) and the same applies to the detection of LDV genomic and subgenomic mRNAs in the spleens by using Northern hybridization analysis (Contag & Plagemann, 1989;Kuo et al, 1992).…”

“…Faaberg, C. Even & P. G. W. Plagemann, unpublished). In adult mice, 5 weeks or older, 5 to 10% of peritoneal macrophages are permissive for LDV replication, whereas in mice younger than 2 weeks of age the proportion of permissive peritoneal macrophages is 60 to 80 % (Inada & Mims, 1985;Onyekaba et al, 1989b). Infection of these macrophages both in vitro and in vivo is cytocidal (Onyekaba et al, 1989b).…”

Interleukin-6 Production by Macrophages from BALB/c Mice with a Chronic Infection of Lactic Dehydrogenase Virus

“…1B, there is no difference between IL-6 activities with and without indomethacin. Most functional alterations of macrophages may be due to cyclooxygenase products after interaction between IC and Fc receptor on macrophages other than direct viral infection in chronically LDV-infected mice [4,7] , since macrophages infected with LDV were less than 10% [10]. Unexpectedly, IL-6 production by macrophages is not impaired in the chronic infection of mice, suggesting that the depressed humoral response to T cell dependent antigens seen in chronic phase of infection [17] may not be involved in the depressed IL-6 production by macrophages as reported here.…”

“…Moreover, the present results suggest that cyclooxygenase products, especially PGEs, one of the regulators of macrophage function such as Ia antigen expression [5,18], IL-1 production [4], and spreading, adhesion and migration [2], may not affect IL-6 production. In addition, though LDV infection causes suppression of autoimmune diseases [3,5,6,10,16], these phenomena may not be due to, at least in part, impaired macrophage IL-6 production, which is known as an enhancer of autoimmune diseases [1,9] . We could not eliminate the possibility that IL-6 production from other immunocompetent cells especially helper T2 cells [13] might be suppressed, since it has been suggested that defective helper T cell function was reported in chronically LDV-infected mice [11].…”

Live Lactate Dehydrogenase-elevating Virus (LDV) Induces Suppressor T Cells that Inhibit the Development of Delayed Hypersensitivity to LDV

“…LDV was donated by Dr K. E. K. Rowson and stock virus preparations were made by collecting serum from mice infected 24 h previously. The assay method has been described (Inada & Mims, 1985 a). The strain and stock virus preparation of murine cytomegalovirus (MCMV) used have also been described (Chong & Mims, 1982).…”