巨细胞病毒也能很善良，可助抗流感
本帖最后由 marine0425030 于 2015-4-15 19:55 编辑人体内有成千上万种不同的病毒，很多对于人类来说都是无害的。而可能在很多时候对我们是有益的，就如很多肠道细菌一样。大家都知道，巨细胞病毒是一种常见的病毒，在美国有一半人感染，而在发展中国家的感染数几乎接近百分之百，而以前，我们对这个病毒并没有什么好感，该病毒通常呈隐性感染，多数感染者无临床症状，但在一定条件下侵袭多个器官和系统可产生严重疾病。
最近科学家发现了一个非常有趣的免疫现象，巨细胞病毒居然可以帮助年轻人提高流感病毒疫苗的反应作用。那么就跟我来看一看，科学家是如何去发现它的神奇。斯坦福大学的研究小组做了这样一系列常见却非常科学的试验。他们采集了上百健康人的血液，并用此来测量血液中季节性流感疫苗的反应。他们非常系统性的测了干扰素，白介素，细胞表型，基因表达和抗体反应等。研究结果表明老人们对疫苗反应弱于年轻人，且和巨细胞病毒是否感染无关，这点非常合乎常理。非常神奇的是，他们发现对于年轻人来说，巨细胞病毒阳性的群体居然对流感疫苗反应强于阴性的群体，也就是说接种了流感疫苗并且巨细胞病毒阳性的群体有可能可以更好的预防新一轮的季节性流感。他们又通过老鼠的体内试验得到了同样的结论。
黑格尔提出这样的哲学观点：存在即合理
这种神秘的辩证，还远远没有被我们所发现，科学之神奇就在于此。
(本文出自marine0425030，转载请注明出处 http://bbs.virology.com.cn/thread-1819-1-1.html)
论文：
Cytomegalovirus infection enhances the immune response to influenza
Cytomegalovirus (CMV) is a β-herpesvirus present in a latent form in most people worldwide. In immunosuppressed individuals, CMV can reactivate and cause serious clinical complications, but the effect of the latent state on healthy people remains elusive. We undertook a systems approach to understand the differences between seropositive and negative subjects and measured hundreds of immune system components from blood samples including cytokines and chemokines, immune cell phenotyping, gene expression, ex vivo cell responses to cytokine stimuli, and the antibody response to seasonal influenza vaccination. As expected, we found decreased responses to vaccination and an overall down-regulation of immune components in aged individuals regardless of CMV status. In contrast, CMV-seropositive young adults exhibited enhanced antibody responses to influenza vaccination, increased CD8+ T cell sensitivity, and elevated levels of circulating interferon-γ compared to seronegative individuals. Experiments with young mice infected with murine CMV also showed significant protection from an influenza virus challenge compared with uninfected animals, although this effect declined with time. These data show that CMV and its murine equivalent can have a beneficial effect on the immune response of young, healthy individuals, which may explain the ubiquity of CMV infection in humans and many other species.
原文：http://stm.sciencemag.org/content/7/281/281ra43
这个很有意思啊！ 本帖最后由 marine0425030 于 2015-4-15 20:24 编辑
rentianyixu 发表于 2015-4-15 20:02
这个很有意思啊！嗯啊，非常有趣呢。在HIV领域也有很多和这个CMV有关的文章，那个hCMV的载体就先不说了。2年前blood有篇文章说CMV特异性的CD4更不容易被HIV感染，这个也蛮有趣的。
Blood. 2013 Feb 14;121(7):1136-44. doi: 10.1182/blood-2012-07-446278. Epub 2012 Dec 20.
Distinct gene-expression profiles associated with the susceptibility of pathogen-specific CD4 T cells to HIV-1 infection.
Hu H1, Nau M, Ehrenberg P, Chenine AL, Macedo C, Zhou Y, Daye ZJ, Wei Z, Vahey M, Michael NL, Kim JH, Marovich M, Ratto-Kim S.
AbstractIn HIV infection, CD4 responses to opportunistic pathogens such as Candida albicans are lost early, but CMV-specific CD4 response persists. Little is currently known about HIV infection of CD4 T cells of different pathogen/antigen specificities. CFSE-labeled PBMCs were stimulated with CMV, tetanus toxoid (TT), and C albicans antigens and subsequently exposed to HIV. HIV infection was monitored by intracellular p24 in CFSE(low) population. We found that although TT- and C albicans-specific CD4 T cells were permissive, CMV-specific CD4 T cells were highly resistant to both R5 and X4 HIV. Quantification of HIV DNA in CFSE(low) cells showed a reduction of strong-stop and full-length DNA in CMV-specific cells compared with TT- and C albicans-specific cells. β-Chemokine neutralization enhanced HIV infection in TT- and C albicans-specific cells, whereas HIV infection in CMV-specific cells remained low despite increased entry by β-chemokine neutralization, suggesting postentry HIV restriction by CMV-specific cells. Microarray analysis (Gene Expression Omnibus accession number: GSE42853) revealed distinct transcriptional profiles that involved selective up-regulation of comprehensive innate antiviral genes in CMV-specific cells, whereas TT- and C albicans-specific cells mainly up-regulated Th17 inflammatory response. Our data suggest a mechanism for the persistence of CMV-specific CD4 response and earlier loss of mucosal Th17-associated TT- and C albicans-specific CD4 response in AIDS.
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