Women are at a greater risk of progressing to AIDS than men, despite having significantly less HIV RNA in circulation and host-mediated pathology is hypothesized to contribute to this sex bias [82] . Plasmacytoid dentritic cells (pDCs) are significant producers of type I interferons (IFN-α), which signal the activation of cytotoxic T cells for the elimination of virally infected cells. pDCs from women react more strongly to HIV-1 encoded toll-like receptor 7 (TLR7) ligands than pDCs derived from men, resulting in higher levels of immune cell activation [83] . Women with higher progesterone (P4) concentrations have greater numbers of activated pDCs in response to the HIV TLR7 ligand than women with lower P4 concentrations [83] . Several genes (for example, the Tlr7 gene that encodes a receptor that recognizes RNA viruses, including influenza viruses) that encode for immunological proteins are on the X chromosome and may escape X inactivation, resulting in higher amounts of expression in women [117] . X chromosomal variation also alters the course of progression of AIDS differently in women than men [84] . Whether female-biased immunopathology contributes to the severity of 2009 H1N1 disease in women requires consideration.