T cell cytokine synthesis at the single-cell level in BALB/c and C57BL/6 mice infected with ectromelia virus.

Background: The purpose of the study was to evaluate synthesis of IFN-γ, IL-2, TNF-α (Th1/Tc1) and IL-4 (Th2/Tc2) at CD4+ T and CD8+ T cell level in BALB/c and C57BL/6 mice in the course of infection with ectromelia virus Moscow strain (ECTV-MOS).

Material/methods: Synthesis of IFN-γ, IL-2, TNF-α and IL-4 in CD4+ T and CD8+ T cells in draining lymph nodes (DLNs) and spleens of BALB/c and C57BL/6 mice was detected by intracellular staining and flow cytometry analysis.

Results: Our results showed an increase in percentage of IFN-γ -synthesizing CD8+ T cells only in DLNs and spleens of C57BL/6 mice at the early stages of infection.

Beclin 1 is involved in regulation of apoptosis and autophagy during replication of ectromelia virus in permissive L929 cells.

Several reports have brought to light new and interesting findings on the involvement of autophagy and apoptosis in pathogenesis of viral and bacterial diseases, as well as presentation of foreign antigens. Our model studies focused on the involvement of apoptosis during replication of highly virulent Moscow strain of ectromelia virus (ECTV-MOS). Here, we show evidence that autophagy is induced during mousepox replication in a cell line.

Antigen presenting and effector cell cluster formation in BALB/c mice during mousepox: model studies*.

Aims: The objective of this study was to access APC-effector cell cluster formation in genetically susceptible BALB/c (H-2(d) ) mice infected with highly virulent Moscow strain of ectromelia virus (ECTV-MOS) and estimate of lymphocyte activation based upon expression of CD62L and CD44 molecules.

Methods And Results: APC-effector cell clusters were obtained by enzymatic digestion from draining lymph nodes (DLNs) and spleens of BALB/c mice. We found that APCs infected with ECTV-MOS form unstable clusters with effector cells, and thus may diminish T-cell activation at the early stage of mousepox.

Contribution of rearranged actin structures to the spread of Ectromelia virus infection in vitro.

We describe here a contribution of virus-induced actin tails and filopodia in transmission of Ectromelia virus (ECTV) infection in permissive cells detected by the immunofluorescence and confocal microscopy. Immunoblot analysis revealed profoundly decreased beta-actin levels during ECTV replicative cycle in the infected cells 24 hrs post infection (p.i.