脑视前神经元群控制疾病期间的发烧和食欲。在感染期间，动物表现出旨在提高生存率的生理和行为适应性变化。尽管存在许多感染原因，但它们会引发类似的定型症状，例如发烧、求热（寻求温暖）、食欲不振和疲劳。神经系统一直在与免疫系统“对接”，免疫系统开启了防御，助生存。本文为感染病学关联基础医学研究论文。
(Google Translate: )
Why does infection with the virus often cause fever? "Nature" study reveals the reason behind the hypothalamus to improve survival rate seeking heat
Brain preoptic neuron population controls fever and appetite during disease. During infection, animals exhibit physiological and behavioral adaptations designed to improve survival. Although there are many causes of infection, they cause similar stereotyped symptoms, such as fever, heat seeking (seeking warmth), loss of appetite, and fatigue. The nervous system has been "docking" with the immune system, which turns on defenses to help survive. This article is a basic medical research paper related to infectious diseases.
（グーグル翻訳： ）
ウイルスに感染するとしばしば発熱するのはなぜですか？ 視床下部が熱を求めて生存率を向上させる理由が「Nature」の研究で明らかに
脳の視索前ニューロン集団は、疾患中の発熱と食欲を制御します。 感染中、動物は生存を改善するように設計された生理学的および行動的適応を示します。 感染症には多くの原因がありますが、発熱、暑熱（熱を求める）、食欲不振、疲労など、似たようなステレオタイプの症状を引き起こします。 神経系は免疫系と「ドッキング」しており、生存を助けるために防御をオンにしています. この記事は、感染症に関する基礎医学研究論文です。
学术经纬
2022/06/13
论文
论文标题：A preoptic neuronal population controls fever and appetite during sickness
作者：Jessica A. Osterhout, Vikrant Kapoor, Stephen W. Eichhorn, Eric Vaughn, Jeffrey D. Moore, Ding Liu, Dean Lee, Laura A. DeNardo, Liqun Luo, Xiaowei Zhuang & Catherine Dulac
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期刊：Nature
发表时间：2022/06/08
数字识别码：10.1038/s41586-022-04793-z
摘要：During infection, animals exhibit adaptive changes in physiology and behaviour aimed at increasing survival. Although many causes of infection exist, they trigger similar stereotyped symptoms such as fever, warmth-seeking, loss of appetite and fatigue1,2. Yet exactly how the nervous system alters body temperature and triggers sickness behaviours to coordinate responses to infection remains unknown. Here we identify a previously uncharacterized population of neurons in the ventral medial preoptic area (VMPO) of the hypothalamus that are activated after sickness induced by lipopolysaccharide (LPS) or polyinosinic:polycytidylic acid. These neurons are crucial for generating a fever response and other sickness symptoms such as warmth-seeking and loss of appetite. Single-nucleus RNA-sequencing and multiplexed error-robust fluorescence in situ hybridization uncovered the identity and distribution of LPS-activated VMPO (VMPOLPS) neurons and non-neuronal cells. Gene expression and electrophysiological measurements implicate a paracrine mechanism in which the release of immune signals by non-neuronal cells during infection activates nearby VMPOLPS neurons. Finally, we show that VMPOLPS neurons exert a broad influence on the activity of brain areas associated with behavioural and homeostatic functions and are synaptically and functionally connected to circuit nodes controlling body temperature and appetite. Together, these results uncover VMPOLPS neurons as a control hub that integrates immune signals to orchestrate multiple sickness symptoms in response to infection.
