Table 1.

Animal models of obesity and outcome of experimental influenza virus infection

Model	Genetics	Weight	Diet	Outcome of infection	References
Genetic leptin knockout (ob/ob)	Spontaneous recessive, homozygous Lepob nonsense mutation	45 g	Normal chow; hyperphagic due to loss of appetite control and satiety	Impaired viral clearance, increased risk of secondary infections, poor wound repair, and diminished memory responses	Campfield et al. 1995; Lutz and Woods 2012; Karlsson et al. 2017a; Meliopoulos et al. 2019
Genetic leptin receptor knockout (db/db)	Spontaneous mutant in Leprdb allele causing abnormal splicing	40 g	Normal chow; hyperphagic due to loss of leptin receptor signal transduction	Reduced viral clearance, impaired adaptive immunity, and increased lung pathology	Lutz and Woods 2012; Radigan et al. 2014
Diet-induced obesity (DIO)	Some strains more susceptible than others	35 g	High-fat, Western, or “cafeteria” diet	Mirrors genetically obese models, but generally moderate phenotypes between genetically obese and control models	Campfield et al. 1995; Smith et al. 2007; Lutz and Woods 2012; O'Brien et al. 2012; Zeeni et al. 2015
Control	Any matched genetic background	25 g	Either low-fat diet or regular chow; diet choice may alter results	Controlled viral spread and replication, reduced lung pathology, improved wound repair, and robust antigenic memory	Lutz and Woods 2012; Zeeni et al. 2015

Adapted from data in Honce and Schultz-Cherry (2019).