Current topics in microbiology and immunology最新文献

{"title":"Lassa Virus Genetics.","authors":"Raphaëlle Klitting,&nbsp;Samar B Mehta,&nbsp;Judith U Oguzie,&nbsp;Paul E Oluniyi,&nbsp;Matthias G Pauthner,&nbsp;Katherine J Siddle,&nbsp;Kristian G Andersen,&nbsp;Christian T Happi,&nbsp;Pardis C Sabeti","doi":"10.1007/82_2020_212","DOIUrl":"https://doi.org/10.1007/82_2020_212","url":null,"abstract":"<p><p>In a pattern repeated across a range of ecological niches, arenaviruses have evolved a compact four-gene genome to orchestrate a complex life cycle in a narrow range of susceptible hosts. A number of mammalian arenaviruses cross-infect humans, often causing a life-threatening viral hemorrhagic fever. Among this group of geographically bound zoonoses, Lassa virus has evolved a unique niche that leads to significant and sustained human morbidity and mortality. As a biosafety level 4 pathogen, direct study of the pathogenesis of Lassa virus is limited by the sparse availability, high operating costs, and technical restrictions of the high-level biocontainment laboratories required for safe experimentation. In this chapter, we introduce the relationship between genome structure and the life cycle of Lassa virus and outline reverse genetic approaches used to probe and describe functional elements of the Lassa virus genome. We then review the tools used to obtain viral genomic sequences used for phylogeny and molecular diagnostics, before shifting to a population perspective to assess the contributions of phylogenetic analysis in understanding the evolution and ecology of Lassa virus in West Africa. We finally consider the future outlook and clinical applications for genetic study of Lassa virus.</p>","PeriodicalId":11102,"journal":{"name":"Current topics in microbiology and immunology","volume":"440 ","pages":"23-65"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/82_2020_212","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9883150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Virus Evolution on Fitness Landscapes.","authors":"Peter Schuster,&nbsp;Peter F Stadler","doi":"10.1007/978-3-031-15640-3_1","DOIUrl":"https://doi.org/10.1007/978-3-031-15640-3_1","url":null,"abstract":"<p><p>The landscape paradigm is revisited in the light of evolution in simple systems. A brief overview of different classes of fitness landscapes is followed by a more detailed discussion of the RNA model, which is currently the only evolutionary model that allows for a comprehensive molecular analysis of a fitness landscape. Neutral networks of genotypes are indispensable for the success of evolution. Important insights into the evolutionary mechanism are gained by considering the topology of sequence and shape spaces. The dynamic concept of molecular quasispecies is viewed in the light of the landscape paradigm. The distribution of fitness values in state space is mirrored by the population structures of mutant distributions. Two classes of thresholds for replication error or mutations are important: (i) the-conventional-genotypic error threshold, which separates ordered replication from random drift on neutral networks, and (ii) a phenotypic error threshold above which the molecular phenotype is lost. Empirical landscapes are reviewed and finally, the implications of the landscape concept for virus evolution are discussed.</p>","PeriodicalId":11102,"journal":{"name":"Current topics in microbiology and immunology","volume":"439 ","pages":"1-94"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10474579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex and Gender Differences in Tuberculosis Pathogenesis and Treatment Outcomes.","authors":"Djeneba Dabitao,&nbsp;William R Bishai","doi":"10.1007/978-3-031-35139-6_6","DOIUrl":"10.1007/978-3-031-35139-6_6","url":null,"abstract":"<p><p>Tuberculosis remains a daunting public health concern in many countries of the world. A consistent observation in the global epidemiology of tuberculosis is an excess of cases of active pulmonary tuberculosis among males compared with females. Data from both humans and animals also suggest that males are more susceptible than females to develop active pulmonary disease. Similarly, male sex has been associated with poor treatment outcomes. Despite this growing body of evidence, little is known about the mechanisms driving sex bias in tuberculosis disease. Two dominant hypotheses have been proposed to explain the predominance of active pulmonary tuberculosis among males. The first is based on the contribution of biological factors, such as sex hormones and genetic factors, on host immunity during tuberculosis. The second is focused on non-biological factors such as smoking, professional exposure, and health-seeking behaviors, known to be influenced by gender. In this chapter, we review the literature regarding these two prevailing hypotheses by presenting human but also experimental animal studies. In addition, we presented studies aiming at examining the impact of sex and gender on other clinical forms of tuberculosis such as latent tuberculosis infection and extrapulmonary tuberculosis, which both appear to have their own specificities in relation to sex. We also highlighted potential intersections between sex and gender in the context of tuberculosis and shared future directions that could guide in elucidating mechanisms of sex-based differences in tuberculosis pathogenesis and treatment outcomes.