Longitudinal Clinical and Molecular Characterization of a Single Pediatric Case of Vertically Acquired HIV-1 Subtype C with Baseline Resistance to Protease Inhibitors.

Transmitted HIV drug resistance can compromise treatment outcomes in children with vertically acquired infection, particularly when baseline resistance testing is unavailable. This case report describes the longitudinal clinical, virological, immunological, and molecular course of a male child diagnosed with vertically acquired HIV-1 subtype C infection, most consistent with mother-to-child transmission. Clinical history, viral load, CD4/CD8 profiles, HIV-1 pol sequencing, phylogenetic analysis, and interpretation were performed using the Stanford HIV Drug Resistance Database (HIVdb). The baseline viral load was 240,993 copies/mL, with a CD4:CD8 ratio of 0.40. Genotypic analysis identified major protease inhibitor resistance mutations V82A and I84I/V, together with M184V. Stanford HIVdb predicted high-level resistance to lopinavir/ritonavir, atazanavir/ritonavir, lamivudine, and emtricitabine; low-level resistance to darunavir/ritonavir and abacavir; and preserved susceptibility to tenofovir, zidovudine, and the evaluated NNRTIs. Initial lopinavir/ritonavir-based regimens failed to achieve sustained virological suppression. Following treatment optimization with an integrase inhibitor-based regimen and subsequent transition to bictegravir/emtricitabine/tenofovir alafenamide (BIC/FTC/TAF), HIV-1 RNA became Target Not Detected (TND) from November 2024 onward. At the latest follow-up, the CD4 count was 877 cells/µL, the CD8 count was 722 cells/µL, and the CD4:CD8 ratio had improved to 1.21, indicating substantial immune recovery. This single-patient case highlights the clinical value of baseline genotypic resistance testing and individualized, genotype-guided antiretroviral therapy in achieving durable virological suppression in pediatric HIV.