Chancroid and human immunodeficiency virus infection – a review

Mohammed, Tahir; Olumide, Yetunde

doi:10.1111/j.1365-4632.2007.03435.x

Cited by 35 publications

(23 citation statements)

References 47 publications

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“…Ulcerative cervico‐vaginal infections, such as herpes simplex virus (HSV) 24 and Haemophilus ducreyi 25 , have been linked to an increased susceptibility to HIV‐1 acquisition. These ulcerative infections result in breaches in the lower genital tract pseudosquamous epithelium and expose lamina propria target cells to infecting virus 24,25 . This review, however, will focus on the more common and often asymptomatic non‐ulcerative infections BV and TV, which facilitate HIV‐1 infection by mechanisms not yet completely elucidated.…”

Section: Prevalence and Symptoms Of Lower Genital Tract Infectionsmentioning

confidence: 99%

Innate Immunity and Inflammatory Response to Trichomonas vaginalis and Bacterial Vaginosis: Relationship to HIV Acquisition

Thurman

Doncel

2011

American Journal of Reproductive Immunology

100

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Most women contract HIV-1 through sexual intercourse with an infected partner. Highly prevalent, unreported and often asymptomatic lower genital tract infections, including bacterial vaginosis (BV) and trichomoniasis (Trichomonas vaginalis- TV), increase a woman's susceptibility to HIV-1 genital infection, given an exposure. A review of the literature from 1989 to the present was conducted. This article will review potential mechanisms by which BV and TV serve as HIV-1-enhancing cofactors including (i) initiation of a clinical or subclinical mucosal inflammatory response, (ii) alteration of innate mucosal immunity, (iii) alteration of normal vaginal microflora and pH, and (iv) weakening or breach of intact cervico-vaginal mucosa. The transmission of HIV-1, in the absence of cofactors, is poorly efficient. Understanding the mechanisms by which these infections enhance HIV-1 acquisition is important to designing effective, safe and evidence-based prevention modalities.

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Section: Prevalence and Symptoms Of Lower Genital Tract Infectionsmentioning

confidence: 99%

Innate Immunity and Inflammatory Response to Trichomonas vaginalis and Bacterial Vaginosis: Relationship to HIV Acquisition

Thurman

Doncel

2011

American Journal of Reproductive Immunology

100

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“…Its evolution (253), host-pathogen interaction (254), and clinical significance (255-257) have been reviewed. Genital ulceration is a major cofactor in the transmission of human immunodeficiency virus (256,257).…”

Section: Other Haemophilus Speciesmentioning

confidence: 99%

Classification, Identification, and Clinical Significance of Haemophilus and Aggregatibacter Species with Host Specificity for Humans

2014

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SUMMARY The aim of this review is to provide a comprehensive update on the current classification and identification of Haemophilus and Aggregatibacter species with exclusive or predominant host specificity for humans. Haemophilus influenzae and some of the other Haemophilus species are commonly encountered in the clinical microbiology laboratory and demonstrate a wide range of pathogenicity, from life-threatening invasive disease to respiratory infections to a nonpathogenic, commensal lifestyle. New species of Haemophilus have been described ( Haemophilus pittmaniae and Haemophilus sputorum ), and the new genus Aggregatibacter was created to accommodate some former Haemophilus and Actinobacillus species ( Aggregatibacter aphrophilus , Aggregatibacter segnis , and Aggregatibacter actinomycetemcomitans ). Aggregatibacter species are now a dominant etiology of infective endocarditis caused by fastidious organisms (HACEK endocarditis), and A. aphrophilus has emerged as an important cause of brain abscesses. Correct identification of Haemophilus and Aggregatibacter species based on phenotypic characterization can be challenging. It has become clear that 15 to 20% of presumptive H. influenzae isolates from the respiratory tracts of healthy individuals do not belong to this species but represent nonhemolytic variants of Haemophilus haemolyticus . Due to the limited pathogenicity of H. haemolyticus , the proportion of misidentified strains may be lower in clinical samples, but even among invasive strains, a misidentification rate of 0.5 to 2% can be found. Several methods have been investigated for differentiation of H. influenzae from its less pathogenic relatives, but a simple method for reliable discrimination is not available. With the implementation of identification by matrix-assisted laser desorption ionization–time of flight mass spectrometry, the more rarely encountered species of Haemophilus and Aggregatibacter will increasingly be identified in clinical microbiology practice. However, identification of some strains will still be problematic, necessitating DNA sequencing of multiple housekeeping gene fragments or full-length 16S rRNA genes.