</p>","PeriodicalId":11102,"journal":{"name":"Current topics in microbiology and immunology","volume":"441 ","pages":"139-183"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10211562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Sex-Differential and Non-specific Effects of Vaccines Over the Life Course.","authors":"Laura A St Clair, Sabal Chaulagain, Sabra L Klein, Christine Stabell Benn, Katie L Flanagan","doi":"10.1007/978-3-031-35139-6_11","DOIUrl":"10.1007/978-3-031-35139-6_11","url":null,"abstract":"","PeriodicalId":11102,"journal":{"name":"Current topics in microbiology and immunology","volume":"441 ","pages":"C1"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11000772/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41129615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Helicobacter pylori-Induced Host Cell DNA Damage and Genetics of Gastric Cancer Development.","authors":"Steffen Backert, Bodo Linz, Nicole Tegtmeyer","doi":"10.1007/978-3-031-47331-9_7","DOIUrl":"10.1007/978-3-031-47331-9_7","url":null,"abstract":"<p><p>Gastric cancer is a very serious and deadly disease worldwide with about one million new cases every year. Most gastric cancer subtypes are associated with genetic and epigenetic aberrations caused by chromosome instability, microsatellite instability or Epstein-Barr virus infection. Another risk factor is an infection with Helicobacter pylori, which also triggers severe alterations in the host genome. This pathogen expresses an extraordinary repertoire of virulence determinants that take over control of important host cell signaling functions. In fact, H. pylori is a paradigm of persistent infection, chronic inflammation and cellular destruction. In particular, H. pylori profoundly induces chromosomal DNA damage by introducing double-strand breaks (DSBs) followed by genomic instability. DSBs appear in response to oxidative stress and pro-inflammatory transcription during the S-phase of the epithelial cell cycle, which mainly depends on the presence of the bacterial cag pathogenicity island (cagPAI)-encoded type IV secretion system (T4SS). This scenario is closely connected with the T4SS-mediated injection of ADP-glycero-β-D-manno-heptose (ADP-heptose) and oncoprotein CagA. While ADP-heptose links transcription factor NF-κB-induced innate immune signaling with RNA-loop-mediated DNA replication stress and introduction of DSBs, intracellular CagA targets the tumor suppressor BRCA1. The latter scenario promotes BRCAness, a disease characterized by the deficiency of effective DSB repair. In addition, genetic studies of patients demonstrated the presence of gastric cancer-associated single nucleotide polymorphisms (SNPs) in immune-regulatory and other genes as well as specific pathogenic germline variants in several crucial genes involved in homologous recombination and DNA repair, all of which are connected to H. pylori infection. Here we review the molecular mechanisms leading to chromosomal DNA damage and specific genetic aberrations in the presence or absence of H. pylori infection, and discuss their importance in gastric carcinogenesis.</p>","PeriodicalId":11102,"journal":{"name":"Current topics in microbiology and immunology","volume":"444 ","pages":"185-206"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139477654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Pathogenesis, Molecular Mechanisms of Gastric Cancer Development.","authors":"Lydia E Wroblewski, Richard M Peek","doi":"10.1007/978-3-031-47331-9_2","DOIUrl":"10.1007/978-3-031-47331-9_2","url":null,"abstract":"<p><p>The human pathogen Helicobacter pylori is the strongest known risk factor for gastric disease and cancer, and gastric cancer remains a leading cause of cancer-related death across the globe. Carcinogenic mechanisms associated with H. pylori are multifactorial and are driven by bacterial virulence constituents, host immune responses, environmental factors such as iron and salt, and the microbiota. Infection with strains that harbor the cytotoxin-associated genes (cag) pathogenicity island, which encodes a type IV secretion system (T4SS) confer increased risk for developing more severe gastric diseases. Other important H. pylori virulence factors that augment disease progression include vacuolating cytotoxin A (VacA), specifically type s1m1 vacA alleles, serine protease HtrA, and the outer-membrane adhesins HopQ, BabA, SabA and OipA. Additional risk factors for gastric cancer include dietary factors such as diets that are high in salt or low in iron, H. pylori-induced perturbations of the gastric microbiome, host genetic polymorphisms, and infection with Epstein-Barr virus. This chapter discusses in detail host factors and how H. pylori virulence factors augment the risk of developing gastric cancer in human patients as well as how the Mongolian gerbil model has been used to define mechanisms of H. pylori-induced inflammation and cancer.</p>","PeriodicalId":11102,"journal":{"name":"Current topics in microbiology and immunology","volume":"444 ","pages":"25-52"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10924282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139477471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex Differences in HIV Infection.","authors":"Marcus Altfeld,&nbsp;Eileen P Scully","doi":"10.1007/978-3-031-35139-6_3","DOIUrl":"10.1007/978-3-031-35139-6_3","url":null,"abstract":"<p><p>Biological sex has wide-ranging impacts on HIV infection spanning differences in acquisition risk, the pathogenesis of untreated infection, impact of chronic treated disease and prospects for HIV eradication or functional cure. This chapter summarizes the scope of these differences and discusses several features of the immune response thought to contribute to the clinical outcomes.