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Abstract

Background Syphilis remains a global public health threat and can lead to severe complications. In addition to resolution of clinical manifestations, a reduction in nontreponemal antibody titers after treatment is regarded as “proof of cure.” However, some patients manifest < 4-fold decline (“serological non-response”) or persistently positive nontreponemal titers despite an appropriate decline (“serofast”) that may represent treatment failure, reinfection, or a benign immune response. To delineate these treatment phenomena, we conducted a systematic review of the literature regarding serological outcomes and associated factors among HIV-infected and -uninfected subjects. Methods Six databases (PubMed, Embase, CINAHL, Web of Science, Scopus, and BIOSIS) were searched with no date restrictions. Relevant articles that evaluated serological treatment responses and correlates of serological cure (≥ four-fold decline in nontreponemal titers) were included. Results We identified 1693 reports in the literature, of which 20 studies met selection criteria. The median proportion of patients who had serological non-response was 12.1 % overall (interquartile range, 4.9–25.6), but varied depending on the time points after therapy. The serofast proportion could only be estimated from 2 studies, which ranged from 35.2–44.4 %. Serological cure was primarily associated with younger age, higher baseline nontreponemal titers, and earlier syphilis stage. The relationship between serological cure and HIV status was inconsistent; among HIV-infected patients, CD4 count and HIV viral load was not associated with serological cure. Conclusions Serological non-response and the serofast state are common syphilis treatment outcomes, highlighting the importance of determining the immunological and clinical significance of persistent nontreponemal antibody titers after therapy. Electronic supplementary material The online version of this article (doi:10.1186/s12879-015-1209-0) contains supplementary material, which is available to authorized users.

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B cells in HIV infection and disease.

Susan Moir, Anthony Fauci (2009)

In recent years, intense research efforts have been dedicated to elucidating the pathogenic mechanisms of HIV-associated disease progression. In addition to the progressive depletion and dysfunction of CD4(+) T cells, HIV infection also leads to extensive defects in the humoral arm of the immune system. The lack of immune control of the virus in almost all infected individuals is a great impediment to the treatment of HIV-associated disease and to the development of a successful HIV vaccine. This Review focuses on advances in our understanding of the mechanisms of B-cell dysfunction in HIV-associated disease and discusses similarities with other diseases that are associated with B-cell dysfunction.

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From epidemiological synergy to public health policy and practice: the contribution of other sexually transmitted diseases to sexual transmission of HIV infection.

D. T. Fleming, J N Wasserheit (1999)

To review the scientific data on the role of sexually transmitted diseases (STDs) in sexual transmission of HIV infection and discuss the implications of these findings for HIV and STD prevention policy and practice. Articles were selected from a review of Medline, accessed with the OVID search engine. The search covered articles from January 1987 to September 1998 and yielded 2101 articles. Methods used to uncover articles which might have been missed included searching for related articles by author, and combing literature reviews. In addition, all abstracts under the category "sexually transmitted diseases" from the XI and XII International Conferences on AIDS (Vancouver 1996 and Geneva 1998) and other relevant scientific meetings were reviewed. Efforts were made to locate journal articles which resulted from the research reported in the identified abstracts. All original journal articles and abstracts which met one of the following criteria were included: (1) studies of the biological plausibility or mechanism of facilitation of HIV infectiousness or susceptibility by STDs, (2) prospective cohort studies (longitudinal or nested case-control) which estimate the risk of HIV infection associated with specific STDs or STD syndromes, or (3) intervention studies which quantitate the effect which STD treatment can have on HIV incidence. Strong evidence indicates that both ulcerative and non-ulcerative STDs promote HIV transmission by augmenting HIV infectiousness and HIV susceptibility via a variety of biological mechanisms. These effects are reflected in the risk estimates found in numerous prospective studies from four continents which range from 2.0 to 23.5, with most clustering between 2 and 5. The relative importance of ulcerative and non-ulcerative STDs appears to be complex. Owing to the greater frequency of non-ulcerative STDs in many populations, these infections may be responsible for more HIV transmission than genital ulcers. However, the limited reciprocal impact of HIV infection on non-ulcerative STDs and the evidence that non-ulcerative STDs may increase risk primarily for the receptive partner (rather than bidirectionally) may modulate the impact of these diseases. The results of two community level randomised, controlled intervention trials conducted in Africa suggest that timely provision of STD services can substantially reduce HIV incidence, but raise additional questions about the optimal way to target and implement these services to achieve the greatest effect on HIV transmission. Available data leave little doubt that other STDs facilitate HIV transmission through direct, biological mechanisms and that early STD treatment should be part of a high quality, comprehensive HIV prevention strategy. Policy makers, HIV prevention programme managers, and providers should focus initial implementation efforts on three key areas: (i) improving access to and quality of STD clinical services; (ii) promoting early and effective STD related healthcare behaviours; and (iii) establishing surveillance systems to monitor STD and HIV trends and their interrelations.

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Biological basis for syphilis.

Rebecca E LaFond, Sheila Lukehart (2006)

Syphilis is a chronic sexually transmitted disease caused by Treponema pallidum subsp. pallidum. Clinical manifestations separate the disease into stages; late stages of disease are now uncommon compared to the preantibiotic era. T. pallidum has an unusually small genome and lacks genes that encode many metabolic functions and classical virulence factors. The organism is extremely sensitive to environmental conditions and has not been continuously cultivated in vitro. Nonetheless, T. pallidum is highly infectious and survives for decades in the untreated host. Early syphilis lesions result from the host's immune response to the treponemes. Bacterial clearance and resolution of early lesions results from a delayed hypersensitivity response, although some organisms escape to cause persistent infection. One factor contributing to T. pallidum's chronicity is the paucity of integral outer membrane proteins, rendering intact organisms virtually invisible to the immune system. Antigenic variation of TprK, a putative surface-exposed protein, is likely to contribute to immune evasion. T. pallidum remains exquisitely sensitive to penicillin, but macrolide resistance has recently been identified in a number of geographic regions. The development of a syphilis vaccine, thus far elusive, would have a significant positive impact on global health.