Globally,asaleadingagentofacuterespiratorytractinfectionsin children 5 years of age and the elderly, the human metapneumovirus (HMPV) has gained considerable attention. As inferred from studies comparing vaccinated and experimentally infected mice,theacquiredimmuneresponseelicitedbythispathogenfails to efficiently clear the virus from the airways, which leads to an exaggerated inflammatory response and lung damage. Furthermore, after disease resolution, there is a poor development of T and B cell immunological memory, which is believed to promote reinfectionsandviralspreadinthecommunity.Inthisarticle,we discuss the molecular mechanisms that shape the interactions of HMPVwithhosttissuesthatleadtopulmonarypathologyandto thedevelopmentofadaptiveimmunitythatfailstoprotectagainst natural infections by this virus.