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NK 细胞改善了持续感染鼠巨细胞病毒的小鼠对友好病毒感染的控制。

NK cells improve control of friend virus infection in mice persistently infected with murine cytomegalovirus.

机构信息

Institute for Virology of the University Hospital in Essen, University of Duisburg-Essen, Essen, Germany.

出版信息

Retrovirology. 2013 Jun 5;10:58. doi: 10.1186/1742-4690-10-58.

DOI:10.1186/1742-4690-10-58
PMID:23738889
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3744174/
Abstract

BACKGROUND

Co-infection of HIV patients with cytomegalovirus (CMV) is associated with enhanced AIDS progression and CMV end-organ diseases. On the other hand, persistent CMV infection has recently been shown to decrease tumor relapse and protect against lethal bacterial infection. The influence of persistent CMV on the outcome of an acute retroviral superinfection is still unknown.

RESULTS

Here we show that a persistent murine CMV (mCMV) infection surprisingly confers higher resistance to a primary Friend retrovirus infection (FV) of mice. Decreased FV titers and augmented FV-specific CD8 T-cell responses were found in mCMV infected mice during primary FV superinfection. NK cells produced higher amounts of IFNgamma after FV infection of persistently mCMV infected mice suggesting that these cells were involved in the 'protective' effect. Depletion of NK1.1+ cells or neutralization of IFNgamma during FV superinfection abrogated the mCMV-mediated effect.

CONCLUSION

Our data demonstrate for the first time that a persistent CMV infection induces long-lasting NK cell responses that can enhance immunity to primary retroviral infections. To our knowledge, studies investigating primary HIV infection have not analyzed the role of the CMV seropositivity in these patients. Our observations suggest that NK cells in CMV seropositive individuals might contribute to the control of primary HIV infection.

摘要

背景

艾滋病毒(HIV)患者合并巨细胞病毒(CMV)感染与艾滋病的进展和 CMV 终末器官疾病有关。另一方面,最近的研究表明,CMV 的持续感染可降低肿瘤复发率,并预防致命的细菌感染。CMV 的持续感染对急性逆转录病毒再感染的结果的影响仍不清楚。

结果

在这里,我们发现持续的鼠巨细胞病毒(mCMV)感染出人意料地赋予了小鼠对原发性 Friend 逆转录病毒感染(FV)更高的抗性。在原发性 FV 超感染期间,感染 mCMV 的小鼠中的 FV 滴度降低,FV 特异性 CD8 T 细胞反应增强。NK 细胞在感染 mCMV 的小鼠中感染 FV 后产生更高水平的 IFNγ,表明这些细胞参与了“保护”作用。在 FV 超感染期间耗尽 NK1.1+细胞或中和 IFNγ 可消除 mCMV 介导的作用。

结论

我们的数据首次证明,持续的 CMV 感染可诱导持久的 NK 细胞反应,从而增强对原发性逆转录病毒感染的免疫力。据我们所知,研究原发性 HIV 感染的研究尚未分析这些患者中 CMV 血清阳性的作用。我们的观察表明,CMV 血清阳性个体中的 NK 细胞可能有助于控制原发性 HIV 感染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fa7/3744174/dfd55b60f5d6/1742-4690-10-58-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fa7/3744174/a38055c8f3b7/1742-4690-10-58-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fa7/3744174/7a225a0e670e/1742-4690-10-58-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fa7/3744174/2ff7243c0b05/1742-4690-10-58-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fa7/3744174/dfd55b60f5d6/1742-4690-10-58-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fa7/3744174/a38055c8f3b7/1742-4690-10-58-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fa7/3744174/7a225a0e670e/1742-4690-10-58-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fa7/3744174/2ff7243c0b05/1742-4690-10-58-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fa7/3744174/dfd55b60f5d6/1742-4690-10-58-4.jpg

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