We recently reported that influenza infection is associated with drastic, depot-specific changes in white adipose tissue (WAT), notably the occurrence of thermogenic brown-like adipocytes within the subcutaneous depot, a process referred to as WAT browning. In mammals, induction of the thermogenic circuit increases heat production and consumes energy, consequently improving host’s metabolism. Importantly, we also demonstrated that mouse and human preadipocytes commit to the thermogenic differentiation program upon in vitro influenza virus infection; this signifies that infection-associated WAT browning may partly rely on a direct effect of the virus on fat. Herein, after a short review of the physiological and cellular mechanisms that have been described to regulate WAT browning, including immune-cell-dependent ones, we will comment on the role that white adipose tissue, which is at the crossroads of metabolism and immunity, may play in influenza pathophysiology.