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Participants were followed for 100 days; deaths were classified as early (\u226414 days) or late (15\u2013100 days). We used clustering, canonical discriminant analysis, bootstrapped correlation networks, and multivariable logistic regression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Twenty-eight participants (18.4%) died: 13 early and 15 late. Early deaths had poorer functional status, greater organ dysfunction, less frequent early antiretroviral initiation, and biochemical evidence of intense systemic inflammation and coagulopathy. Unsupervised clustering did not clearly segregate outcomes, but early deaths displayed higher innate\/chemotactic mediators and persistently dense, hyperconnected cytokine networks at baseline and day 7. Mortality was associated with higher day-7 Tumor Necrosis Factor (TNF)-\u03b1, interleukin (IL)\u20136, and Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) and lower day-7 IL-2, as well as higher baseline IL-1ra and lower baseline TNF-\u03b2 and IL-5; baseline international normalized ratio was the only biochemical predictor.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Early mortality in this Brazilian cohort was characterized by a dysregulated, hyperconnected inflammatory state consistent with sepsis-like hyperinflammation, supporting immune-informed risk stratification and carefully designed host-directed studies.<\/jats:p>\n                  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