SUMMARYThe lipid homeostasis pathways of bacterial pathogens have been studied comprehensively for their biochemical functionality. However, new and refined technologies have supported the interrogation of bacterial lipid and fatty acid homeostasis mechanisms in more complex environments, such as mammalian host niches. In particular, emerging findings on the breadth and depth of host fatty acid uptake have demonstrated their importance beyond merely fatty acid utilization for membrane synthesis, as they can contribute to virulence factor regulation, pathogenesis, and group-based behaviors. Lipid homeostasis is also intertwined with other metabolic and physiological processes in the bacterial cells, which appear to be largely unique per species, but overarching themes can be derived. This review combines the latest biochemical and structural findings and places these in the context of bacterial pathogenesis, thereby shedding light on the far-reaching implications of lipid homeostasis on bacterial success.
{"title":"Bacterial acquisition of host fatty acids has far-reaching implications on virulence.","authors":"Jack K Waters, Bart A Eijkelkamp","doi":"10.1128/mmbr.00126-24","DOIUrl":"https://doi.org/10.1128/mmbr.00126-24","url":null,"abstract":"<p><p>SUMMARYThe lipid homeostasis pathways of bacterial pathogens have been studied comprehensively for their biochemical functionality. However, new and refined technologies have supported the interrogation of bacterial lipid and fatty acid homeostasis mechanisms in more complex environments, such as mammalian host niches. In particular, emerging findings on the breadth and depth of host fatty acid uptake have demonstrated their importance beyond merely fatty acid utilization for membrane synthesis, as they can contribute to virulence factor regulation, pathogenesis, and group-based behaviors. Lipid homeostasis is also intertwined with other metabolic and physiological processes in the bacterial cells, which appear to be largely unique per species, but overarching themes can be derived. This review combines the latest biochemical and structural findings and places these in the context of bacterial pathogenesis, thereby shedding light on the far-reaching implications of lipid homeostasis on bacterial success.</p>","PeriodicalId":18520,"journal":{"name":"Microbiology and Molecular Biology Reviews","volume":null,"pages":null},"PeriodicalIF":8.0,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142546266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
SUMMARYHepatitis B virus (HBV) is an important human pathogen that chronically infects approximately 250 million people in the world, resulting in ~1 million deaths annually. This virus is a hepatotropic virus and can cause severe liver diseases including cirrhosis and hepatocellular carcinoma. The entry of HBV into hepatocytes is initiated by the interaction of its envelope proteins with its receptors. This is followed by the delivery of the viral nucleocapsid to the nucleus for the release of its genomic DNA and the transcription of viral RNAs. The assembly of the viral capsid particles may then take place in the nucleus or the cytoplasm and may involve cellular membranes. This is followed by the egress of the virus from infected cells. In recent years, significant research progresses had been made toward understanding the entry, the assembly, and the egress of HBV particles. In this review, we discuss the molecular pathways of these processes and compare them with those used by hepatitis delta virus and hepatitis C virus , two other hepatotropic viruses that are also enveloped. The understanding of these processes will help us to understand how HBV replicates and causes diseases, which will help to improve the treatments for HBV patients.
