Current Clinical Microbiology Reports最新文献_第10页

Molecular Pathogenesis of Middle East Respiratory Syndrome (MERS) Coronavirus. 中东呼吸综合征(MERS)冠状病毒的分子发病机制

IF 5.2

Current Clinical Microbiology Reports Pub Date : 2019-01-01 Epub Date: 2019-07-05 DOI: 10.1007/s40588-019-00122-7

Arinjay Banerjee, Kaushal Baid, Karen Mossman

{"title":"Molecular Pathogenesis of Middle East Respiratory Syndrome (MERS) Coronavirus.","authors":"Arinjay Banerjee, Kaushal Baid, Karen Mossman","doi":"10.1007/s40588-019-00122-7","DOIUrl":"10.1007/s40588-019-00122-7","url":null,"abstract":"Purpose of review: Middle East respiratory syndrome coronavirus (MERS-CoV) emerged in 2012 and is listed in the World Health Organization's blueprint of priority diseases that need immediate research. Camels are reservoirs of this virus, and the virus spills over into humans through direct contact with camels. Human-to-human transmission and travel-associated cases have been identified as well. Limited studies have characterized the molecular pathogenesis of MERS-CoV. Most studies have used ectopic expression of viral proteins to characterize MERS-CoV and its ability to modulate antiviral responses in human cells. Studies with live virus are limited, largely due to the requirement of high containment laboratories. In this review, we have summarized current studies on MERS-CoV molecular pathogenesis and have mentioned some recent strategies that are being developed to control MERS-CoV infection.Recent findings: Multiple antiviral molecules with the potential to inhibit MERS-CoV infection by disrupting virus-receptor interactions are being developed and tested. Although human vaccine candidates are still being developed, a candidate camel vaccine is being tested for efficacy. Combination of supportive treatment with interferon and antivirals is also being explored.Summary: New antiviral molecules that inhibit MERS-CoV and host cell receptor interaction may become available in the future. Additional studies are required to identify and characterize the pathogenesis of MERS-CoV EMC/2012 and other circulating strains. An effective MERS-CoV vaccine, for humans and/or camels, along with an efficient combination antiviral therapy may help us prevent future MERS cases.","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"6 3","pages":"139-147"},"PeriodicalIF":5.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s40588-019-00122-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37784719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 15

Tissue Destruction Caused by Entamoeba histolytica Parasite: Cell Death, Inflammation, Invasion, and the Gut Microbiome. 由溶组织内阿米巴原虫引起的组织破坏:细胞死亡、炎症、入侵和肠道微生物群。

IF 5.2

Current Clinical Microbiology Reports Pub Date : 2019-01-01 Epub Date: 2019-01-21 DOI: 10.1007/s40588-019-0113-6

Swagata Ghosh, Jay Padalia, Shannon Moonah

{"title":"Tissue Destruction Caused by Entamoeba histolytica Parasite: Cell Death, Inflammation, Invasion, and the Gut Microbiome.","authors":"Swagata Ghosh, Jay Padalia, Shannon Moonah","doi":"10.1007/s40588-019-0113-6","DOIUrl":"https://doi.org/10.1007/s40588-019-0113-6","url":null,"abstract":"Purpose of review: Entamoeba histolytica is a protozoan parasite that causes amebiasis, which remains a significant cause of morbidity and mortality worldwide. E. histolytica causes tissue destruction which leads to clinical disease. This review outlines some of the recent advances that have furthered our understanding of the processes that lead to the tissue damage caused by E. histolytica.Recent findings: Recent studies have identified new mechanisms involved in E. histolytica-induced tissue damage. These include (i) new form of contact-dependent killing called trogocytosis; (ii) parasite-produced cytokine, macrophage migration inhibitory factor, that contributes to inflammation; (iii) exploitation of host immune response to promote invasion; and (iv) the contribution of the gut microbiome to clinical disease.Summary: Targeting these mechanisms that result in tissue injury should be a focus of future research for the development of improved preventive and therapeutic strategies for amebiasis.","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"6 1","pages":"51-57"},"PeriodicalIF":5.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s40588-019-0113-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37174042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 41

