Facts about syphilis. There are currently no items to display. Prevention and control Guidance on prevention of sexually transmitted diseases. Facts Syphilis is a sexually transmitted infection caused by the bacterium Treponema pallidum. Related diseases.
Disease programmes and networks. Peer-Reviewed Publication Gender violence, poverty and HIV infection risk among persons engaged in the sex industry: Cross-national analysis of the political economy of sex markets in 30 European and Central Asian countries Jan This spectacle of two personified pathogens worked, also, as recognition of the distinctiveness of each disease.
Much work was needed to bring them together into one frame of reference, so that they could circulate on Twitter and elsewhere together. Already in the late s, papers were being published that not only argued for the inclusion of TB on the list of AIDS index diseases but that also pointed to the changing biology of TB in cases of HIV, and thus to the drastic increase of complexity when dealing with patients who manifest both diseases Nambuya et al.
Since the emergence of a significant number of TB cases in people with HIV during the last two decades, the infection of one person with TB and HIV simultaneously has been called a broad variety of names. In , 1. Yet does one plus one really equal two? The objective of a syndemics approach is to acknowledge co-occurring epidemics as fundamentally entangled and structured by similar epidemiological conditions of poverty, inequality, and discrimination, all adding up to states of bad health Singer et al.
Within a concept of syndemics, co-infections are thus framed as multiplied deadly afflictions, which constitute first and foremost a deadly phenomenon, as well as an intriguing practical problem in the clinic and in public health, determined by structural factors. In the syndemics literature, it is argued that these structural factors not only add up to bad health, but also multiply the vectors of overall disease burden Singer , In the end, the concept of syndemics shows how single-disease approaches that do not take into account structural inequalities constantly fail.
Its proponents usually make a prescriptive argument that such inequalities should be addressed in conjunction with each other, taking into account the multiplied complexity for treatment and prevention in dire socioeconomic conditions when more than one epidemic occurs at a time.
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Proposing syndemics as a way to conceive of the practical and structural problems co-infections create does not, however, seem entirely satisfactory to us, as it does not fundamentally question the single-disease framework and its associated ways of research. We suggest, with this perspective, that one plus one does not equal two: co-infections are more than deadly duos, they are more than complex syndemics. We understand epistemological obstacles to be productive: they challenge established ways of seeing and dealing with disease, and allow us to investigate new avenues for different kinds of research on epidemics.
Managing tuberculosis and HIV in sub-Sahara Africa | SpringerLink
Seeing diseases as co-infections allows us to think and analyse beyond the given narratives of specific diseases, and draws our attention to common problems, shared underlying conditions, and the ways in which strategies and concepts, which have been developed to tackle one disease, travel on to another. It thus takes a great deal of intellectual effort and creativity to bridge their histories, to relate them; to find concepts, practices, and ideas in the in-between of two diseases; and to follow how one disease informs the ways in which another disease is approached.
Some work has already be done to show how epidemics simultaneously reveal and veil each other, most recently by Julie Livingston , who shows the interrelations between AIDS and cancer in Botswana, and by Johanna Crane , who links the conceptualisation of treatment resistance in the field of HIV to the problematisation of multiresistant tuberculosis.
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Even as we write this, other co-infections like AIDS and hepatitis C are becoming new grounds of research and funding see, for example, Chabrol c. As researchers in the field of anthropology and the history of infectious diseases, we wish to slightly step back from the dire reality of multiplied disease loads, and instead interrogate the historical conditions in which co-infections became problems of health politics and policies in the first place.
While this is a preliminary investigation of the global health and medicine policy documents that shaped the discourse on co-infection in the late s and early s, our larger epistemological argument suggests ways in which historical and ethnographic research on diseases of co-infection might be conceptualised in the future.
These systems are designed to order complexities, rather than perceive them. As such, co-infections pose challenges to treatment guidelines, clinical protocols, randomised trials, epidemiological models, and practices of care — as well as the epistemological premises of writing and thinking about diseases in the social sciences and humanities. We take from Fleck the observation that if an entangled object made of different collectives appears, there ought to be a common ground in both diseases that permits the entangling of the object in the first place.