{"title":"Hepatitis B virus entry, assembly, and egress.","authors":"Yu-Chen Chuang, J-H James Ou","doi":"10.1128/mmbr.00014-24","DOIUrl":"https://doi.org/10.1128/mmbr.00014-24","url":null,"abstract":"<p><p>SUMMARYHepatitis B virus (HBV) is an important human pathogen that chronically infects approximately 250 million people in the world, resulting in ~1 million deaths annually. This virus is a hepatotropic virus and can cause severe liver diseases including cirrhosis and hepatocellular carcinoma. The entry of HBV into hepatocytes is initiated by the interaction of its envelope proteins with its receptors. This is followed by the delivery of the viral nucleocapsid to the nucleus for the release of its genomic DNA and the transcription of viral RNAs. The assembly of the viral capsid particles may then take place in the nucleus or the cytoplasm and may involve cellular membranes. This is followed by the egress of the virus from infected cells. In recent years, significant research progresses had been made toward understanding the entry, the assembly, and the egress of HBV particles. In this review, we discuss the molecular pathways of these processes and compare them with those used by hepatitis delta virus and hepatitis C virus , two other hepatotropic viruses that are also enveloped. The understanding of these processes will help us to understand how HBV replicates and causes diseases, which will help to improve the treatments for HBV patients.</p>","PeriodicalId":18520,"journal":{"name":"Microbiology and Molecular Biology Reviews","volume":null,"pages":null},"PeriodicalIF":8.0,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142503754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
SUMMARYUrinary tract infection (UTI) is one of the most common infections in otherwise healthy individuals. UTI is also common in healthcare settings where patients often require urinary catheters to alleviate urinary retention. The placement of a urinary catheter often leads to catheter-associated urinary tract infection (CAUTI) caused by a broad range of opportunistic pathogens, commonly referred to as ESKAPE (Enterococcus, Staphylococcus, Klebsiella, Acinetobacter, Pseudomonas, and Enterobacter) pathogens. Our understanding of CAUTI is complicated by the differences in pathogens, in initial microbial load, changes that occur due to the duration of catheterization, and the relationship between infection (colonization) and disease symptoms. To advance our understanding of CAUTI, we reviewed UTI and CAUTI caused by Pseudomonas aeruginosa which is unique in that it is not commonly found associated with human microbiomes. For this reason, the ability of P. aeruginosa to cause UTI and CAUTI requires the introduction of the bacteria to the bladder from catheterization. Once in the host, the virulence factors used by P. aeruginosa in these infections remain an area of ongoing research. In this review, we will discuss studies that focus on P. aeruginosa UTI and CAUTI to better understand the infection dynamics and outcome in clinical settings, virulence factors associated with P. aeruginosa isolated from the urinary tract, and animal studies to test which bacterial factors are required for this infection. Understanding how P. aeruginosa can cause UTI and CAUTI can provide an understanding of how these infections initiate and progress and may provide possible strategies to limit these infections.
摘要尿路感染(UTI)是健康人最常见的感染之一。尿路感染在医疗机构中也很常见,因为病人通常需要使用导尿管来缓解尿潴留。导尿管的放置通常会导致导尿管相关性尿路感染(CAUTI),由多种机会性病原体引起,这些病原体通常被称为 ESKAPE(肠球菌、葡萄球菌、克雷伯氏菌、不动杆菌、假单胞菌和肠杆菌)病原体。我们对 CAUTI 的了解因病原体、初始微生物负荷、导管插入时间的变化以及感染(定植)和疾病症状之间的关系而变得复杂。为了加深对 CAUTI 的了解,我们回顾了由铜绿假单胞菌引起的 UTI 和 CAUTI。因此,铜绿假单胞菌引起尿道炎和膀胱炎需要通过导尿将细菌引入膀胱。一旦进入宿主体内,铜绿假单胞菌在这些感染中使用的毒力因子仍是一个持续研究的领域。在本综述中,我们将讨论以铜绿假单胞菌UTI和CAUTI为重点的研究,以便更好地了解临床环境中的感染动态和结果、从泌尿道分离出的铜绿假单胞菌的相关毒力因子,以及测试这种感染需要哪些细菌因子的动物研究。了解铜绿假单胞菌如何引起UTI和CAUTI,就能了解这些感染是如何开始和发展的,并为限制这些感染提供可能的策略。
