We found that infection with influenza A virus causes a rapid increase in the number of cDCs in the lungs of mice. All cDCs originate from precursors, which, like for all other white blood cells, develop in the bone marrow and then travel via the blood as pre-cDCs to colonise all tissues. In the absence of infection, we found that steady-state colonisation and subsequent cell division leads to groups of sister cDCs forming in tissues. But, upon influenza A virus infection, the steady-state trickle of pre-cDCs into the lung gives way to large scale influx of many pre-cDCs that accumulate specifically at the lung sites where the virus is replicating. We found that part of this is driven by a chemokine receptor known as CCR2 because, when we remove CCR2 from pre-cDCs, they can still colonise the lung normally in the absence of infection but lose the ability to home to virus-containing lung sites in influenza A virus-infected mice. As a consequence, there are fewer cDCs at infection foci to be activated by the virus and to migrate to lymph nodes to transmit information about the infection to T cells. We find that this results in a diminished T cell response to the virus that is insufficient to prevent re-infection. In other words, the results from our project thus-far tell us that the generation of cDCs is elastic and responsive to demand and show that pre-cDC “backup” from bone marrow is essential to sustain an immune response against a respiratory virus.