Macrophage activities contribute to many co- morbidities [8,9], including aging [28], obesity [29], diabetes [30], exposure to pollutants [31], and microbiome properties [32]. Macrophage functions alter with age, together with adaptive immune processes such as thymic involution, which deplete T lymphocyte reserves. Chronic, low grade inflammation (INFLAMMAGING) has been proposed as a predisposing factor [33]. This may result from failure of macrophages and NK cells to clear increasing accumulation of senescent cells, that enhance basal levels of inflammation and interfere with subsequent adaptive immunity upon infection [28]. Baseline inflammation may not be detrimental in itself, but can initiate an inflammatory cascade that amplifies excessive inflammation occurring in response to pathogens. Age-related metabolic correlates of macrophage dysfunction include innate lymphoid cell interactions with adipose tissue and associated macrophages, as well as inflammasome activation [34,35]. This affects thermogenesis, part of a wider metabolic syndrome involving glucose and lipid metabolism [36], elevated body mass index (BMI), type 1 and type 2 diabetes, obesity and atherosclerosis [37]. These correlate with macrophage metabolic and mitochondrial activities [38] and, possibly, ACE2 expression and hypertension, another co-morbidity [37]. ACE2, the COVID-19 entry receptor, is widely expressed on microvascular endothelium and binds the SARS-CoV2 spike glycoprotein implicated in angiotensin regulation by its competition with ACE1, and potential role as an anti-inflammatory agent [39]. Macrophages in tuberculosis and sarcoidosis express ACE1 [40], but expression of ACE2 by monocytes and tissue macrophages has not been validated [41]; evidence for productive infection of macrophages via ACE2 is incomplete [15]. Macrophages express scavenger receptors including Axl and MERTK, tyrosine kinase receptors implicated in phosphatidyl serine recognition and phagocytosis of apoptotic cells [21]; Axl is a coreceptor for ACE2+ dependent infection of other cell types by COVID-19 and other enveloped viruses via surface or endocytic routes [42], the basis for a clinical trial involving an Axl inhibitor.