The prevalence of HBV, titres of HBV DNA and development of hepatocellular carcinoma are higher in males than females and involve the effects of hormones on viral and host gene expression [67, 68, 119] . Among HBV positive males, elevated concentrations of testosterone and expression of certain androgen receptor gene alleles correlate with an increased risk of hepatocellular carcinoma [120, 121] . In HBV transgenic mice, castration of males reduces, whereas replacement of testosterone in castrated males increases, serum HBsAg concentrations [122] . Chemically-induced hepatocellular carcinoma is more severe in male than female mice, which is mediated by increased inflammatory cytokine production by liver cells in males and can be reversed with oestradiol (E2) treatment [123] . Sex steroids modulate sex differences in the prevalence of HBV and development of liver cancer through effects on immune responses to HBV. Whether sex steroids affect the pathogenesis of influenza virus infection should be examined.