{"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":"<p><strong>Purpose of review: </strong>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.</p><p><strong>Recent findings: </strong>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.</p><p><strong>Summary: </strong>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.</p>","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}
{"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":"<p><strong>Purpose of review: </strong>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 <i>IFITM3</i> gene and severe virus infections.</p><p><strong>Recent findings: </strong>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 <i>IFITM3</i> 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 <i>IFITM3</i> promoter has also recently been reported to be a risk allele for severe influenza virus infections.</p><p><strong>Summary: </strong>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.</p>","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}
{"title":"Chlamydia psittaci in Ocular Adnexal MALT Lymphoma: a Possible Causative Agent in the Pathogenesis of This Disease","authors":"Maximilian C. Köller, A. Aigelsreiter","doi":"10.1007/s40588-018-0108-8","DOIUrl":"https://doi.org/10.1007/s40588-018-0108-8","url":null,"abstract":"","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"701 1","pages":"261 - 267"},"PeriodicalIF":5.2,"publicationDate":"2018-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s40588-018-0108-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"52839507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Cryptococcus neoformans Titan Cell: From In Vivo Phenomenon to In Vitro Model","authors":"Xiaoping Zhou, Elizabeth R. Ballou","doi":"10.1007/s40588-018-0107-9","DOIUrl":"https://doi.org/10.1007/s40588-018-0107-9","url":null,"abstract":"","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"5 1","pages":"252 - 260"},"PeriodicalIF":5.2,"publicationDate":"2018-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s40588-018-0107-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"52839486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Adaptation of <i>Candida albicans</i> 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":"<p><strong>Purpose of review: </strong>Colonization of the gastrointestinal (GI) tract with <i>Candida albicans</i> (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.</p><p><strong>Recent findings: </strong>Recent data reveal the importance of 1) CA genetic determinants; 2) host factors; and 3) environmental factors in modulating CA GI colonization in humans.</p><p><strong>Summary: </strong>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.</p>","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}
{"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":"<p><strong>Purpose of review: </strong>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, <i>Mucor circinelloides</i> and <i>Rhizopus delemar.</i></p><p><strong>Recent findings: </strong>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.</p><p><strong>Summary: </strong>We present how these genetic methods have been applied to understand basic biology, morphogenesis, pathogenesis, and host-pathogen interactions in the two Mucoralean fungi, <i>M. circinelloides</i> and <i>R. delemar.</i> With these advances in Mucorales the opportunity to further understand the pathogenesis of these organisms is opened.</p>","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}
{"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":"<p><strong>Purpose of review: </strong>Invasive fungal infections caused by the commensal yeast <i>Candida</i> and the ubiquitous, inhaled mold <i>Aspergillus</i> 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.</p><p><strong>Recent findings: </strong>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.</p><p><strong>Summary: </strong>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.</p>","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}
{"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":"<p><strong>Purpose of review: </strong>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.</p><p><strong>Recent findings: </strong>Three IRIS animal models have been reported. They are Mycobacterial IRIS (M-IRIS), cryptococcal IRIS (C-IRIS) and <i>Pneumocystis</i>-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.</p><p><strong>Summary: </strong>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<sup>+</sup> 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.</p>","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}
C. Delaney, Ryan Kean, B. Short, M. Tumelty, W. McLean, C. Nile, G. Ramage
{"title":"Fungi at the Scene of the Crime: Innocent Bystanders or Accomplices in Oral Infections?","authors":"C. Delaney, Ryan Kean, B. Short, M. Tumelty, W. McLean, C. Nile, G. Ramage","doi":"10.1007/s40588-018-0100-3","DOIUrl":"https://doi.org/10.1007/s40588-018-0100-3","url":null,"abstract":"","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"5 1","pages":"190 - 200"},"PeriodicalIF":5.2,"publicationDate":"2018-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s40588-018-0100-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"52839466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}