{"title":"Bacterial structure and functional relation to abscess formation.","authors":"A O Tzianabos, A B Onderdonk, D L Kasper","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The capsular polysaccharide complex (CPC) of Bacteroides fragilis exhibits unusual biologic properties. This polysaccharide complex promotes the formation of abscesses and prevents abscess induction in a rat model of intra-abdominal sepsis. Each of these biologic properties is mediated by a T cell-dependent immune mechanism. The CPC consists of two distinct polysaccharides, PS A and PS B, each with repeating units that have positively charged amino groups and negatively charged carboxyl or phosphate groups. Analysis of these polysaccharides as well as other charged carbohydrates before and after chemical modification revealed that these oppositely charged groups are required for promotion of intra-abdominal abscesses as well as for protection against abscess induction. These studies provide a structural rationale for the distinct properties associated with the B. fragilis CPC, and delineate one mechanism by which this host response occurs.</p>","PeriodicalId":77176,"journal":{"name":"Infectious agents and disease","volume":"3 5","pages":"256-65"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18864857","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 destruction of smallpox virus stocks in national repositories: a grave mistake and a bad precedent.","authors":"B Roizman, W Joklik, B Fields, B Moss","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77176,"journal":{"name":"Infectious agents and disease","volume":"3 5","pages":"215-7"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18864853","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":"Overview of issues related to medical compliance with implications for the outpatient management of infectious diseases.","authors":"D A Sclar, T A Tartaglione, M J Fine","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Noncompliance with therapeutic drug regimens is a public health problem with major health and economic implications. Reported rates of noncompliance for all types of drugs range from 13% to 93% among adults and from 25% to 82% among children. In recent years, sophisticated techniques for evaluating noncompliance have evolved, as has our understanding of factors associated with noncompliance. A key factor is the prescribed dosing schedule for a drug. Studies indicate that there is a direct relationship between frequency of dose and compliance. A study of compliance with short-term regimens of oral antibiotic therapy found mean compliance rates of 80%, 69%, and 38% for administration once a day (QD), twice a day (BID), and three times a day (TID), respectively. Pharmacoeconomic analyses of dose-related compliance have demonstrated that significant savings can be achieved with QD dosing of antihypertensive medication. Although similar analyses have not been performed for drug regimens used in the treatment of infectious diseases that are usually treated on an outpatient basis, it is probable that comparable savings will be attained when economic analyses of dose/compliance relationships in short-term antibiotic therapy for such common disorders as sinusitis, pharyngitis, otitis media, urinary tract infections, and community-acquired pneumonia are undertaken.</p>","PeriodicalId":77176,"journal":{"name":"Infectious agents and disease","volume":"3 5","pages":"266-73"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18864858","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}
E A Duarte, I S Novella, S C Weaver, E Domingo, S Wain-Hobson, D K Clarke, A Moya, S F Elena, J C de la Torre, J J Holland
{"title":"RNA virus quasispecies: significance for viral disease and epidemiology.","authors":"E A Duarte, I S Novella, S C Weaver, E Domingo, S Wain-Hobson, D K Clarke, A Moya, S F Elena, J C de la Torre, J J Holland","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The experimental evidence available for animal and plant RNA viruses, as well as other RNA genetic elements (viroids, satellites, retroelements, etc.), reinforces the view that many different types of genetic alterations may occur during RNA genome replication. This is fundamentally because of infidelity of genome replication and large population sizes. Homologous and heterologous recombination, as well as gene reassortments occur frequently during replication of retroviruses and most riboviruses, especially those that use enzymes with limited processivity. Following the generation of variant genomes, selection, which is dependent on environmental parameters in ways that are poorly understood, sorts out those genome fits enough to generate viable quasispecies. Chance events can also be destabilizing, as illustrated by recent results on fitness loss and other phenotypic changes accompanying bottleneck transmission. Variation, selection, and random sampling of genomes occur continuously and unavoidably during virus evolution. Evolution of RNA viruses is largely unpredictable because of the stochastic nature of mutation and recombination events, as well as the subtle effects of chance transmission events and host/environmental factors. Among environmental factors, alterations resulting from human intervention (deforestation, agricultural activities, global climatic changes, etc.) may alter dispersal patterns and provide new adaptive possibilities to viral quasispecies. Current understanding of RNA virus evolution suggests several strategies to control and diagnose viral diseases. The new generation of chemically defined vaccines and diagnostic reagents (monoclonal antibodies, peptide antigens, oligonucleotides for polymerase chain reaction amplification, etc.) may be adequate to prevent disease and detect some or even most of the circulating quasispecies of any given RNA pathogen. However, the dynamics of viral quasispecies mandate careful consideration of those reagents to be incorporated into diagnostic kits. Broadening diagnosis without jeopardizing specificity of detection will be challenging. There is a finite probability (impossible to quantify at present) that a defined vaccine may promote selection of escape mutants or a particular diagnostic kit may fail to detect a viral pathogen. Of particular concern are the potential long-term effects of weak selective pressures that may initially go unnoticed. Variant viruses resulting from evolutionary pressure imposed by vaccines or drugs may insidiously and gradually replace previous quasispecies. The great potential for variation and phenotypic diversity of some important RNA virus pathogens (human immunodeficiency virus, the hepatitis viruses, the newly recognized human hantaviruses, etc.) has become clear. Prevention and therapy should rely on multicomponent vaccines and antiviral agents to address the complexity of RNA quasispecies mutant spectra.