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“…Chancroid is endemic in some developing countries in Africa, Asia, and South America, where it accounts for almost half of all GUD cases, although these numbers could be higher as H. ducreyi cases remain poorly documented (55,57). GUD is a recognized cofactor for human immunodeficiency virus acquisition and transmission (25,37), and a better understanding of H. ducreyi pathogenesis is necessary to allow a rational approach to the identification of vaccine candidates that could be used to prevent chancroid.H. ducreyi is a strict human pathogen, and it is likely that during the different stages of ulcer production (i.e., progression of a papule into a pustule followed by frank ulceration [1,8,50]), this pathogen controls gene expression to enhance its growth and to evade the host immune system.…”

mentioning

confidence: 99%

mentioning

confidence: 99%

Regulation of Expression of the Haemophilus ducreyi LspB and LspA2 Proteins by CpxR

2009

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The LspA1, LspA2, and LspB proteins of Haemophilus ducreyi comprise a two-partner secretion system that has been shown to be necessary for H. ducreyi to inhibit phagocytosis by immune cells in vitro. Inactivation of lspA1 resulted in increased levels of LspA2, suggesting that these two proteins are differentially controlled (C. J. Ward et al., Infect. Immun. 71:2478-2486, 2003). Expression of LspA2 but not LspA1 was shown to be both growth phase dependent and affected by the presence of fetal calf serum (FCS) in the growth medium. In addition, neither LspA1 nor LspA2 could be detected in culture supernatant fluid in the absence of FCS. DNA microarray analysis revealed that 324 H. ducreyi genes were differentially regulated after growth in the presence of FCS. Among these, the CpxRA two-component sensory transduction system was downregulated by the presence of FCS. Inactivation of cpxR resulted in increased expression of both LspB and LspA2. Electrophoretic mobility shift assays showed that a recombinant H. ducreyi CpxR protein bound the promoter region of the lspB-lspA2 operon. The cpxR and cpxA genes were shown to be part of an operon containing two additional genes in H. ducreyi 35000HP. This is the first description of a two-component sensory transduction system regulating a proven virulence factor of H. ducreyi.Haemophilus ducreyi is a gram-negative coccobacillus and the causative agent of the sexually transmitted genital ulcer disease (GUD) chancroid (1,8). Globally, chancroid is a significant sexually transmitted disease, with more than 6 million cases reported in 1997 (60). In the United States, several outbreaks were reported between 1980 and 2000 (24, 36, 51), but since then the number of cases has greatly diminished, and today the soft chancres characteristic of H. ducreyi infection occur only in isolated cases that are typically associated with the sex trade industry (57). Chancroid is endemic in some developing countries in Africa, Asia, and South America, where it accounts for almost half of all GUD cases, although these numbers could be higher as H. ducreyi cases remain poorly documented (55,57). GUD is a recognized cofactor for human immunodeficiency virus acquisition and transmission (25,37), and a better understanding of H. ducreyi pathogenesis is necessary to allow a rational approach to the identification of vaccine candidates that could be used to prevent chancroid.H. ducreyi is a strict human pathogen, and it is likely that during the different stages of ulcer production (i.e., progression of a papule into a pustule followed by frank ulceration [1,8,50]), this pathogen controls gene expression to enhance its growth and to evade the host immune system. Information about regulatory networks that might control the expression of H. ducreyi virulence factors is very limited at present. Although nucleotide sequence analysis of the H. ducreyi 35000HP genome (GenBank accession no. NC002940) revealed the presence of several genes encoding predicted proteins with homology to known bacterial regulators...

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Chancroid and human immunodeficiency virus infection – a review

Cited by 35 publications

References 47 publications

Innate Immunity and Inflammatory Response to Trichomonas vaginalis and Bacterial Vaginosis: Relationship to HIV Acquisition

Innate Immunity and Inflammatory Response to Trichomonas vaginalis and Bacterial Vaginosis: Relationship to HIV Acquisition

Classification, Identification, and Clinical Significance of Haemophilus and Aggregatibacter Species with Host Specificity for Humans

Regulation of Expression of the Haemophilus ducreyi LspB and LspA2 Proteins by CpxR

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