Commensal colonization of C. albicans is common in humans and attenuated host immunity is a perquisite for the transition from commensal colonization to infection. Historically, it was believed that C. albicans switched from a commensal to a pathogen using distinct pathogen-associated genetic programs when the host immune status was altered. An intriguing review challenges this notion, Hube postulates that C. albicans exists in a permanent hostpathogen interplay where overgrowth and invasion is only observed under immunocompromising conditions [44] . The review puts forth two-models of a permanent infection strategy: (1) constitutive gene expression where attenuated immunity induces little or no change in the pathogenic profile of C. albicans or (2) a variable transcriptional profile where C. albicans expression is dependent on the stage-and tissue-specific interactions with the host. Our study indicates the existence of permanent hostpathogen interplay with variable gene expression over the course of infection. The serological response to the entire C. albicans cell surface protein microarray detected considerable homogeneity as well as differences in the patterns of antigens recognized among patients and healthy individuals. The majority of healthy individuals and uninfected hospital patients have moderate to strong IgG responses to many C. albicans cell surface proteins that have long been associated with virulence or hyphal-regulation (a hallmark of virulence in itself). In agreement with our protein microarray data, Naglik et al. observed similar levels of IgG titers to the hyphal wall protein Hwp1 in patients with oral candidiasis and asymptomatic mucosal infections as well as healthy culturenegative controls [23] . These serodominant cross-reactive antigens include adhesins such as Als1, Als3, Als5, Hwp1 and Int1 and hyphal-regulated genes such as Als3, Hwp1, Ece1, Hyr1, and Cdc24. Both functional groups are known to be important for invasion and virulence [45] . Among the identified serodominant antigens are many previously characterized immunogenic peptides such as Bgl2 [17] , Tkl1 [15] , Hwp1 [13, 23] , Eft2 [15] , and Cdc24 [13] . Intriguingly, the average signal intensities to the top-forty serodominant antigens are higher in the healthy individuals than the uninfected hospital patients and acute candidiasis patients (10,380 vs. 8,837 and 8,825, respectively). It is interesting to speculate whether the healthy individuals' IgG response limits colonization and overgrowth since many of the serodominant antigens are against adhesins. In particular is the strong humoral response to the integrin-like protein, Int1, which may play dual roles in limiting both intestinal colonization of the cecum and systemic invasion of deep tissue organs [46, 47] . Another interesting serodominant antibody response is to the protein Ece1, which has been shown to promote adhesion and is important for GI colonization [48] . ECE1 transcription is highly expressed during GI colonization and invasion of host tissue [33, 48] . However, one can not discount that the high IgG titer of colonized individuals may be due to a previous superficial infections such candidal vaginitis [49, 50] .