Transcriptional and post-transcriptional regulation of viral gene expression in the gamma-herpesvirus Kaposi's sarcoma-associated herpesvirus. γ -疱疹病毒卡波西肉瘤相关疱疹病毒病毒基因表达的转录和转录后调控

IF 5.2

Current Clinical Microbiology Reports Pub Date : 2018-12-01 Epub Date: 2018-08-03 DOI: 10.1007/s40588-018-0102-1

Matthew Butnaru, Marta M Gaglia

{"title":"Transcriptional and post-transcriptional regulation of viral gene expression in the gamma-herpesvirus Kaposi's sarcoma-associated herpesvirus.","authors":"Matthew Butnaru, Marta M Gaglia","doi":"10.1007/s40588-018-0102-1","DOIUrl":"https://doi.org/10.1007/s40588-018-0102-1","url":null,"abstract":"Purpose of review: Kaposi's sarcoma-associated herpesvirus (KSHV), the etiological agent of the AIDS-associated tumor Kaposi's sarcoma, is a complex virus that expresses ~90 proteins in a regulated temporal cascade during its replication cycle. Although KSHV relies on cellular machinery for gene expression, it also uses specialized regulators to control nearly every step of the process. In this review we discuss the current understanding of KSHV gene regulation.Recent findings: High-throughput sequencing and a new robust system to mutate KSHV have paved the way for comprehensive studies of KSHV gene expression, leading to the characterization of new viral factors that control late gene expression and post-transcriptional steps of gene regulation. They have also revealed key aspects of chromatin-based control of gene expression in the latent and lytic cycle.Summary: The combination of mutant analysis and high-throughput sequencing will continue to expand our model of KSHV gene regulation and point to potential new targets for anti-KSHV drugs.","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"5 4","pages":"219-228"},"PeriodicalIF":5.2,"publicationDate":"2018-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s40588-018-0102-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37041543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Antiviral Protection by IFITM3 In Vivo. IFITM3体内抗病毒保护。

IF 5.2

Current Clinical Microbiology Reports Pub Date : 2018-12-01 Epub Date: 2018-08-03 DOI: 10.1007/s40588-018-0103-0

Ashley Zani, Jacob S Yount

{"title":"Antiviral Protection by IFITM3 In Vivo.","authors":"Ashley Zani, Jacob S Yount","doi":"10.1007/s40588-018-0103-0","DOIUrl":"10.1007/s40588-018-0103-0","url":null,"abstract":"Purpose of review: Interferon-induced transmembrane protein 3 (IFITM3) is a cellular restriction factor that blocks fusion between virus and host membranes. Here, we provide an introduction to IFITM3 and the biochemical regulation underlying its antiviral activity. Further, we analyze and summarize the published literature examining phenotypes of IFITM3 knockout mice upon infections with viral pathogens and discuss the controversial association between single nucleotide polymorphisms (SNPs) in the human IFITM3 gene and severe virus infections.Recent findings: Recent publications show that IFITM3 knockout mice experience more severe pathologies than wild-type mice in diverse virus infections, including infections with influenza A virus, West Nile virus, Chikungunya virus, Venezuelan equine encephalitis virus, respiratory syncytial virus, and cytomegalovirus. Likewise, numerous studies of humans of Chinese ancestry have associated the IFITM3 SNP rs12252-C with severe influenza virus infections, though examinations of other populations, such as Europeans, in which this SNP is rare, have largely failed to identify an association with severe infections. A second SNP, rs34481144-A, found in the human IFITM3 promoter has also recently been reported to be a risk allele for severe influenza virus infections.Summary: There is significant evidence for a protective role of IFITM3 against virus infections in both mice and humans, though additional work is required to identify the range of pathogens restricted by IFITM3 and the mechanisms by which human SNPs affect IFITM3 levels or functionality.","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"5 4","pages":"229-237"},"PeriodicalIF":5.2,"publicationDate":"2018-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6334760/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36870450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Chlamydia psittaci in Ocular Adnexal MALT Lymphoma: a Possible Causative Agent in the Pathogenesis of This Disease 眼附件MALT淋巴瘤中的鹦鹉热衣原体:一种可能的致病因子

