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疱疹病毒与单纯疱疹病毒的合作导致皮肤感染的难治性病变。

The cooperation between orf virus and leads to intractable lesions in skin infection.

机构信息

College of Biological Science and Technology, Heilongjiang Bayi Agricultural University, Daqing, China.

College of Veterinary Medicine, China Agricultural University, Beijing, China.

出版信息

Front Cell Infect Microbiol. 2024 Jan 8;13:1213694. doi: 10.3389/fcimb.2023.1213694. eCollection 2023.

DOI:10.3389/fcimb.2023.1213694
PMID:38259972
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10800892/
Abstract

A large amount of evidence shows that different kinds of microorganisms can jointly cope with environmental pressures including cell hosts. For example, in many cases, it has been found that secondary or mixed infection of animals caused by ORFV (an epitheliophilic Parapoxvirus) and bacteria (such as Staphylococcus aureus or Streptococcus) shows a mutual aid mode that indirectly leads to the deterioration of the disease. However, the lack of research on the co-pathogenic mechanism, including how to hijack and destroy the cell host in the pathological microenvironment, has hindered the in-depth understanding of the pathogenic process and consequences of this complex infection and the development of clinical treatment methods. Here, we summarized the current strategies of trapping cell hosts together, based on the previously defined ORFV-Host (O-H) system. The opportunistic invasion of destroyed the delicate dynamic balance of the O-H, thus aggravating tissue damage through bacterial products (mediated by Agr), even causing sepsis or inducing cytokine storms. In fact, the virus products from its adaptive regulatory system (VARS) weaken the immune attacks and block molecular pathways, so that can settle there more smoothly, and the toxins can penetrate into local tissues more quickly. This paper focuses on the main challenges faced by cell hosts in dealing with mixed infection, which provides a starting point for us to deal with this disease in the future.

摘要

大量证据表明,不同种类的微生物可以共同应对包括细胞宿主在内的环境压力。例如,在许多情况下,已经发现动物的 ORFV(一种上皮亲嗜性痘病毒)和细菌(如金黄色葡萄球菌或链球菌)的继发或混合感染表现出一种互助模式,这种模式间接导致疾病恶化。然而,由于缺乏对共病原体机制的研究,包括如何在病理微环境中劫持和破坏细胞宿主,这阻碍了对这种复杂感染的致病过程和后果的深入了解,以及临床治疗方法的发展。在这里,我们根据先前定义的 ORFV-宿主(O-H)系统,总结了目前共同捕获细胞宿主的策略。 的机会性入侵破坏了 O-H 的微妙动态平衡,从而通过细菌产物(Agr 介导)加重组织损伤,甚至导致败血症或诱导细胞因子风暴。事实上,其适应性调节系统(VARS)的病毒产物削弱了免疫攻击并阻断了分子途径,从而使 更顺利地定植,毒素更快地渗透到局部组织中。本文重点关注细胞宿主在应对混合感染时面临的主要挑战,为我们今后应对这种疾病提供了一个起点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3700/10800892/6b9eb75661ab/fcimb-13-1213694-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3700/10800892/f3a0e588b69e/fcimb-13-1213694-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3700/10800892/6b9eb75661ab/fcimb-13-1213694-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3700/10800892/f3a0e588b69e/fcimb-13-1213694-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3700/10800892/6b9eb75661ab/fcimb-13-1213694-g002.jpg

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Laboratory Diagnosis of a NZ7-like Orf Virus Infection and Pathogen Genetic Characterization, Particularly in the Gene.
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