Table 1.

Evidence of the influence of host features on viral infection. TNF = tumour necrosis factor; DHF = dengue hemorrhagic fever; HCV = hepatitis C virus; RSV = human respiratory syncytial virus; IAV = influenza A virus; WNV = West Nile virus; IFN = interferon; DC = dendritic cells; ACE2 = angiotensin-converting enzyme; Nab = neutralising antibody; HRV = human rhinovirus.

Feature	Virus	Effect on Host	Refs.
Host genetic susceptibility
TNF-α (−308) GG genotype IL-10 (-592/-819/-1082) CCA/ATA genotype IL-10 (-592/-819/-1082) ATA/ATG genotype	Dengue	Development of severe dengue in Sri Lankan patients. Risk factor to developing DHF. Protective factor from DHF.	[16]
G6PD gene	Dengue, coronavirus, enterovirus	Deficiency enhances viral infection.	[17,18,19]
A117V polymorphism in the NS2A	Zika	Increased virulence by reducing host innate immune responses and viral-induced apoptosis in vitro.	[20]
HLA DRB1*11	HCV	Protects from disease progression.	[21]
HLA*0405, HLA DRB1*0301, DQB1*0201	HCV	Viral persistence and chronic infection.	[22]
IFIH1	RSV	Deficient individuals unable to induce IFN-β, rendering them susceptible to infection.	[23]
Q421X	IAV	Impaired IFN-α production causes life-threatening condition.	[24]
Ageing
Axl, Mertk	WNV	Age-related upregulation of regulatory receptors facilitates viral uptake by increasing blood–brain barrier permeability.	[25]
T-cell defects	WNV	Insufficient number and quality of effector antiviral T-cells underlie age-related susceptibility to WNV.	[26]
Histone modifications	IAV	Age-associated altered histone expression decreases IFN production by myeloid DCs.	[27]
miR-181a deficiency in T-cells	WNV	Hallmark of ageing. Impairs T-cell expansion, viral clearance, and recall response.	[28]
Ethnicity
IFN	HCV	IFN effectiveness in blocking viral production significantly greater in White versus African-American patients.	[29]
ACE2	COVID-19	ACE2 (receptor for cellular entry) expression significantly higher among Asians compared to African-Americans and Caucasians.	[30]
Nab	Rubella	Individuals of African descent have significantly higher rubella-specific NAb levels than European or Hispanic individuals.	[31]
Co-morbidities
Obesity	Influenza H1N1	Decreased CD8+ T-cell activation results in inability to mount protective immune response	[32]
Asthma	IAV	Increased susceptibility to heterologous secondary influenza due to defective mucosal antibody responses.	[33]
Cancer (melanoma/RCC)		Tumour antigen-specific Th2-type polarisation of CD4+ T-cell responses in the peripheral blood of patients with RCC or melanoma.	[34]
Type 2 airway disorders (allergic asthma, allergic rhinitis, CRSwNP)	HRV16	Type 2 cytokines increase susceptibility to viral infection in airways via changing the epithelial structure and production of interferons. A Th2 bias induces a deficit in defending the mucosa against viral and bacterial infections.	[35]