Viral infections cause a variety of symptoms and negatively impact health. Most research focuses on the localised site of infection and the “anti-viral” immune response. As a result, we have a detailed understanding of how our immune system destroys viruses. However, growing evidence suggests that viruses (and inflammation in general) also cause serious long-term effects throughout the body, including changes in the bone marrow. The bone marrow serves as the site of immune cell production and also houses cells that maintain bone structure. Regulation of the bone marrow must be delicately balanced to deal with infection, while maintaining long-term bone health. In initial studies, we assessed the impact of pneumonia virus of mice (PVM) infection on hematopoietic cell development in the bone marrow. Our findings demonstrated a rapid induction of inflammatory mediators in the lung and serum, increasing myeloid progenitors in the bone marrow. Induction of hematopoiesis was dampened through systemic administration of blocking antibodies against either TNFα or IFNγ. Intriguingly, we also noted decreases in key bone structural cell populations (including osteoblasts) following viral lung infection. Further, we could identify similar changes in other inflammatory disease models (including systemic chronic viral infection and ulcerative colitis). While bone structural cells are obviously important for the long-term maintenance of bone integrity, they also form a key part of the hematopoietic stem cell niche, regulating hematopoiesis. The regulation of these cell populations is important for the development of appropriate immune responses during acute infection and also limiting pathology in the context of chronic inflammation.
This research was funded through fellowships from the Canadian Institutes for Health Research (CIHR) and the University of Newcastle.