Thus, co-infection allows us to interrogate the pasts and presents of diseases for their common ground and shared traits. If translation is successful, and communication takes place, then transformation is inevitable.
This means that the concepts a gain strength and significance within the existing collectives, and simultaneously b become altered in between the thought collectives. For Fleck, this doubled process of alteration and corroboration is the basis for an epistemological approach to the genesis and development of any knowledge.
Our brief evaluation of both diseases in their own spheres, and of efforts to address their short entangled history, reveals both the sturdiness of certain aspects of each disease as well as the fluidity and contingency of the very same cultural, social, and biological elements involved in their making.
While the lens of co-infection might partly dissolve the existence of single-disease concepts in medicine and public health, their practical use endures, solidly anchored. Given the endurance of single-disease concepts, we begin in the next section by engaging with the histories and presents of TB and HIV. We then use this analysis as a tool to open up new research questions and to propose strategic entry points for future ethnographic and historical research in this emergent field of histories and anthropologies of co-infection.
The idea of morbid categories, or single-disease concepts, is of course older and can easily be traced back to Hippocrates and beyond — if it is understood as a set of abstract signs that describe disease, used to organise diagnostics, treatment, and surveillance. The single-disease concept became fundamental to medicine and the history of medicine and anthropology at the beginning of the nineteenth century, with the birth of modern medicine and its empirical lab procedures and scientific principles of proof.
But neither do single diseases, however, easily come into clinical existence as such. Since then, the TB community has become international in scope, consisting of national and international medical associations like the International Union of Tuberculosis and Lung Disease, bacteriological reference laboratories, vertical disease-control programmes see Harper , and medical institutions like dispensaries and treatment centres across the world.
At the European level, nationalised public health strategies include screening see Armstrong ; Welshman and Bashford , contact tracing see Kehr a , and isolation see Strange and Bashford TB has always disproportionately affected poor, disadvantaged, and dominated populations. It thus exemplifies the complex relationship between social inequalities, biological processes, biomedical research, and the unequal development of disease in different groups of people, making it a truly biosocial phenomenon. TB is therefore an interesting object for the social history of medicine Amrith ; Barnes ; Bryder ; Condrau and Worboys ; Packard , critical medical anthropology Draus ; Farmer ; Kehr b; Keshavjee ; Koch b , and social epidemiology Gandy and Zumla , fields of research that we also see as part of the TB community.
TB is, in other words, a vantage point from which both the history and the present of complex interrelations between disease, medicine, and society can be examined. Why is this so? One reason is that TB began to disappear as a major public health problem in Europe and North America in the s, which led to considerable neglect of this disease during the s and s in the international arena and in research Ogden et al.
Long sanatorium stays and yearlong treatments were transformed into short-term relations between patients and health professionals, mediated through the mostly technical administration of drugs. Additionally, economic and social developments like universal access to health care, social insurance, improved living conditions, and a decrease in poverty in the postwar years proliferated in the North. The de facto availability of treatment coupled with these welfare advances thereby effectively contributed to declining TB disease rates in Europe and North America.
TB thus became less and less visible in Northern societies, as prevention campaigns and mass-screening measures, such as mobile X-ray vans, gradually ceased to operate.
The epidemiological decrease in disease rates in the North was paralleled by a strong belief in ever-advancing modernisation and development in the s on a global scale, which helped make TB invisible as a public health problem. In sum, biomedical science gradually stopped basing its future on old diseases like tuberculosis, turning instead to new, scientifically more interesting, and more profitable challenges Kehr b.
In the South, though, among the newly independent nations, tuberculosis did not disappear as a major public health problem. Just a little more than a decade ago, TB as a site of research and action began to be invested in again, with the creation of such powerful organisations as the Global Fund and the TB Alliance.
