Varicella-zoster virus reactivation and cardiovascular risk: implications for patients receiving JAK inhibitors.

Beyond its classical clinical manifestations, recent evidence shows that VZV reactivation may contribute to acute cardiovascular events.

除了其经典临床表现外，最近的证据表明VZV的再激活可能与急性心血管事件有关。

Vaccination reduces the incidenceof herpes zoster and may confer cardiovascular benefits, although causality remains unproven.

接种疫苗可以减少带状疱疹的发病率，并可能带来心血管益处，尽管因果关系尚未得到证实。

To summarise current evidence linking VZV infection to cardiovascular risk, evaluate the impact of VZV vaccination in the general and immune-mediated inflammatory disease (IMID) populations, and discuss the hypothesis that increased VZV reactivation under Janus kinase inhibitor (JAKi) therapy may partially explain the major adverse cardiovascular event (MACE) signal observed in the ORAL Surveillance trial. Epidemiologic studies show a consistent association between herpes zoster and a transient increase in MACEs.

总结当前将水痘带状疱疹病毒（VZV）感染与心血管风险相关联的证据，评估在普通人群和免疫介导炎症性疾病（IMID）人群中接种VZV疫苗的影响，并讨论在Janus激酶抑制剂（JAKi）治疗下VZV再激活增加可能部分解释在ORAL Surveillance试验中观察到的主要不良心血管事件（MACE）信号的假设。流行病学研究显示带状疱疹与MACE短暂增加之间存在一致的关联。

Mechanistic insights support VZV's ability to infect vascular tissues, induce inflammation, destabilise atherosclerotic plaques, and enhance thrombogenicity.

机制洞察支持水痘带状疱疹病毒（VZV）感染血管组织、诱导炎症、破坏动脉粥样硬化斑块和增强血栓形成的能力。

Vaccination with the recombinant zoster vaccine (RZV) effectively prevents herpes zoster and is associated with reduced MACEs in large observational cohorts, although randomised trials powered for cardiovascular endpoints are lacking.

重组带状疱疹疫苗（RZV）接种有效预防带状疱疹，并与大型观察性队列中主要心血管不良事件（MACEs）的减少相关，尽管缺乏针对心血管终点的随机试验的证据。

In IMID populations, vaccination reduces herpes zoster incidencebut has not consistently demonstrated cardiovascular benefit.

在炎症性肠病（IMID）人群中，疫苗接种减少了带状疱疹的发生率，但并未一致显示出心血管方面的益处。

JAKis, which increase VZV reactivation risk by impairing antiviral immunity, may create episodic vascular insults that contribute to the elevated MACE rates observed with tofacitinib in the ORAL Surveillance trial. VZV reactivation is a plausible and potentially preventable contributor to cardiovascular risk, particularly in older and immunosuppressed individuals.

JAK抑制剂（JAKis）因损害抗病毒免疫而增加水痘带状疱疹病毒（VZV）再激活的风险，可能造成间歇性的血管损伤，这可能是托法替尼在ORAL Surveillance试验中观察到的主要不良心血管事件（MACE）率升高的原因之一。VZV再激活是心血管风险的一个合理且可能可预防的贡献因素，特别是在老年人和免疫抑制的个体中。

While vaccination shows promise in reducing zoster-associated cardiovascular risk, definitive causal evidence remains lacking.

尽管疫苗接种显示出减少带状疱疹相关心血管风险的潜力，但缺乏明确的因果证据。

The hypothesised JAKi-VZV-vascular pathway warrants prospective evaluation.

所假设的JAKi-VZV-血管通路值得前瞻性评估。