The UN Truth Commission tasked with accounting for El Salvador’s armed conflict described it as a war in which “nobody won” (“nadie ganaba”). Between 1980 and 1992, the small Central American country was devastated by a civil war that claimed the lives of more than 70,000 and exposed its people to gross human rights violations committed, overwhelmingly, at the hands of state security forces. This project asks how the armed conflict in El Salvador existed within a broader ecosystem of right-wing state terror by examining one particularly crucial relationship: that between El Salvador and Argentina in the period immediately before the outbreak of war (1978-1980). I argue that the military regimes in El Salvador and Argentina took on a consultatory relationship during the late 1970s in which Argentina passed its “successful” model of repression onto key Salvadoran military officials. As El Salvador barreled toward war in late 1979 and early 1980, those very same Salvadoran officials came to occupy the highest positions of power, paving the way for an urban war campaign that looked eerily like Argentina’s “dirty war.” By pairing archival research conducted at the Historical Archive of the Chancellery (Archivo Histórico de la Cancillería) in Buenos Aires with existing scholarship on Argentine involvement in Central America, I trace the rise of Argentine influence in El Salvador from a few well-placed offers of aid to the minds of four of El Salvador’s top-ranking wartime officials. In doing so, I look beyond the Cold War in Latin America as a phenomenon imposed from above by the United States and instead interrogate the middle layer, in which Latin American states, driven by politics, culture, and their own will to survive, reproduced the Cold War along more local and regional lines.

Merkel cell carcinoma (MCC) is a rare and aggressive cancer of the skin with a mortality rate of ~30%. In the US, most MCC tumors arise from integration of the Merkel cell polyomavirus (MCPyV) DNA into a host chromosome, leading to expression of viral T-Antigen (T-Ag) oncoproteins that drive tumorigenesis. Though current treatment options have significantly improved MCC prognosis, new therapies are needed to address recurrent/resistant disease. While T-Ag-specific antibodies are usually detected in the blood of patients with virus-driven MCC, the role of these antibodies in tumor immunity remains unclear. Here, we analyzed blood samples from 100 MCC patients prior to definitive treatment, 51 of whom had high titers of antibodies recognizing the T-Ags. These 51 high titer samples were assessed for binding across two domains of the T-Ag. Suprisingly, we found that patients who had high titers of antibodies binding both regions of the T-Ag had worse MCC control than patients whose antibodies predominantly bound one region (median PFS 5.5 vs. 14.2 months, p=0.003). These data suggest that careful mapping of circulating antibody reactivity to different regions of T-Ag can serve as a biomarker to identify high-risk patients for which a more aggressive treatment regimen is needed. Future work is also focused on understanding the immune response resulting in differential response to T-Ag domains.