硒--降低病毒感染风险最正确的营养素

2020年伊始，“新冠肺炎”在全球爆发，感染人数极速增长，口罩等防护用品紧缺。我们个人除了日常戴好口罩，勤洗手，加强锻炼外，防止病毒传染，最重要的是，增强自身抗病毒的免疫力。

一篇"陈君石院士谈硒免疫力"的文章在朋友圈多次被提到，文中指出硒是唯一与病毒感染有直接关系的营养素，硒的抗氧化功能有可能防止或减轻SARS病毒对肺组织造成的损伤，硒能调节机体的免疫功能，从而增强人体抗病能力，适当补硒可能有助于提高对非典病人的疗效。

今天，关于硒的作用，我们将通过国外一些权威医学或研究机构的数据来分享给大家：

1、我们先来看看硒和免疫相关的研究数据：

硒在免疫组织如脾脏、淋巴结和肝脏中有大量的分布。研究发现，硒的状态会影响免疫系统对感染和癌症的应答能力，低于最适量的硒摄入可损害免疫系统的发育与功能，补充足够的硒可增强非特异性免疫功能；非特异性免疫的效应细胞包括：巨噬细胞、单核细胞和中性粒细胞，主要功能是吞噬细胞、溶解作用和杀伤感染的微生物。

文献来源：Wuryastuti, H., et al., Journal of animal science, 1993.71(9): p.2464-2472.

Carlson, B.A., trying al., The Proceedings of the Nutrition Society, 2010. 69(3): p.300-310

划重点：

硒与细胞免疫：补硒可增强细胞免疫中淋巴细胞的数量，以及单个淋巴细胞的免疫活性。

Kiremidjian等人给硒状态正常的志愿者补硒200微克／天，8周后其免疫细胞对肿瘤细胞的杀伤活性提高118%。2000年，他们中另一项临床研究中发现，头颈鳞状细胞癌患者的血硒水平明显低于健康人，并且处于三期和四期的病人血硒低于早期患者，给放射治疗的头颈鳞状细胞癌患者补充硒200微克/天，8周后和对照组患者相比，免疫细胞的应答能力增强。

文献来源：Kiremidjian-Schumacher, L., et al., 1994.41(1-2): p.115-127.

Kiremidjian-Schumacher, L., et al., 2000. 73(2): p. 97-111.

Dylewski等给雌鼠饲料喂养低硒饮食，则新生大鼠中具有免疫活性的细胞比例明显减少并且胸腺细胞对抗原刺激的反应能力也有下降。实验表明，硒缺乏小鼠的腹腔渗出液淋巴细胞杀伤一定数量的肿瘤细胞所需的淋巴细胞数量较对照组增加72%，而补硒组较对照组下降54%，说明补硒增强了单个淋巴细胞的免疫活性。

文献来源：Dylewski, M.L., A.M. Maestro, and M.F. Picciano, 2002. 82(2): p.122-7.

2、我们再来看看，国内外对硒与病毒方面的研究。

   2001年，美国北卡罗来纳大学的研究者利用H3N2流感病毒分别感染饮食中缺硒和补硒的小鼠，结果发现缺硒小鼠感染后间质性肺炎更严重，表现出更明显的病毒感染症状，这表明缺硒是增加流行性感冒发病的营养因素之一，补充适量的硒可以保护机体免受病毒感染。

(图示：缺硒小鼠和补硒小鼠感染流感病毒后的肺部病理学评分，可以看出缺硒小鼠的肺部病理学评分更高，病变更严重）

   2011年，哈尔滨医科大学相关专家的研究发现，同样剂量的流感病毒感染缺硒小鼠后，死亡率达75%，而同样剂量的流感病毒感染补硒小鼠后，死亡率大幅度降低至25%，研究者认为补硒可改善机体对流感病毒的免疫应答能力，减轻流感病毒的危害。

   2015年，哈尔滨医科大学四附院的程昱等专家，利用流感病毒感染小鼠，之后比较体内硒充足和缺硒小鼠对流感病毒的抵抗力，结果发现：缺硒组小鼠的死亡率高于正常给硒组和补充硒组（P＜0.05);缺硒组小鼠的血清硒水平明显低于正常给硒组和补充硒组（P＜0.05); 在病毒感染第5天，缺硒组小鼠的免疫相关因子TNF-α和IFN-γ含量低于正常给硒组和补充硒组（P＜0.05)。

   以上研究一致表明补硒可以增强机体对流感病毒的免疫反应，减轻感染后的疾病症状。

文献资料：

1. Beck, M.A., H. K. Nelson, et al. (2001)."Se;enigma deficiency increases the pathology of an influenza virus infection." Faseb Journal Official Publication of the Federation of American Societies for Experimental Biology 15(8): 1481-1483.