(ABSTRACT TRUNCATED AT 400 WORDS)</p>","PeriodicalId":77176,"journal":{"name":"Infectious agents and disease","volume":"3 4","pages":"201-14"},"PeriodicalIF":0.0,"publicationDate":"1994-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18827485","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":"Trypanosomatid protozoa provide paradigms of eukaryotic biology.","authors":"C Tschudi, E Ullu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Over the last 10 years, trypanosomatid protozoa have been the subject of intense investigation particularly focusing on their parasitic lifestyle and their intriguing and novel cell properties. These studies have furthered our understanding of the physiology and functioning of these cells and have identified a large number of biochemical and metabolic peculiarities, including mitochondrial function, enzymatic compartmentalization, and gene expression. This review focuses on the mode of gene expression and highlights areas of trypanosome research that have provided paradigms of eukaryotic biology.</p>","PeriodicalId":77176,"journal":{"name":"Infectious agents and disease","volume":"3 4","pages":"181-6"},"PeriodicalIF":0.0,"publicationDate":"1994-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18829498","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":"Promoting laboratory research during infectious diseases fellowship training or telling the truth about training in clinical research.","authors":"K Joiner","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77176,"journal":{"name":"Infectious agents and disease","volume":"3 4","pages":"163-7"},"PeriodicalIF":0.0,"publicationDate":"1994-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18829496","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":"Whatever happened to AIDS?","authors":"J E Osborn","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The HIV/AIDS epidemic has caught millions of people in its path worldwide during the first 13 years since it surfaced; half a million Americans have been diagnosed with AIDS, and hundreds of thousands more are in earlier stages of HIV disease. Yet the sense of urgency one would expect should attend such awful numbers is strangely absent, prompting the bitter query \"Whatever happened to AIDS?\" This paper discusses the present status of progress with respect to the epidemic and explores some of the reasons that might partially explain both the inherent difficulties of research and the inappropriate public sense of quiescence. It then puts forward some suggested areas of research endeavor and/or public policy that could re-energize the flagging public response to this massive health disaster.</p>","PeriodicalId":77176,"journal":{"name":"Infectious agents and disease","volume":"3 4","pages":"194-200"},"PeriodicalIF":0.0,"publicationDate":"1994-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18827482","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":"Human papillomavirus vaccines: a warty problem.","authors":"D A Galloway","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Infection of the genital tract with human papillomaviruses (HPVs) is a common occurrence, and manifestations can include genital warts (condyloma acuminata), dysplasia, and invasive cancer. Approaches to diagnose and treat HPV infections are costly and are not fully effective. Even in populations at low risk for sexually transmitted diseases (STDs), HPV infection is severalfold more prevalent than all other STDs combined, and worldwide, uterine cervical cancer remains the most common cancer in women. It should be feasible to develop prophylactic vaccines to prevent HPV infection using the L1 and L2 capsid proteins or therapeutic vaccines to modulate the development or recurrence of disease based on the E6 and E7 oncoproteins or other viral proteins. In favor of success is (a) the relative simplicity of the HPV genome (only two proteins in the viral coat, and a small number of other genes), (b) the lack of genetic variability within types and stability of the genome, and (c) the encouraging results with vaccines against animal PVs. However, it is difficult to provide evidence of the efficacy of HPV vaccines because of the inability to propagate the virus in culture or in animal models and because of the incomplete understanding of the natural history of HPV infection.</p>","PeriodicalId":77176,"journal":{"name":"Infectious agents and disease","volume":"3 4","pages":"187-93"},"PeriodicalIF":0.0,"publicationDate":"1994-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18829499","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":"Rabies--an historical perspective.","authors":"G M Baer","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77176,"journal":{"name":"Infectious agents and disease","volume":"3 4","pages":"168-80"},"PeriodicalIF":0.0,"publicationDate":"1994-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18829497","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":"Pathogenesis associated with replication of hepatitis delta virus.","authors":"V Bichko, H J Netter, T T Wu, J Taylor","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Hepatitis delta virus (HDV) is a subviral satellite of human hepatitis B virus (HBV). HDV was discovered in patients chronically infected with HBV who had a more severe form of disease. Subsequent studies have attempted to understand the cytopathic effects due to HDV, and this article reviews the progress along with newer studies that suggest that HDV genome replication per se causes no more than a moderate inhibition of cellular growth rate. This inhibition nevertheless provides a selective pressure for reduced levels of HDV genome replication. Such a reduction is apparently achieved by a host cell activity that edits the HDV RNA genome.</p>","PeriodicalId":77176,"journal":{"name":"Infectious agents and disease","volume":"3 2-3","pages":"94-7"},"PeriodicalIF":0.0,"publicationDate":"1994-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18811625","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}