Hsp-27, hsp-70 and hsp-90 expression and apoptosis in macrophages during ectromelia (mousepox) virus infection

Viruses remain one of the inducers of the stress response in the infected cells. Heat shock response induced by Moscow strain of ectromelia (mousepox) virus (ECTV-MOS) was studied in vitro in mouse monocyte cell line, RAW 264.7 and in vivo in BALB/c (H-2(d)) mice. In our studies we found that ECTV-MOS-infected RAW 264.7 cells up-regulated hsp-70 and hsp-90 expression during the phase of intensive virus replication in vitro. In spleen, lymph nodes (DLN) and liver of BALB/c mice inoculated with ECTV-MOS, virus replication was not accompanied by apoptosis of macrophages identified as CD11b(+) cells and high loads of CD11b(+)/ECTV-MOS+ cells could be detected. Intensive virus replication in the spleen and lymph nodes was accompanied with elevated expression of hsp-27, hsp-70, and hsp-90. Particularly, CD11b(+) cells showed up-regulation of hsp-27 (spleen, lymph nodes) and hsp-70 (spleen) at the peak of virus replication and up-regulation of hsp-90 during later stages of infection (15 and 20 day post infection). We conclude that during ECTV-MOS infection in vivo, hsps expressed by CD11b(+) cells may play a dual role as anti-apoptotic factors fostering virus replication and as regulators of anti-viral response.