</p>","PeriodicalId":11102,"journal":{"name":"Current topics in microbiology and immunology","volume":"441 ","pages":"61-73"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10202939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetics of Sex Differences in Immunity.","authors":"Shani T Gal-Oz,&nbsp;Tal Shay","doi":"10.1007/978-3-031-35139-6_1","DOIUrl":"10.1007/978-3-031-35139-6_1","url":null,"abstract":"<p><p>Women have a stronger immune response and a higher frequency of most autoimmune diseases than men. While much of the difference between men and women is due to the effect of gonadal hormones, genetic differences play a major role in the difference between the immune response and disease frequencies in women and men. Here, we focus on the immune differences between the sexes that are not downstream of the gonadal hormones. These differences include the gene content of the sex chromosomes, the inactivation of chromosome X in women, the consequences of non-random X inactivation and escape from inactivation, and the states that are uniquely met by the immune system of women-pregnancy, birth, and breast feeding. While these female-specific states are temporary and involve gonadal hormonal changes, they may leave a long-lasting footprint on the health of women, for example, by fetal cells that remain in the mother's body for decades. We also briefly discuss the immune phenotype of congenital sex chromosomal aberrations and experimental models that enable hormonal and the non-hormonal effects of the sex chromosomes to be disentangled. The increasing human life expectancy lengthens the period during which gonadal hormones levels are reduced in both sexes. A better understanding of the non-hormonal effects of sex chromosomes thus becomes more important for improving the life quality during that period.</p>","PeriodicalId":11102,"journal":{"name":"Current topics in microbiology and immunology","volume":"441 ","pages":"1-19"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10202944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of MHC and MHC-Like Molecules by Varicella Zoster Virus.","authors":"Allison Abendroth,&nbsp;Barry Slobedman","doi":"10.1007/82_2022_254","DOIUrl":"https://doi.org/10.1007/82_2022_254","url":null,"abstract":"<p><p>Varicella zoster virus (VZV) is a medically important human herpesvirus that has co-evolved with the human host to become a highly successful and ubiquitous pathogen. Whilst it is clear the innate and adaptive arms of the immune response play key roles in controlling this virus during both primary and reactivated infections, it is also apparent that VZV \"fights back\" by encoding multiple functions that impair a wide range of immune molecules. This capacity to manipulate the immune response is likely to be important in underpinning the success of VZV as a human pathogen. In this review, we will focus on the plethora of mechanisms that VZV has evolved to prevent and/or delay immune functions via regulating the expression of major histocompatibility complex (MHC) class I and MHC class II molecules, as well as several MHC-like molecules. In doing so, we will highlight both established and newly emerged VZV-encoded immunomodulatory capabilities and provide context to new avenues of research that seek to build the most comprehensive understanding of how this virus interfaces with these aspects of host immunity.</p>","PeriodicalId":11102,"journal":{"name":"Current topics in microbiology and immunology","volume":" ","pages":"85-102"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40327263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Management of Gastric Cancer Treatment Regimens.","authors":"Juliette Boilève, Yann Touchefeu, Tamara Matysiak-Budnik","doi":"10.1007/978-3-031-47331-9_11","DOIUrl":"10.1007/978-3-031-47331-9_11","url":null,"abstract":"<p><p>Gastric cancer is the fifth most common cancer and the fourth leading cause of cancer-associated death in the world. Endoscopic resection can be the treatment in selected cases of very early gastric cancer. Surgery is recommended for tumors that do not meet the criteria for endoscopic resection or for tumors with lymph node invasion but without distant metastases. Gastrectomy should include D2 lymphadenectomy without splenectomy. Perioperative or adjuvant chemotherapy improves survival and is recommended in locally advanced gastric cancer (>T1 and/or with lymph nodes positive). In locally advanced cancer with microsatellite instability (MSI), immunotherapy should be considered. Advanced unresectable or metastatic gastric cancer has a poor prognosis. The basis of the treatment is cytotoxic chemotherapy, with platinum and fluoropyrimidine doublet in the first line. Targeted therapies can be combined with chemotherapy. Trastuzumab (anti-HER2) is recommended in the first line in HER2-positive cancer. Ramucirumab (anti-VEGFR2) is recommended in the second line, in addition to paclitaxel chemotherapy. Zolbetuximab (anti-Claudine 18.2) should also be considered in the first line in Claudine 18.2-positive cancer. Immunotherapy can also be associated with chemotherapy in the first line of PD-L1-positive cancer. In HER2-positive and PD-L1-positive cancer, adjunction of trastuzumab and immunotherapy should be considered. In advanced and metastatic cancer with microsatellite instability (MSI), immunotherapy should be the first choice depending on its availability. Important progress has been made in recent years in the treatment of gastric cancer, especially due to a better understanding of molecular characteristics and heterogeneity of this disease. New targets and therapeutic approaches are being developed, which will very likely lead to changes in the management of gastric cancer.</p>","PeriodicalId":11102,"journal":{"name":"Current topics in microbiology and immunology","volume":"444 ","pages":"279-304"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139477469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}