2. You, L., L. Sun, et al. (2011). "Protection from H1N1 influenza virus infections in mice by supplementation with selenium: a comparison with selenium-deficient mice." Biological Trace Element Research 141(1): 254

3. Chen Yu, Wang Songbai, et al. (2015). "Selenium's protective effect for influenza A (H1N1) infected mice." Progress in Modern Biomedicine 15(17): 3220-3222

划重点：

Beck实验室的工作进一步证明了宿主的营养状态（尤其是硒缺乏）是除肠道病毒以外很多病毒家族恶化的重要因子。

如下图所示流感病毒组硒缺乏宿主内出现快速的致病力变化。正常小鼠分别给予硒缺乏饮食和硒充足饮食4周，然后接种流感病毒H3N2，21天后硒缺乏小鼠出现严重的肺炎症状肺炎持续时间更长，免疫细胞低下，而硒充足小鼠只出现轻度肺炎症状，肺炎时间和免疫细胞水平都相对正常。

   更为重要的是，硒缺乏老鼠中的病毒出现强致病力变异，基因组发生显著变化，引起HA和NA基因发生变异。这些突变并不是随机的。相反，在硒充足动物中，只发现很少的病毒基因突变。这些证据表明宿主硒水平对病毒突变有很强的影响，硒缺乏能够促进病毒基因组快速进化。

   病毒感染会引起宿主细胞内部氧化还原状态变化，导致抗氧化系统紊乱。

   许多研究表明人类或动物营养缺乏更容易受到感染。膳食硒缺乏会导致宿主氧化应激，组氧化应激压力下，可能会引起病毒基因组发生变化，致使正常的或低毒弱毒的病毒变成强致病力的病毒。

    小编在此要重点科普下：硒是具有抗氧化防御，维持氧化还原平衡的重要微量元素。

    其主要生物活性是通过融入硒代半胱氨酸，形成一系列必须含硒蛋白的活性中心来实现的。硒缺乏是导致硒蛋白表达变化的主要因素，且与一些病毒的致病性紧密相关。一些硒蛋白如谷胱甘肽过氧化物酶和硫氧蛋白还原酶在许多模型中对病毒复制具有重要影响。

Se-The most correct nutrient for reducing the risk of virus infection

At the beginning of 2020, "COVID-19" broke out in the world, the number of infections is growing rapidly, and all the personal protective equipment like facemask is in shortage. For ourselves, except wearing facemasks, washing hands, and doing more exercise, the most important way to prevent virus infection is to boost our immunity.

Recently, an article, "Academician Mr. Chen Junshi talk about Se immunity", has been mentioned many times on Wechat, and it indicates that Se is the only nutrient which has a direct connection with virus infection. In addition, the antioxidant function of Se is probable to prevent or reduce the lung tissue injury which is caused by SARS virus. Se can regulate immune function to strengthen the human body's disease resistance, so proper Se supplementation probably can contribute to improving the efficacy of SARS patients.

Now, with regard to the effect of Se, we will share the information from some Foreign authoritative medical or research institutions:

1、Let's have a look at the relevant research data on Se and immunity.

Se is widely distributed in the immunologic tissue such as spleen, lymph gland and liver. The research finds out that the state of Se will affect the response of immunologic tissue for infection and cancer, the under appropriate amount of Se intake will damage the development and function of immunologic tissue, and enough supplementation of Se can enhance the non-specific immune function. The effector cells of non-specific immunity include macrophages, monocytes, and neutrophils, and their main functions are devouring cells, dissolution, and killing the infected microbes.

Literature sources：

Wuryastuti, H., et al., Journal of animal science, 1993.71(9): p.2464-2472.

Carlson, B.A., trying al., The Proceedings of the Nutrition Society, 2010. 69(3): p.300-310

Highlight:

Se and cellular immunity: Se supplementation can increase the number of lymphocytes in cellular immunity, and it also can increase the immunological competence of single lymphocyte.

Kiremidjian et al. supplemented Se in 200ug/day for volunteers whose Se state were normal, and after 8 weeks their immunocytes' killing activity for tumor cells increased 118%. In 2000, they had a new founding on another clinical research. The head and neck squamous cell carcinoma (HNSCC) patients' level of blood selenium was significantly lower than healthy people, and stage 3 and stage 4 paitents' level of blood selenium was lower than the early stage patients. They had supplemented Se in 200ug/day for the HNSCC patients who were under radiation therapy, and after 8 weeks, compared with the control group patients, their immunocytes' response increased. 

Literature sources：

Kiremidjian-Schumacher, L., et al., 1994.41(1-2): p.115-127.

Kiremidjian-Schumacher, L., et al., 2000. 73(2): p. 97-111.

