Feline eosinophils and neutrophils readily adhered in vitro to the sheaths of microfilariae of Brugia pahangi in the presence of suitable serum. Both cell types flattened along the surface of the parasite undergoing cytoplasmic changes which included degranulation. Adherence was dependent on properties of both the serum and the history of the microfilaria used. Two types of serum factor were found to mediate adherence. Heat labile factors were present in sera from infected and uninfected cats as well as in sera from other species. They were removed by preincubation of sera with zymosan suggesting that complement components were involved. This suggestion was supported by the demonstration of C3 on the surface of microfilariae participating in adherence reactions. A heat stable factor, present in the serum of less than 10% of infected cats, also mediated adherence. This factor was demonstrated to be IgG by immunoadsorption and immunofluorescence. The ability of the microfilariae to participate in the adherence reaction mediated by complement factor varied with maturation of the parasite. Microfilariae obtained directly from the uteri of adult worms, or produced in vitro, did not possess the ability to participate in adherence. Young blood microfilariae (i.e. taken from the blood of cats recently patent) were similar to the in vitro produced parasites; however, the majority of blood microfilariae from infections of greater than three weeks patency participated in this form of adherence. No difference between blood and uterine/in vitro microfilariae was seen in adherence reactions mediated by heat stable antibody.
One-day-old chickens were inoculated with turkey herpesvirus (HVT). Using an indirect immunofluorescence assay with a monoclonal antibody against HVT glycoprotein B (gB), we determined the course of productive HVT infection in peripheral blood mononuclear cells (PBMCs), spleen, thymus, and bursa. PBMCs were examined from days 4 through 35 postinfection (PI). The spleen, thymus, and bursa were examined from 21 through 70 days PI. Although productive infection in PBMCs was detected at 4 to 12 days PI, it ended by 14 days PI. Splenic cells expressed gB at 21, 28, 35, and 70 days PI, whereas the thymus was positive for gB expression at 21 and 35 days PI. The bursa was never positive for gB expression. At 21, 28, 35, and 70 days PI, plaque formation after co-cultivation of PBMCs with chicken embryo fibroblasts indicated the presence of HVT in infected chickens by co-cultivation assays. On the basis of indirect immunofluorescence assay, gB expression in the spleen and thymus indicates a productive HVT infection in chickens.
The interaction between host and infecting organism plays an important role in the survival of both of these components. The mechanisms whereby survival of one, or both, is achieved can be considered at various anatomical levels and degrees of complexity; those involving whole tissues together with events occurring at the cellular and subcellular levels. The involvement of sequestration, or the ‘standing apart’ of an invading organism from the host, as a mechanism of survival can also be examined at these various levels.
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