{"title":"Urinary tract infections and catheter-associated urinary tract infections caused by <i>Pseudomonas aeruginosa</i>.","authors":"Nour El Husseini, Jared A Carter, Vincent T Lee","doi":"10.1128/mmbr.00066-22","DOIUrl":"https://doi.org/10.1128/mmbr.00066-22","url":null,"abstract":"<p><p>SUMMARYUrinary tract infection (UTI) is one of the most common infections in otherwise healthy individuals. UTI is also common in healthcare settings where patients often require urinary catheters to alleviate urinary retention. The placement of a urinary catheter often leads to catheter-associated urinary tract infection (CAUTI) caused by a broad range of opportunistic pathogens, commonly referred to as ESKAPE (<i>Enterococcus</i>, <i>Staphylococcus</i>, <i>Klebsiella</i>, <i>Acinetobacter</i>, <i>Pseudomonas</i>, and <i>Enterobacter</i>) pathogens. Our understanding of CAUTI is complicated by the differences in pathogens, in initial microbial load, changes that occur due to the duration of catheterization, and the relationship between infection (colonization) and disease symptoms. To advance our understanding of CAUTI, we reviewed UTI and CAUTI caused by <i>Pseudomonas aeruginosa</i> which is unique in that it is not commonly found associated with human microbiomes. For this reason, the ability of <i>P. aeruginosa</i> to cause UTI and CAUTI requires the introduction of the bacteria to the bladder from catheterization. Once in the host, the virulence factors used by <i>P. aeruginosa</i> in these infections remain an area of ongoing research. In this review, we will discuss studies that focus on <i>P. aeruginosa</i> UTI and CAUTI to better understand the infection dynamics and outcome in clinical settings, virulence factors associated with <i>P. aeruginosa</i> isolated from the urinary tract, and animal studies to test which bacterial factors are required for this infection. Understanding how <i>P. aeruginosa</i> can cause UTI and CAUTI can provide an understanding of how these infections initiate and progress and may provide possible strategies to limit these infections.</p>","PeriodicalId":18520,"journal":{"name":"Microbiology and Molecular Biology Reviews","volume":null,"pages":null},"PeriodicalIF":8.0,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142469743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
SUMMARYMyzozoans encompass apicomplexans and dinoflagellates that manifest diverse lifestyles in highly varied environments. They show enormous propensity to employ different metabolic programs and exploit different nutrient resources and niches, and yet, they share much core biology that underlies this evolutionary success and impact. This review discusses apicomplexan parasites of medical significance and the traits and properties they share with non-pathogenic myzozoans. These include the versatility of myzozoan plastids, which scale from fully photosynthetic organelles to the site of very select key metabolic pathways. Pivotal evolutionary innovations, such as the apical complex, have allowed myzozoans to shift from predatory to parasitic and other symbiotic lifestyles multiple times in both apicomplexan and dinoflagellate branches of the myzozoan evolutionary tree. Such traits, along with shared mechanisms for nutrient acquisition, appear to underpin the prosperity of myzozoans in their varied habitats. Understanding the mechanisms of these shared traits has the potential to spawn new strategic interventions against medically and veterinary relevant parasites within this grouping.
{"title":"Adaptations and metabolic evolution of myzozoan protists across diverse lifestyles and environments.","authors":"Ross F Waller, Vern B Carruthers","doi":"10.1128/mmbr.00197-22","DOIUrl":"https://doi.org/10.1128/mmbr.00197-22","url":null,"abstract":"<p><p>SUMMARYMyzozoans encompass apicomplexans and dinoflagellates that manifest diverse lifestyles in highly varied environments. They show enormous propensity to employ different metabolic programs and exploit different nutrient resources and niches, and yet, they share much core biology that underlies this evolutionary success and impact. This review discusses apicomplexan parasites of medical significance and the traits and properties they share with non-pathogenic myzozoans. These include the versatility of myzozoan plastids, which scale from fully photosynthetic organelles to the site of very select key metabolic pathways. Pivotal evolutionary innovations, such as the apical complex, have allowed myzozoans to shift from predatory to parasitic and other symbiotic lifestyles multiple times in both apicomplexan and dinoflagellate branches of the myzozoan evolutionary tree. Such traits, along with shared mechanisms for nutrient acquisition, appear to underpin the prosperity of myzozoans in their varied habitats. Understanding the mechanisms of these shared traits has the potential to spawn new strategic interventions against medically and veterinary relevant parasites within this grouping.</p>","PeriodicalId":18520,"journal":{"name":"Microbiology and Molecular Biology Reviews","volume":null,"pages":null},"PeriodicalIF":8.0,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142469742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