IF 5.2

Current Clinical Microbiology Reports Pub Date : 2018-11-16 DOI: 10.1007/s40588-018-0108-8

Maximilian C. Köller, A. Aigelsreiter

引用次数: 3

The Cryptococcus neoformans Titan Cell: From In Vivo Phenomenon to In Vitro Model 新型隐球菌泰坦细胞:从体内现象到体外模型

IF 5.2

Current Clinical Microbiology Reports Pub Date : 2018-09-14 DOI: 10.1007/s40588-018-0107-9

Xiaoping Zhou, Elizabeth R. Ballou

引用次数: 30

Adaptation of Candida albicans during gastrointestinal tract colonization. 白色念珠菌在胃肠道定植过程中的适应性。

IF 5.2

Current Clinical Microbiology Reports Pub Date : 2018-09-01 Epub Date: 2018-06-16 DOI: 10.1007/s40588-018-0096-8

Animesh A Mishra, Andrew Y Koh

{"title":"Adaptation of Candida albicans during gastrointestinal tract colonization.","authors":"Animesh A Mishra, Andrew Y Koh","doi":"10.1007/s40588-018-0096-8","DOIUrl":"https://doi.org/10.1007/s40588-018-0096-8","url":null,"abstract":"Purpose of review: Colonization of the gastrointestinal (GI) tract with Candida albicans (CA), the most common human fungal pathogen, is the first step towards the development of invasive infection. Yet the fungal virulence factors and host factors that modulate CA GI colonization are still poorly understood. In this review, we will review emerging evidence of the importance of select CA genetic determinants and CA's interaction with the host that contribute to its successful adaptation as a pathobiont in the human GI tract.Recent findings: Recent data reveal the importance of 1) CA genetic determinants; 2) host factors; and 3) environmental factors in modulating CA GI colonization in humans.Summary: As evidence continues to grow supporting the notion that the GI tract and its resident microbiota are an integral part of the host immune system, it will be critical for studies to interrogate the interaction of CA with the host (including both the host innate and adaptive immune system as well as the endogenous gut microbiota) in order to dissect the mechanisms of CA pathogenesis and thus lay the foundation for novel therapeutic approaches to prevent and/or treat invasive fungal infections.","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"5 3","pages":"165-172"},"PeriodicalIF":5.2,"publicationDate":"2018-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s40588-018-0096-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36792287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 17

Genetic tools for investigating Mucorales fungal pathogenesis. 研究粘菌类真菌致病机理的遗传工具。

IF 3.1

Current Clinical Microbiology Reports Pub Date : 2018-09-01 Epub Date: 2018-06-18 DOI: 10.1007/s40588-018-0097-7

Alexis Garcia, Sandeep Vellanki, Soo Chan Lee

{"title":"Genetic tools for investigating Mucorales fungal pathogenesis.","authors":"Alexis Garcia, Sandeep Vellanki, Soo Chan Lee","doi":"10.1007/s40588-018-0097-7","DOIUrl":"10.1007/s40588-018-0097-7","url":null,"abstract":"Purpose of review: Mucormycosis is an emerging opportunistic fungal infection whose causative agents are found within the Mucorales family. A recent increase in immunocompromised cohorts with solid organ transplants, diabetes mellitus, and other medical conditions have resulted in increased fungal infections including mucormycosis. Our current knowledge about Mucoralean fungi is in its infancy compared to other fungal pathogens, which may be due to lack of robust genetic tools for Mucorales. In this review we summarize recent advances in genetic tools to study the two most prevalent and genetically amenable Mucoralean fungi, Mucor circinelloides and Rhizopus delemar.Recent findings: There have been advances made in the study of Mucorales family genetics. These findings include the construction of recyclable markers to manipulate the genome, as well as silencing vectors, and the adaptation of the CRISPR/Cas9 gene editing system.Summary: We present how these genetic methods have been applied to understand basic biology, morphogenesis, pathogenesis, and host-pathogen interactions in the two Mucoralean fungi, M. circinelloides and R. delemar. With these advances in Mucorales the opportunity to further understand the pathogenesis of these organisms is opened.","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"5 3","pages":"173-180"},"PeriodicalIF":3.1,"publicationDate":"2018-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6296817/pdf/nihms-975966.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36804314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of neutrophils in host defense against invasive fungal infections. 中性粒细胞在宿主防御侵袭性真菌感染中的作用。

