Memorias do Instituto Oswaldo Cruz · 2026
Aedes aegypti salivary gland extract enhances Zika virus replication through immune modulation.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Hilario Gabriel, Dorneles Gilson Pires, Freitas Deise Nascimento de, Silva Onilda Santos da, Prophiro Josiane Somariva, Fazolo Tiago, Machado Rafael Rahal Guaragna, Bonorino Cristina, Oliveira Danielle Bruna Leal, Fonseca Simone Gonçalves da, Romão Pedro Roosevelt Torres, Rodrigues Luiz Carlos
Аннотация
BACKGROUND: Mosquito saliva contains bioactive molecules that modulate host immunity and may influence arboviral infection. The contribution of Aedes aegypti salivary gland extract (SGE) to viral replication and immune regulation during Zika virus (ZIKV) infection remains poorly understood.
OBJECTIVES: To investigate the immunomodulatory effects of Ae. aegypti SGE during ZIKV infection.
METHODS: Peripheral blood mononuclear cells (PBMCs) and murine antigen-presenting cell lines were exposed to ZIKV with or without SGE. Viral replication was measured by quantitative polymerase chain reaction (qPCR), cell death and immune subsets by flow cytometry, oxidative stress markers by biochemical assays, and cytokine production by enzyme-linked immunosorbent assay (ELISA).
FINDINGS: SGE enhanced ZIKV replication, particularly in PBMCs, with increased RNA copies (median Δ = +1,779), reduced late apoptosis of CD4⁺ T cells (p = 0.0055), dendritic cell death (p < 0.01), and impaired T-cell proliferation. SGE attenuated ZIKV-induced oxidative damage by restoring glutathione levels, reducing lipid and protein oxidation (p < 0.001), and increasing nitric oxide (NO) production. Cytokine profiling revealed suppression of interferon-y (IFN-γ) (p < 0.001) and induction of interleukin-4 (IL-4) (p < 0.0001), indicating a Th2-skewed response. Murine cell lines confirmed SGE-driven cytokine modulation.
MAIN CONCLUSIONS: Ae. aegypti SGE alters host immune homeostasis, favouring ZIKV infection by weakening antiviral defences and redirecting immune and redox pathways, thereby facilitating viral expansion.
OBJECTIVES: To investigate the immunomodulatory effects of Ae. aegypti SGE during ZIKV infection.
METHODS: Peripheral blood mononuclear cells (PBMCs) and murine antigen-presenting cell lines were exposed to ZIKV with or without SGE. Viral replication was measured by quantitative polymerase chain reaction (qPCR), cell death and immune subsets by flow cytometry, oxidative stress markers by biochemical assays, and cytokine production by enzyme-linked immunosorbent assay (ELISA).
FINDINGS: SGE enhanced ZIKV replication, particularly in PBMCs, with increased RNA copies (median Δ = +1,779), reduced late apoptosis of CD4⁺ T cells (p = 0.0055), dendritic cell death (p < 0.01), and impaired T-cell proliferation. SGE attenuated ZIKV-induced oxidative damage by restoring glutathione levels, reducing lipid and protein oxidation (p < 0.001), and increasing nitric oxide (NO) production. Cytokine profiling revealed suppression of interferon-y (IFN-γ) (p < 0.001) and induction of interleukin-4 (IL-4) (p < 0.0001), indicating a Th2-skewed response. Murine cell lines confirmed SGE-driven cytokine modulation.
MAIN CONCLUSIONS: Ae. aegypti SGE alters host immune homeostasis, favouring ZIKV infection by weakening antiviral defences and redirecting immune and redox pathways, thereby facilitating viral expansion.