SUMMARYLipopolysaccharides (LPS) are an integral part of the outer membrane of Gram-negative bacteria and play essential structural and functional roles in maintaining membrane integrity as well as in stress response and virulence. LPS comprises a membrane-anchored lipid A group, a sugar-based core region, and an O-antigen formed by repeating oligosaccharide units. 3-Deoxy-D-manno-octulosonic acid-lipid A (Kdo2-lipid A) is the minimum LPS component required for bacterial survival. While LPS modifications are not essential, they play multifaceted roles in stress response and host-pathogen interactions. Gram-negative bacteria encode several distinct LPS-modifying phosphoethanolamine transferases (PET) that add phosphoethanolamine (pEtN) to lipid A or the core region of LPS. The pet genes differ in their genomic locations, regulation mechanisms, and modification targets of the encoded enzyme, consistent with their various roles in different growth niches and under varied stress conditions. The discovery of mobile colistin resistance genes, which represent lipid A-modifying pet genes that are encoded on mobile elements and associated with resistance to the last-resort antibiotic colistin, has led to substantial interest in PETs and pEtN-modified LPS over the last decade. Here, we will review the current knowledge of the functional diversity of pEtN-based LPS modifications, including possible roles in niche-specific fitness advantages and resistance to host-produced antimicrobial peptides, and discuss how the genetic and structural diversities of PETs may impact their function. An improved understanding of the PET group will further enhance our comprehension of the stress response and virulence of Gram-negative bacteria and help contextualize host-pathogen interactions.
摘要脂多糖(LPS)是革兰氏阴性细菌外膜的一个组成部分,在维持膜完整性、应激反应和毒力方面发挥着重要的结构和功能作用。LPS 由膜锚定脂质 A 基团、糖基核心区和由重复寡糖单位形成的 O 抗原组成。3-Deoxy-D-manno-octulosonic acid-lipid A(Kdo2-lipid A)是细菌生存所需的最小 LPS 成分。虽然 LPS 修饰并非必不可少,但它们在应激反应和宿主-病原体相互作用中发挥着多方面的作用。革兰氏阴性细菌编码几种不同的 LPS 修饰磷乙醇胺转移酶(PET),可将磷乙醇胺(pEtN)添加到脂质 A 或 LPS 的核心区域。这些 PET 基因的基因组位置、调控机制和编码酶的修饰靶标各不相同,这与它们在不同生长环境和不同压力条件下的不同作用是一致的。移动可乐菌素抗性基因是在移动元件上编码的脂质 A 修饰 pet 基因,与对最后一种抗生素可乐菌素的抗性有关,该基因的发现在过去十年中引起了人们对 PET 和 pEtN 修饰 LPS 的极大兴趣。在这里,我们将回顾目前关于基于 pEtN 的 LPS 修饰功能多样性的知识,包括在特定生态位的适应优势和对宿主产生的抗菌肽的抗性方面可能发挥的作用,并讨论 PET 的遗传和结构多样性可能如何影响其功能。加深对 PET 组的了解将进一步提高我们对革兰氏阴性细菌的应激反应和毒力的理解,并有助于了解宿主与病原体之间相互作用的背景。
{"title":"The multifaceted roles of phosphoethanolamine-modified lipopolysaccharides: from stress response and virulence to cationic antimicrobial resistance.","authors":"Anna Schumann, Ahmed Gaballa, Martin Wiedmann","doi":"10.1128/mmbr.00193-23","DOIUrl":"https://doi.org/10.1128/mmbr.00193-23","url":null,"abstract":"<p><p>SUMMARYLipopolysaccharides (LPS) are an integral part of the outer membrane of Gram-negative bacteria and play essential structural and functional roles in maintaining membrane integrity as well as in stress response and virulence. LPS comprises a membrane-anchored lipid A group, a sugar-based core region, and an O-antigen formed by repeating oligosaccharide units. 3-Deoxy-D-<i>manno</i>-octulosonic acid-lipid A (Kdo<sub>2</sub>-lipid A) is the minimum LPS component required for bacterial survival. While LPS modifications are not essential, they play multifaceted roles in stress response and host-pathogen interactions. Gram-negative bacteria encode several distinct LPS-modifying phosphoethanolamine transferases (PET) that add phosphoethanolamine (pEtN) to lipid A or the core region of LPS. The <i>pet</i> genes differ in their genomic locations, regulation mechanisms, and modification targets of the encoded enzyme, consistent with their various roles in different growth niches and under varied stress conditions. The discovery of mobile colistin resistance genes, which represent lipid A-modifying <i>pet</i> genes that are encoded on mobile elements and associated with resistance to the last-resort antibiotic colistin, has led to substantial interest in PETs and pEtN-modified LPS over the last decade. Here, we will review the current knowledge of the functional diversity of pEtN-based LPS modifications, including possible roles in niche-specific fitness advantages and resistance to host-produced antimicrobial peptides, and discuss how the genetic and structural diversities of PETs may impact their function. An improved understanding of the PET group will further enhance our comprehension of the stress response and virulence of Gram-negative bacteria and help contextualize host-pathogen interactions.