Dylewski et al. fed female mice with low-selenium food, so the immunological competent cells' ratio of newborn mice was significantly decreased, and the thymocytes' response ability to antagonize the original stimulus was also decreasing. The experiment showed that the Se-deficient mice's peritoneal exudate needed 72% more lymphocytes to kill a certain amount of tumor cells than the control group, and the Se supplementation group needed 54% less lymphocytes than the control group. It can indicate the Se supplementation can promote the immunological competence of single lymphocyte.

Literature sources：

Dylewski, M.L., A.M. Maestro, and M.F. Picciano, 2002. 82(2): p.122-7.

2、Let's focus on the domestic and foreign researches on Se and virus.

In 2001, researchers at the University of North Carolina used the H3N2 influenza virus to inflect the Se shortage and Se supplementmice separately, and the result showed that after the infection, the Se shortage mice's interstitial pneumonia was much more serious because they had more obvious symptoms of virus infection. This experiment indicates that the shortage of Se is one of the nutritional factors to increase the onset of flu, and proper Se supplementation can protect the body from the virus infection.

(Diagram: pulmonary pathology scores of Se shortage rats and Se supplement mice after influenza virus inflection, and it shows the pulmonary pathology score of Se shortage mice is higher)

   In 2011, the research of experts from Harbin Medical University had the finding that the death rate of the Se shortage mice which had infected the same doses of the flu virus was 75%. However, the death rate of the Se supplement mice which had infected the same doses of the flu virus was dropped to 25%. So the researchers believed the Se supplementation could improve body's immune response on flu virus, and decrease the damages which were caused by the flu virus.

   In 2015, the experts from The Fourth Affiliated Hospital of Harbin Medical University used the flu virus to infected the mice, and compared the flu virus resistance on selenium-sufficient mice andselenium-deficient mice. The result showed that the selenium-deficient mice's death rate was higher than selenium-sufficient group and selenium-supplementary group (P＜0.05); selenium-deficient mice's serum selenium level was obviously lower than that of selenium-sufficient group and selenium-supplementary group (P＜0.05). On the day 5^th day of infection, the selenium-deficient mice's content of immune-related factors TNF-αand IFN-γ is also lower than the selenium-sufficient group and selenium-supplementary group (P＜0.05).

   The above researches have consistently shown that Se supplementation can increase the body's immune response on flu virus, and decrease the disease symptoms after infection. 

Literature sources:

1. Beck, M.A., H. K. Nelson, et al. (2001)."Se;enigma deficiency increases the pathology of an influenza virus infection." Faseb Journal Official Publication of the Federation of American Societies for Experimental Biology 15(8): 1481-1483.

2. You, L., L. Sun, et al. (2011). "Protection from H1N1 influenza virus infections in mice by supplementation with selenium: a comparison with selenium-deficient mice." Biological Trace Element Research 141(1): 254

3. Chen Yu, Wang Songbai, et al. (2015). "Selenium's protective effect for influenza A (H1N1) infected mice." Progress in Modern Biomedicine 15(17): 3220-3222

Highlight:

The work of Beck lab further proved that except for the enterovirus, the host's state of nutrition (especially the Se deficiency) is the main factor of many virus families' deterioration.

   As shown below, flu virus has the rapid pathogenicity change in theselenium-deficient host. Normal mice have been separately fed by theselenium-sufficient food and selenium-deficient food for 4 weeks, and they also have been inoculated the flu virus H3N2. After 21 days, the selenium-deficient mice have the serious symptoms of pneumonia, and the pneumonia has a long duration with less immunocytes. However, the selenium-sufficient mice only have mild symptoms, and the pneumonia duration and immunocytes level are relatively ordinary.

   More importantly, the virus in the selenium-deficient mice has the pathogenicity mutation, and the genome changes significantly, which causes the mutation in HA and NA genes. These mutations are not random. On the contrary, in the selenium-sufficient mice, only very few virus gene mutations can be found. The evidences can prove that the host's Se level has a great impact on the virus mutation, and the selenium deficiency can accelarate the tachytelic evolution of virus genome.

   Virus infection will cause the cell's inside redox state change of the host, and disrupt the antioxidant system.

   Many researches indicate that the nutrient-deficient humans or animals are more easily to be infected. Selenium-deficient diet will cause the host's oxidative stress, and under the oxidative stress, the virus genome is probably to change, which will make the normal or low toxic virus become strong pathogenic virus.

   The editor hereby emphasizes that Se is an important microelement which can defend the antioxidation and maintain the redox balance. It's realization of selenium's main bioactivity is the integration of selenocysteine (Sec) which can form a series of obligatory selenoprotein's active center. Se deficiency is the main factor to lead to the expression change of selenoprotein, and it is also closely related to the pathogenicity of some viruses. In many models, some selenoproteins such as the glutathione peroxidase and thioredoxin reductase have a great influence on the virus replication.

转自： 恩施市硒资源保护与开发中心