IF 3.1

Current Clinical Microbiology Reports Pub Date : 2018-09-01 Epub Date: 2018-06-22 DOI: 10.1007/s40588-018-0098-6

Jigar V Desai, Michail S Lionakis

{"title":"The role of neutrophils in host defense against invasive fungal infections.","authors":"Jigar V Desai, Michail S Lionakis","doi":"10.1007/s40588-018-0098-6","DOIUrl":"10.1007/s40588-018-0098-6","url":null,"abstract":"Purpose of review: Invasive fungal infections caused by the commensal yeast Candida and the ubiquitous, inhaled mold Aspergillus have emerged as major causes of morbidity and mortality in critically ill and immunosuppressed patient populations. Here, we review how neutrophils contribute to effective immunity against these infections.Recent findings: Studies in mouse models of invasive candidiasis and aspergillosis, and observations in hematological patients with chemotherapy-induced neutropenia and in patients with primary immunodeficiency disorders that manifest with these infections have highlighted the critical role of neutrophils and have identified key immune factors that promote neutrophil-mediated effective host defense against invasive fungal disease.Summary: Neutrophils are crucial in host protection against invasive candidiasis and aspergillosis. Recent advances in our understanding of the molecular cues that mediate protective neutrophil recruitment and effector function against these infections hold promise for developing immune-based strategies to improve the outcomes of affected patients.","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"5 1","pages":"181-189"},"PeriodicalIF":3.1,"publicationDate":"2018-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6758935/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"52839440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Understanding mechanisms underlying the pathology of immune reconstitution inflammatory syndrome (IRIS) by using animal models. 利用动物模型了解免疫重建炎症综合征(IRIS)的病理机制。

IF 5.2

Current Clinical Microbiology Reports Pub Date : 2018-09-01 Epub Date: 2018-06-22 DOI: 10.1007/s40588-018-0099-5

Nupur Aggarwal, William Barclay, Mari L Shinohara

{"title":"Understanding mechanisms underlying the pathology of immune reconstitution inflammatory syndrome (IRIS) by using animal models.","authors":"Nupur Aggarwal, William Barclay, Mari L Shinohara","doi":"10.1007/s40588-018-0099-5","DOIUrl":"https://doi.org/10.1007/s40588-018-0099-5","url":null,"abstract":"Purpose of review: Despite the increasing number of clinical reports on immune reconstitution inflammatory syndrome (IRIS), mechanistic understanding of IRIS is still largely limited. The main focus of this review is to summarize animal studies, which were performed to better understand the cellular and molecular mechanisms underlying the pathology of IRIS.Recent findings: Three IRIS animal models have been reported. They are Mycobacterial IRIS (M-IRIS), cryptococcal IRIS (C-IRIS) and Pneumocystis-IRIS. M-IRIS animal model suggested that, rather than lymphopenia itself, the failure to clear the pathogen by T cells results in excessive priming of the innate immune system. If this happens before T cell reconstitution, hosts likely suffer IRIS upon T cell reconstitution. Interestingly, T cells specific to self-antigens, not only pathogen-specific, could drive IRIS as well.Summary: The mechanism to develop IRIS is quite complicated, including multiple layers of host immune responses; the innate immune system that detects pathogens and prime host immunity, and the adaptive immune system that is reconstituted but hyper-activated particularly through CD4+ T cells. Animal models of IRIS, although there are still small numbers of studies available, have already provided significant insights on the mechanistic understanding of IRIS.","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"5 3","pages":"201-209"},"PeriodicalIF":5.2,"publicationDate":"2018-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s40588-018-0099-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36776572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 10