</p>","PeriodicalId":18520,"journal":{"name":"Microbiology and Molecular Biology Reviews","volume":null,"pages":null},"PeriodicalIF":8.0,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142391730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Katrina M Jackson, Marcus de Melo Teixeira, Bridget M Barker
SUMMARYCoccidioides immitis and Coccidioides posadasii are fungal pathogens that cause systemic mycoses and are prevalent in arid regions in the Americas. While C. immitis mainly occurs in California and Washington, C. posadasii is widely distributed across North and South America. Both species induce coccidioidomycosis (San Joaquin Valley fever or, more commonly, Valley fever), with reported cases surging in the United States, notably in California and Arizona. Moreover, cases in Argentina, Brazil, and Mexico are on the rise. Climate change and environmental alterations conducive to Coccidioides spp. proliferation have been recently explored. Diagnostic challenges contribute to delayed treatment initiation, compounded by limited therapeutic options. Although antifungal drugs are often effective treatments, some patients do not respond to current therapies, underscoring the urgent need for a vaccine, particularly for vulnerable populations over 60 years old relocating to endemic areas. Despite recent progress, gaps persist in the understanding of Coccidioides ecology, host immune responses, and vaccine development. This review synthesizes recent research advancements in Coccidioides ecology, genomics, and immune responses, emphasizing ongoing efforts to develop a human vaccine.
摘要:水霉球孢子菌(Coccidioides immitis)和柱孢球孢子菌(Coccidioides posadasii)是引起系统性真菌病的真菌病原体,在美洲干旱地区十分普遍。C. immitis 主要分布在加利福尼亚州和华盛顿州,而 C. posadasii 则广泛分布在北美洲和南美洲。这两种球孢子菌都会诱发球孢子菌病(圣华金谷热或更常见的谷热),在美国,特别是加利福尼亚州和亚利桑那州报告的病例激增。此外,阿根廷、巴西和墨西哥的病例也在增加。气候变化和环境变化有利于球孢子虫属的扩散,最近对此进行了探讨。诊断方面的挑战导致治疗启动延迟,而有限的治疗方案又使情况更加复杂。虽然抗真菌药物通常是有效的治疗方法,但有些患者对目前的疗法没有反应,这突出表明迫切需要疫苗,特别是针对迁往流行地区的 60 岁以上易感人群。尽管最近取得了进展,但人们对球孢子菌生态学、宿主免疫反应和疫苗开发的认识仍存在差距。这篇综述综述了球孢子菌生态学、基因组学和免疫反应方面的最新研究进展,并强调了正在进行的人类疫苗开发工作。
{"title":"From soil to clinic: current advances in understanding <i>Coccidioides</i> and coccidioidomycosis.","authors":"Katrina M Jackson, Marcus de Melo Teixeira, Bridget M Barker","doi":"10.1128/mmbr.00161-23","DOIUrl":"https://doi.org/10.1128/mmbr.00161-23","url":null,"abstract":"<p><p>SUMMARY<i>Coccidioides immitis</i> and <i>Coccidioides posadasii</i> are fungal pathogens that cause systemic mycoses and are prevalent in arid regions in the Americas. While <i>C. immitis</i> mainly occurs in California and Washington, <i>C. posadasii</i> is widely distributed across North and South America. Both species induce coccidioidomycosis (San Joaquin Valley fever or, more commonly, Valley fever), with reported cases surging in the United States, notably in California and Arizona. Moreover, cases in Argentina, Brazil, and Mexico are on the rise. Climate change and environmental alterations conducive to <i>Coccidioides</i> spp. proliferation have been recently explored. Diagnostic challenges contribute to delayed treatment initiation, compounded by limited therapeutic options. Although antifungal drugs are often effective treatments, some patients do not respond to current therapies, underscoring the urgent need for a vaccine, particularly for vulnerable populations over 60 years old relocating to endemic areas. Despite recent progress, gaps persist in the understanding of <i>Coccidioides</i> ecology, host immune responses, and vaccine development. This review synthesizes recent research advancements in <i>Coccidioides</i> ecology, genomics, and immune responses, emphasizing ongoing efforts to develop a human vaccine.</p>","PeriodicalId":18520,"journal":{"name":"Microbiology and Molecular Biology Reviews","volume":null,"pages":null},"PeriodicalIF":8.0,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-26Epub Date: 2024-06-24DOI: 10.1128/mmbr.00001-23
