It has long been known that measles virus is spread between persons via the respiratory route, that is in fluid droplets in coughs and sneezes.  It was originally thought that we breathed in the virus particles which then attached to receptors on the apical surface of epithelial cells that line the alveoli of the lung. From here they were thought to spread to other cells of the body, including cells of the immune system, producing a viremia. This was followed by viral proliferation in other organs including, in addition to the lymph nodes, the spleen, kidneys, liver and skin (producing the characteristic measles rash). The virus particles then reinfect lung epithelial cells and migrate back to the alveoli to start another round of infection.  

However, models of the progress of a measles infection in animals produced a puzzling result. The lung epithelial cells which, if the above is true, should be the earliest sites of infection in the body are in fact only infected late in the course of the disease. It is immune cells in the lungs that are the primary sites of infection and it is these cells that carry the virus to the lymph nodes and other replication sites in the body. There is also another puzzle in the way measles spreads from the lungs and that is that the receptor for measles virus on lung epithelial cells, called nectin-4, is an immunoglobulin-like protein found on the basolateral surface of lung epithelial cells in the intercellular adhesion points called adherens junctions, whereas if the classical route of infection is true the receptor would have to be on the apical surface of these cells. However, nectin-4 is clearly a measles virus receptor since, when this protein is expressed in cells that are normally resistant to measles virus infection, they become infected. 

These data are now part of a new model of virus infection. It appears that the primary site of infection is lymphocytes in the alveoli. These cells are infected via another receptor called CD150 or SLAM (Signaling lymphocyte activation molecule). Because lung epithelial cells do not have CD150 and because nectin-4 is not expressed on the surface of the epithelial cells that faces the alveoli, these cells are not infected at this stage. The infected lymphocytes take the virus particles to various organs where they replicate, including to the lungs. Here, the basolateral surface of the epithelial cells, exposed to the blood stream and containing nectin-4, takes up the virus which replicates and is shed into the alveoli.

See:

Mühlebach MD, Mateo M, Sinn PL, Prüfer S, Uhlig KM, Leonard VH, Navaratnarajah CK, Frenzke M, Wong XX, Sawatsky B, Ramachandran S, McCray PB Jr, Cichutek K, von Messling V, Lopez M, Cattaneo R. Adherens junction protein nectin-4 is the epithelial receptor for measles virus. Nature. 2011 Nov 2;480 (7378):530-3 

Noyce RS, Bondre DG, Ha MN, Lin LT, Sisson G, Tsao MS, Richardson CD. Tumor cell marker PVRL4 (nectin 4) is an epithelial cell receptor for measles virus. PLoS Pathog. 2011 Aug;7(8):e1002240. Epub 2011 Aug 25.