HIV-induced apoptosis is a contradictory complicated phenomenon that occurs at the intersection of viral persistence and host defense. HIV primarily affects CD4 T cells during an infection, causing widespread immune cell death through both direct infection and indirect (bystander) mechanisms. This immunopathologic process is caused by viral proteins such as Tat, Nef, Env, and Vpr, which modify host signaling cascades such as the PI3K/Akt, p53, NF-κB, and mitochondrial pathways. Dysregulation of pro- and anti-apoptotic mediators, particularly Bax, Bcl-2, and caspase activation, which results in mitochondrial depolarization, oxidative stress, and cytochrome c release, exacerbates immune depletion. Although apoptosis serves as a host antiviral mechanism to limit viral replication and spread, HIV exploits it to evade immune surveillance and establish chronic infection. HIV pathogenesis, which includes lymphoid tissue destruction, microbial translocation, and persistent inflammation, is significantly influenced by apoptosis of both infected and bystander cells. Furthermore, alterations in death receptor signaling (Fas/FasL and TNF pathways) and mitochondrial dysfunction highlight the delicate balance between immune defense and viral manipulation. Despite considerable progress in antiretroviral therapy, immune restoration is still incomplete due to ongoing apoptotic loss and immune exhaustion. This review examines the biological mechanisms underlying HIV-induced apoptosis, evaluates the dual role of cell death in host defense versus viral persistence, and highlights novel therapeutic targets intended to restore immune homeostasis and reduce HIV-associated immunopathology.

Background: Children living with perinatally-acquired HIV-1 (CPHIV) face significant health challenges despite advancements in antiretroviral therapy (ART). This study aimed to determine the association between unsuppressed HIV RNA viral load (VL), proinflammatory markers, sociodemographic, and clinical factors among CPHIV attending routine ART clinic at Arthur Davison Children’s Hospital (ADH), Ndola, Zambia. Methods: We conducted a cross-sectional study on 135 CPHIV, aged 2−18 years, who had been on ART for over 12 months. Sociodemographic, clinical, and laboratory data were collected using a standardized questionnaire and a data collection form. The primary outcome was unsuppressed HIV RNA VL defined as a viral load greater than 1000 copies/mL of HIV-1 RNA after at least 6 months of ART treatment. Bivariate and multivariate logistic analyses were conducted to assess associations with unsuppressed HIV viral load. Results: Overall median (Q1 - Q3) age was 15 years (12–17) and 59.3% were male. The proportion of CPHIV with unsuppressed HIV VL was 15.6% (n = 21, 95% confidence interval (CI): 9.9–22.8%). Factors associated with unsuppressed VL in multivariate logistic regression were poor adherence to ART (missing two or more doses in 2 weeks) (adjusted OR (AOR) = 14.96; 95% CI: 2.39–93.49, p = 0.004) and lower CD4 count (AOR; 0.99, 0.99–1.00, p = 0.026). Proinflammatory markers tumor necrosis factor-alpha (TNF-α) (p = 0.196) and D-dimer (p = 0.709) did not differ between the suppressed and unsuppressed CPHIV. Conclusion: One in six children with perinatally acquired HIV in Ndola, Zambia, had unsuppressed viral load, which was associated with poor ART adherence and lower CD4 counts. Proinflammatory markers, TNF-α and D-dimer, showed no significant differences between suppressed and unsuppressed groups, suggesting they may not be reliable indicators of viral control. Enhanced adherence support and further research on immune dysregulation are needed.

The Haemoglobin-to-Red Cell Distribution Width ratio (Hb/RDW) is an emerging marker of inflammation and clinical risk, but its correlates in patients with

Ischemic stroke remains a leading cause of death and disability worldwide, with blood–brain barrier (BBB) disruption playing a central role in vasogenic edema, neuroinflammation, hemorrhagic transformation, and secondary neuronal injury. The BBB is a specialized neurovascular unit composed of endothelial tight junctions, pericytes, astrocytes, and basement membrane structures that undergo coordinated molecular and cellular changes during ischemia–reperfusion injury, generating diverse biomarker signatures including endothelial dysfunction, oxidative stress, inflammatory mediators, and extracellular matrix remodeling. However, conventional biomarkers and imaging approaches fail to fully capture the dynamic and heterogeneous nature of BBB injury. Meaningful interpretation of BBB‐derived biomarkers requires mechanistic understanding of their molecular and cellular origins, making the integration of BBB pathophysiology with computational modeling essential for clinically relevant translation. Recent advances in machine learning (ML) and deep learning (DL) enable integration of neuroimaging, molecular, clinical, and multi‐omics data to characterize BBB dysfunction and improve prediction of stroke outcomes. ML‐based models have demonstrated value in identifying BBB‐related signatures associated with infarct progression, hemorrhagic transformation, and functional recovery, while deep neural networks enhance lesion segmentation and prognostic modeling. Despite this progress, challenges including data heterogeneity, limited longitudinal datasets, and model interpretability remain barriers to clinical translation. This review integrates the molecular and cellular mechanisms of BBB disruption with machine learning approaches for BBB biomarker profiling, highlighting a pathway toward biologically informed, personalized ischemic stroke management.