Immunity, inflammation and disease · 2026
Expression of Purinergic and Endothelial Activation Markers in Brain Tissue From Fatal Microcephaly Associated With ZIKV.
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Sousa Jorge Rodrigues de, Batista Ferro Gustavo, Vieira Teixeira Leticia, Silva Carlos, Lima Ligia, Neto Orlando, Azevedo Raimunda, Chiang Jannifer Oliveira, Casseb Livia Medeiros Neves, Filho Arnaldo Jorge Martins, Martins Lívia Caricio, Quaresma Juarez Antônio Simões, Vasconcelos Pedro Fernando da Costa
Аннотация
BACKGROUND: Zika virus (ZIKV) is a flavivirus that has gained global attention due to its association with congenital microcephaly and neuroinflammatory responses. Markers of endothelial activation and purinergic signaling have been identified in the context of ZIKV neuropathogenesis, although the underlying mechanisms remain poorly understood.
METHODS: Brain tissue samples from fatal cases of ZIKV-induced microcephaly were analyzed using immunohistochemistry to detect endothelial activation markers (E-selectin, P-selectin, ICAM-1, and VCAM-1) and purinergic receptors (P2X4, P2X7, and P2Y2). Quantitative analysis measured the expression patterns of these molecules and assessed their contribution to neuroinflammation and blood-brain barrier disruption.
RESULTS: ZIKV-positive cases exhibited significant endothelial activation, with increased expression of adhesion molecules mediating leukocyte recruitment. Purinergic receptor upregulation suggested a role in excitotoxicity and neuroinflammatory exacerbation. Statistical analysis revealed a marked difference in marker expression between ZIKV-infected cases and controls (p < 0.0001).
CONCLUSION: The interaction between endothelial activation and purinergic signaling may be associated with the vascular dysfunction and neuronal damage observed in ZIKV-associated microcephaly. Understanding these associations could contribute to the development of targeted interventions for Zika congenital syndrome.
METHODS: Brain tissue samples from fatal cases of ZIKV-induced microcephaly were analyzed using immunohistochemistry to detect endothelial activation markers (E-selectin, P-selectin, ICAM-1, and VCAM-1) and purinergic receptors (P2X4, P2X7, and P2Y2). Quantitative analysis measured the expression patterns of these molecules and assessed their contribution to neuroinflammation and blood-brain barrier disruption.
RESULTS: ZIKV-positive cases exhibited significant endothelial activation, with increased expression of adhesion molecules mediating leukocyte recruitment. Purinergic receptor upregulation suggested a role in excitotoxicity and neuroinflammatory exacerbation. Statistical analysis revealed a marked difference in marker expression between ZIKV-infected cases and controls (p < 0.0001).
CONCLUSION: The interaction between endothelial activation and purinergic signaling may be associated with the vascular dysfunction and neuronal damage observed in ZIKV-associated microcephaly. Understanding these associations could contribute to the development of targeted interventions for Zika congenital syndrome.