Table 1.

Similarities and differences between IAV and SARS-CoV2 infection.

Feature	IAV	SARS-CoV2
Receptor	α 2,6 sialic acids (human) α 2,3 sialic acids (avian)	ACE2
Genome	Multisegmented RNA	Single RNA Segment
Mechanisms of Genome Variation	Reassortment Point mutation	Point mutation
Morbidity and Mortality	Bacterial Superinfection>Viral Pneumonia	Viral Pneumonia, ?Bacterial Superinfection Cytokine storm with IL-6 Thrombosis
Current Antiviral Therapy	M protein inhibitors, neuraminidase inhibitors	Remdesivir
Emerging Therapy	Favipiravir	Interferons Favipiravir
Increased Susceptibility for Older Adults	Yes (unless previously immune)	Yes
Co-morbidities Related to Severe Illness	Cardiovascular Disease, Obesity, Diabetes, COPD	Cardiovascular Disease, Obesity, Diabetes, COPD
Anti-inflammatory Therapy	None approved	Dexamethasone ? Cytokine blockers
Animal Reservoirs	Birds, Pigs	Bats, ?Felines ?Pangolins
Binding protein	HA	S protein
Binding protein glycosylation	High in seasonal, human adapted strains Low in pandemic and avian strains	High
Cell Targets	Respiratory Epithelial Cells	Respiratory Epithelial Cells, Endothelial Cells, ?others with ACE2 expression
Neutrophilic infiltration	Yes—early influx beneficial late influx maybe harmful	Yes—role not yet evaluated but may be similar
Inflammasome activation	Yes	Likely (confirmed for SARS-CoV1)
Type III IFN production	Contributes to host defense and bacterial superinfection	Contributes to host defense and bacterial superinfection
Viral proteins to block IFN action	Yes	Yes
Elevated CRP and SAA	Yes	Yes
Role of SP-D	Antiviral and anti-inflammatory (seasonal glycosylated strains inhibited)	Unknown
Role of antimicrobial peptides	Antiviral and anti-inflammatory	Unknown

? Indicates possible features of SARS-CoV infection pending further study.