Viruses manipulate host cells to enhance their replication, and the identification of cellular factors targeted by viruses has led to key insights into both viral pathogenesis and cell biology. In this study, we develop an HIV reporter virus HIV-AFMACS displaying a streptavidin-binding affinity tag at the surface of infected cells, allowing facile one-step selection with streptavidin-conjugated magnetic beads. We therefore provide a high-coverage functional proteomic atlas of HIV infection, and a mechanistic account of host factors subverted by the virus in its natural target cell.
Remodelling of the host proteome during viral infection may reflect direct effects of viral proteins, secondary effects or cytopathicity accompanying viral replication, or host countermeasures such as the interferon IFN response. By defining time-dependent changes in protein levels in infected cells, and correlating temporal profiles of cellular and viral proteins, we have shown that it is possible to differentiate these phenomena, and identify direct cellular targets of human cytomegalovirus HCMV and HIV Greenwood et al.
To enable time course analysis and minimise confounding effects from uninfected bystander cells, pure populations of synchronously infected cells must be sampled sequentially as they progress through a single round of viral replication. The utility of cancer cell line models such as CEM-T4 is, however, limited by the extent to which they retain the characteristics of the primary cells from which they were derived, and cancer-specific and in vitro culture-dependent reprogramming are well described Gillet et al. To this end, we have developed an HIV reporter virus encoding a cell surface streptavidin-binding affinity tag, allowing antibody-free magnetic cell sorting of infected cells AFMACS Matheson et al.
Length is indicated in base pairs bp. The complete sequence is available in Supplementary file 1. Cells expressing this marker may be selected directly with streptavidin-conjugated magnetic beads, washed to remove unbound cells, then released by incubation with the naturally occurring vitamin biotin Matheson et al. Further details relating to construct design are described in the Materials and methods and Supplementary file 1.
To confirm that HIV-AFMACS virus could be used for cell selection Figure 1A , infected primary T cells were captured by streptavidin-conjugated magnetic beads, released by incubation with excess biotin, then analysed by flow cytometry. Interpretation of HIV-dependent proteomic remodelling in primary T cells is complicated by concurrent changes in relative protein abundance resulting from T cell activation Geiger et al.
We therefore exploited multiplex TMT labelling to measure parallel protein abundances in resting and activated uninfected T cells from the same donor, as well as control mock-infected T cells obtained at each time point. A Overview of time course proteomic experiment. Mock-infected cells are shown in grey. Axes, scales and colours are as in C. Expression profiles of other accessory protein targets are shown in Figure 2—figure supplement 1B.
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Log2 ratio s of abundances in experimental Expt :control Ctrl cells are shown for 45 accessory protein targets as in Figure 2—figure supplement 3A. In total, we quantitated cellular proteins across 10 different conditions. As previously reported Geiger et al. All data from infected and uninfected cells have been made available via ProteomeXchange with identifier PXD, and are summarised in an interactive spreadsheet allowing generation of temporal profiles for any quantitated proteins of interest Figure 2—source data 1.
In the absence of donor haplotyping, polymorphisms at the MHC-I locus make routine proteomic quantification problematic. Together with cellular proteins, we identified gene products from seven viral open reading frames ORFs; Figure 2—figure supplement 1C. Conversely, viral structural proteins expressed from unspliced, Rev-dependent transcripts Gag and Gagpol were expressed late in infection, increasing progressively from 24 to 48 hr.
Managing tuberculosis and HIV in sub-Sahara Africa
Viral accessory proteins expressed from partially spliced transcripts were either not detected Vpr and Vpu or incompletely quantitated Vif. Inter-individual variability is known to affect gene expression during T cell activation Ye et al. Whilst some donor-dependent differences were apparent, most sample-sample variability was accounted for by HIV infection Figure 3—figure supplement 1B , and all accessory protein substrates from Figure 2C—D and Figure 2—figure supplement 1B were significantly depleted by WT HIV Figure 3C , left panel.
A Overview of single time point proteomic experiment.
Volcano plots show statistical significance y axis vs fold change x axis for cellular and six viral proteins quantitated in cells from all three donors no missing values.
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