Arthur Wickenhagen, Sarah van Tol, Vincent Munster
SUMMARYSeveral examples of high-impact cross-species transmission of newly emerging or re-emerging bat-borne viruses, such as Sudan virus, Nipah virus, and severe acute respiratory syndrome coronavirus 2, have occurred in the past decades. Recent advancements in next-generation sequencing have strengthened ongoing efforts to catalog the global virome, in particular from the multitude of different bat species. However, functional characterization of these novel viruses and virus sequences is typically limited with regard to assessment of their cross-species potential. Our understanding of the intricate interplay between virus and host underlying successful cross-species transmission has focused on the basic mechanisms of entry and replication, as well as the importance of host innate immune responses. In this review, we discuss the various roles of the respective molecular mechanisms underlying cross-species transmission using different recent bat-borne viruses as examples. To delineate the crucial cellular and molecular steps underlying cross-species transmission, we propose a framework of overall characterization to improve our capacity to characterize viruses as benign, of interest, or of concern.
{"title":"Molecular determinants of cross-species transmission in emerging viral infections.","authors":"Arthur Wickenhagen, Sarah van Tol, Vincent Munster","doi":"10.1128/mmbr.00001-23","DOIUrl":"10.1128/mmbr.00001-23","url":null,"abstract":"<p><p>SUMMARYSeveral examples of high-impact cross-species transmission of newly emerging or re-emerging bat-borne viruses, such as Sudan virus, Nipah virus, and severe acute respiratory syndrome coronavirus 2, have occurred in the past decades. Recent advancements in next-generation sequencing have strengthened ongoing efforts to catalog the global virome, in particular from the multitude of different bat species. However, functional characterization of these novel viruses and virus sequences is typically limited with regard to assessment of their cross-species potential. Our understanding of the intricate interplay between virus and host underlying successful cross-species transmission has focused on the basic mechanisms of entry and replication, as well as the importance of host innate immune responses. In this review, we discuss the various roles of the respective molecular mechanisms underlying cross-species transmission using different recent bat-borne viruses as examples. To delineate the crucial cellular and molecular steps underlying cross-species transmission, we propose a framework of overall characterization to improve our capacity to characterize viruses as benign, of interest, or of concern.</p>","PeriodicalId":18520,"journal":{"name":"Microbiology and Molecular Biology Reviews","volume":null,"pages":null},"PeriodicalIF":8.0,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11426021/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141443060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-26Epub Date: 2024-07-12DOI: 10.1128/mmbr.00006-24
Alexander Ewerling, Helen Louise May-Simera
SUMMARYCilia and the nucleus were two defining features of the last eukaryotic common ancestor. In early eukaryotic evolution, these structures evolved through the diversification of a common membrane-coating ancestor, the protocoatomer. While in cilia, the descendants of this protein complex evolved into parts of the intraflagellar transport complexes and BBSome, the nucleus gained its selectivity by recruiting protocoatomer-like proteins to the nuclear envelope to form the selective nuclear pore complexes. Recent studies show a growing number of proteins shared between the proteomes of the respective organelles, and it is currently unknown how ciliary transport proteins could acquire nuclear functions and vice versa. The nuclear functions of ciliary proteins are still observable today and remain relevant for the understanding of the disease mechanisms behind ciliopathies. In this work, we review the evolutionary history of cilia and nucleus and their respective defining proteins and integrate current knowledge into theories for early eukaryotic evolution. We postulate a scenario where both compartments co-evolved and that fits current models of eukaryotic evolution, explaining how ciliary proteins and nucleoporins acquired their dual functions.
