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Is There such a Thing as Post-Viral Depression?: Implications for Precision Medicine

機譯:是否有病毒后抑郁癥這樣的東西?:對精準(zhǔn)醫(yī)療的影響

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摘要

Viral infections are increasingly recognized as triggers for depressive disorders, particularly following the SARS-CoV-2 pandemic and the rise of long COVID. Viruses such as Herpes Simplex Virus (HSV), Epstein-Barr Virus (EBV), Cytomegalovirus (CMV), and Human Immunodeficiency Virus (HIV) are linked to depression through complex neurobiological mechanisms. These include immune system dysregulation, chronic inflammation, and neurotransmitter imbalances that affect brain function and mood regulation. Viral activation of the immune system leads to the release of pro-inflammatory cytokines, resulting in neuroinflammation and associated depressive symptoms. Furthermore, specific viruses can disrupt neurotransmitter systems, including serotonin, dopamine, and glutamate, all of which are essential for mood stabilization. The unique interactions of different viruses with these systems underscore the need for virus-specific therapeutic approaches. Current broad-spectrum treatments often overlook the precise neurobiological pathways involved in post-viral depression, reducing their efficacy. This review emphasizes the need to understand these virus-specific interactions to create tailored interventions that directly address the neurobiological effects induced by each type of virus. These interventions may include immunomodulatory treatments that target persistent inflammation, antiviral therapies to reduce the viral load, or neuroprotective strategies that restore neurotransmitter balance. Precision medicine offers promising avenues for the effective management of virus-induced depression, providing patient-specific approaches that address the specific biological mechanisms involved. By focusing on the development of these targeted treatments, this review aims to pave the way for a new era in psychiatric care that fully addresses the root causes of depression induced by viral infections.
機譯:病毒感染越來越被認(rèn)為是抑郁癥的誘因,尤其是在 SARS-CoV-2 大流行和長期 COVID 的興起之后。單純皰疹病毒 (HSV)、EB 病毒 (EBV)、巨細(xì)胞病毒 (CMV) 和人類免疫缺陷病毒 (HIV) 等病毒通過復(fù)雜的神經(jīng)生物學(xué)機制與抑郁癥有關(guān)。這些包括影響大腦功能和情緒調(diào)節(jié)的免疫系統(tǒng)失調(diào)、慢性炎癥和神經(jīng)遞質(zhì)失衡。免疫系統(tǒng)的病毒激活導(dǎo)致促炎細(xì)胞因子的釋放,從而導(dǎo)致神經(jīng)炎癥和相關(guān)的抑郁癥狀。此外,特定病毒可以破壞神經(jīng)遞質(zhì)系統(tǒng),包括血清素、多巴胺和谷氨酸,所有這些都對穩(wěn)定情緒至關(guān)重要。不同病毒與這些系統(tǒng)的獨特相互作用強調(diào)了對病毒特異性治療方法的需求。目前的廣譜治療往往忽視了病毒后抑郁癥所涉及的精確神經(jīng)生物學(xué)途徑,從而降低了它們的療效。本綜述強調(diào)需要了解這些病毒特異性相互作用,以制定量身定制的干預(yù)措施,直接解決每種病毒誘導(dǎo)的神經(jīng)生物學(xué)影響。這些干預(yù)措施可能包括針對持續(xù)性炎癥的免疫調(diào)節(jié)治療、降低病毒載量的抗病毒治療或恢復(fù)神經(jīng)遞質(zhì)平衡的神經(jīng)保護策略。精準(zhǔn)醫(yī)學(xué)為有效管理病毒誘導(dǎo)的抑郁癥提供了有前途的途徑,為解決所涉及的特定生物學(xué)機制提供了針對患者的特定方法。通過專注于這些靶向治療的發(fā)展,本綜述旨在為精神病護理的新時代鋪平道路,以充分解決病毒感染誘發(fā)抑郁癥的根本原因。

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