Health disparities increase with each step down the socioeconomic status (SES) ladder (Adler & Rehkopf, 2008). Adults with lower incomes, less education, and less prestigious jobs are at greater risk for chronic disease, disability, and premature mortality (Stowe et al., 2010). Although income clearly limits health care access, the connection between lower SES and poor health still exists in countries with universal health care; thus, health care access is not the sole mechanism (Cohen, Doyle, & Baum, 2006). Understanding why SES-related health disparities exist could lead to improvements in health. Maladaptive alterations in immune function are central to SES health disparities. Research addressing pathogen burden has provided some of the strongest data in this regard, with the herpesviruses playing a pivotal role (Stowe, et al., 2010). Once a person has been infected with one of the herpesviruses, they will carry the virus for the rest of their life (Glaser & Kiecolt-Glaser, 1994). Herpesviruses create persistent latent infections, in which the virus remains “dormant” in latently infected cells. Under a variety of conditions, the virus may be triggered to reactivate in those cells and replicate, thereby producing new virus particles that kill cells. Persistent infections fuel chronic inflammatory responses, which in turn are linked to a range of age-related diseases (Steptoe et al., 2007). SES researchers have focused on Epstein-Barr virus (EBV), herpes simplex virus type 1 (HSV-1), and cytomegalovirus (CMV) infections (Simanek, Dowd, & Aiello, 2009; Steptoe, et al., 2007; Stowe, et al., 2010); these herpesviruses are ubiquitous in adults. More than 90% of adults are EBV seropositive (previously infected) (Glaser & Kiecolt-Glaser, 1994), and more than 90% of individuals have antibody to HSV-1 by their forties (Nahmias & Roizman, 1973). Lower SES individuals are more likely to be infected with each of these herpesviruses earlier in life than higher SES individuals; they are also more likely to be seropositive for multiple pathogens, and to show evidence of viral reactivation (Stowe, et al., 2010). Psychological stress and depression can drive herpesvirus reactivation or replication by impairing the ability of the cellular immune system to control viral latency (Glaser & Kiecolt-Glaser, 1994). Both stress and depression are higher among those with lower incomes and less education (Adler & Rehkopf, 2008). When the cellular immune system is compromised, EBV and other herpesviruses reactivate; the increased antiviral antibody production reflects the immune system’s response to heightened herpesvirus replication (Glaser & Kiecolt-Glaser, 1994). Supportive interpersonal relationships can buffer the negative effects of stress on the cellular immune system and herpesvirus latency. For example, dementia spousal caregivers who reported lower levels of social support upon entry into a longitudinal study showed greater negative changes in immune function a year later, including increases in EBV antibody titers (Kiecolt-Glaser, Dura, Speicher, Trask, & Glaser, 1991). Lonelier medical students had higher EBV antibody titers than their fellow students who were not as lonely (Kiecolt-Glaser et al., 1984). The experience of awaiting or receiving a breast cancer diagnosis is highly stressful, and supportive interpersonal relationships can buffer this distress (Hegel et al., 2006). Indeed, one study found that the elevated distress observed before a diagnostic breast biopsy remained high after the biopsy, regardless of the diagnostic outcome (Witek-Janusek, Gabram, & Mathews, 2007). Supportive interpersonal relationships predict better adjustment among women diagnosed with breast cancer (Arora, Finney Rutten, Gustafson, Moser, & Hawkins, 2007; Burgess et al., 2005; Epplein et al., 2010). Lower SES individuals may not obtain the same stress reducing benefits from social support as higher SES individuals (Riley & Eckenrode, 1986). Lower SES people receive lower quality support from others than those who are higher SES (Belle, 1982, 1990; Krause & Borawski-Clark, 1995). Higher SES individuals are more likely to seek support in times of high stress compared to those who are lower SES (Krause, 1997). This difference is important because people benefit most from social support when they experience stress (Cohen & Wills, 1985). Accordingly, SES may moderate the link between social support and health. This study investigated how SES and social support were related to cellular immune function in a highly stressed sample of newly diagnosed breast cancer patients or those awaiting a potential breast cancer diagnosis. Specifically, we addressed the question of whether SES moderated the association between social support and EBV antibody titers. Psychological stress and depression can drive herpesvirus reactivation, and people benefit most from social support when stressed (Cohen, 2004; Cohen & Wills, 1985). Given the heightened distress surrounding an abnormal mammogram or breast cancer diagnosis, we studied these relationships in both groups. Although we did not expect differential results between those awaiting a breast cancer diagnosis or newly diagnosed with breast cancer based on related studies (Witek-Janusek, et al., 2007), we tested for these differences. As an ancillary analysis, we also assessed relationships between SES, social support, and blood pressure.