{"title":"Evolutionary trajectory for nuclear functions of ciliary transport complex proteins.","authors":"Alexander Ewerling, Helen Louise May-Simera","doi":"10.1128/mmbr.00006-24","DOIUrl":"10.1128/mmbr.00006-24","url":null,"abstract":"<p><p>SUMMARYCilia and the nucleus were two defining features of the last eukaryotic common ancestor. In early eukaryotic evolution, these structures evolved through the diversification of a common membrane-coating ancestor, the protocoatomer. While in cilia, the descendants of this protein complex evolved into parts of the intraflagellar transport complexes and BBSome, the nucleus gained its selectivity by recruiting protocoatomer-like proteins to the nuclear envelope to form the selective nuclear pore complexes. Recent studies show a growing number of proteins shared between the proteomes of the respective organelles, and it is currently unknown how ciliary transport proteins could acquire nuclear functions and <i>vice versa</i>. The nuclear functions of ciliary proteins are still observable today and remain relevant for the understanding of the disease mechanisms behind ciliopathies. In this work, we review the evolutionary history of cilia and nucleus and their respective defining proteins and integrate current knowledge into theories for early eukaryotic evolution. We postulate a scenario where both compartments co-evolved and that fits current models of eukaryotic evolution, explaining how ciliary proteins and nucleoporins acquired their dual functions.</p>","PeriodicalId":18520,"journal":{"name":"Microbiology and Molecular Biology Reviews","volume":null,"pages":null},"PeriodicalIF":8.0,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11426024/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141590737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-26Epub Date: 2024-06-12DOI: 10.1128/mmbr.00140-23
Archana Shrestha, Iman Mehdizadeh Gohari, Jihong Li, Mauricio Navarro, Francisco A Uzal, Bruce A McClane
SUMMARYIn the 2018-revised Clostridium perfringens typing classification system, isolates carrying the enterotoxin (cpe) and alpha toxin genes but no other typing toxin genes are now designated as type F. Type F isolates cause food poisoning and nonfoodborne human gastrointestinal (GI) diseases, which most commonly involve type F isolates carrying, respectivefooly, a chromosomal or plasmid-borne cpe gene. Compared to spores of other C. perfringens isolates, spores of type F chromosomal cpe isolates often exhibit greater resistance to food environment stresses, likely facilitating their survival in improperly prepared or stored foods. Multiple factors contribute to this spore resistance phenotype, including the production of a variant small acid-soluble protein-4. The pathogenicity of type F isolates involves sporulation-dependent C. perfringens enterotoxin (CPE) production. C. perfringens sporulation is initiated by orphan histidine kinases and sporulation-associated sigma factors that drive cpe transcription. CPE-induced cytotoxicity starts when CPE binds to claudin receptors to form a small complex (which also includes nonreceptor claudins). Approximately six small complexes oligomerize on the host cell plasma membrane surface to form a prepore. CPE molecules in that prepore apparently extend β-hairpin loops to form a β-barrel pore, allowing a Ca2+ influx that activates calpain. With low-dose CPE treatment, caspase-3-dependent apoptosis develops, while high-CPE dose treatment induces necroptosis. Those effects cause histologic damage along with fluid and electrolyte losses from the colon and small intestine. Sialidases likely contribute to type F disease by enhancing CPE action and, for NanI-producing nonfoodborne human GI disease isolates, increasing intestinal growth and colonization.
{"title":"The biology and pathogenicity of <i>Clostridium perfringens</i> type F: a common human enteropathogen with a new(ish) name.","authors":"Archana Shrestha, Iman Mehdizadeh Gohari, Jihong Li, Mauricio Navarro, Francisco A Uzal, Bruce A McClane","doi":"10.1128/mmbr.00140-23","DOIUrl":"10.1128/mmbr.00140-23","url":null,"abstract":"<p><p>SUMMARYIn the 2018-revised <i>Clostridium perfringens</i> typing classification system, isolates carrying the enterotoxin (<i>cpe</i>) and alpha toxin genes but no other typing toxin genes are now designated as type F. Type F isolates cause food poisoning and nonfoodborne human gastrointestinal (GI) diseases, which most commonly involve type F isolates carrying, respectivefooly, a chromosomal or plasmid-borne <i>cpe</i> gene. Compared to spores of other <i>C. perfringens</i> isolates, spores of type F chromosomal <i>cpe</i> isolates often exhibit greater resistance to food environment stresses, likely facilitating their survival in improperly prepared or stored foods. Multiple factors contribute to this spore resistance phenotype, including the production of a variant small acid-soluble protein-4. The pathogenicity of type F isolates involves sporulation-dependent <i>C. perfringens</i> enterotoxin (CPE) production. <i>C. perfringens</i> sporulation is initiated by orphan histidine kinases and sporulation-associated sigma factors that drive <i>cpe</i> transcription. CPE-induced cytotoxicity starts when CPE binds to claudin receptors to form a small complex (which also includes nonreceptor claudins). Approximately six small complexes oligomerize on the host cell plasma membrane surface to form a prepore. CPE molecules in that prepore apparently extend β-hairpin loops to form a β-barrel pore, allowing a Ca<sup>2+</sup> influx that activates calpain. With low-dose CPE treatment, caspase-3-dependent apoptosis develops, while high-CPE dose treatment induces necroptosis. Those effects cause histologic damage along with fluid and electrolyte losses from the colon and small intestine. Sialidases likely contribute to type F disease by enhancing CPE action and, for NanI-producing nonfoodborne human GI disease isolates, increasing intestinal growth and colonization.</p>","PeriodicalId":18520,"journal":{"name":"Microbiology and Molecular Biology Reviews","volume":null,"pages":null},"PeriodicalIF":8.0,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11426027/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141306279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-26Epub Date: 2024-06-20DOI: 10.1128/mmbr.00013-24
Aaron M Neiman
SUMMARYIn ascomycete fungi, sexual spores, termed ascospores, are formed after meiosis. Ascospore formation is an unusual cell division in which daughter cells are created within the cytoplasm of the mother cell by de novo generation of membranes that encapsulate each of the haploid chromosome sets created by meiosis. This review describes the molecular events underlying the creation, expansion, and closure of these membranes in the budding yeast, Saccharomyces cerevisiae. Recent advances in our understanding of the regulation of gene expression and the dynamic behavior of different membrane-bound organelles during this process are detailed. While less is known about ascospore formation in other systems, comparison to the distantly related fission yeast suggests that the molecular events will be broadly similar throughout the ascomycetes.
{"title":"Membrane and organelle rearrangement during ascospore formation in budding yeast.","authors":"Aaron M Neiman","doi":"10.1128/mmbr.00013-24","DOIUrl":"10.1128/mmbr.00013-24","url":null,"abstract":"<p><p>SUMMARYIn ascomycete fungi, sexual spores, termed ascospores, are formed after meiosis. Ascospore formation is an unusual cell division in which daughter cells are created within the cytoplasm of the mother cell by <i>de novo</i> generation of membranes that encapsulate each of the haploid chromosome sets created by meiosis. This review describes the molecular events underlying the creation, expansion, and closure of these membranes in the budding yeast, <i>Saccharomyces cerevisiae</i>. Recent advances in our understanding of the regulation of gene expression and the dynamic behavior of different membrane-bound organelles during this process are detailed. While less is known about ascospore formation in other systems, comparison to the distantly related fission yeast suggests that the molecular events will be broadly similar throughout the ascomycetes.</p>","PeriodicalId":18520,"journal":{"name":"Microbiology and Molecular Biology Reviews","volume":null,"pages":null},"PeriodicalIF":8.0,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11426023/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141427193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}