12 research outputs found

    The Global Fund to Fight AIDS, Tuberculosis and Malaria's investments in harm reduction through the rounds-based funding model (2002-2014)

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    Background: Harm reduction is an evidence-based, effective response to HIV transmission and other harms faced by people who inject drugs, and is explicitly supported by the Global Fund to Fight AIDS, Tuberculosis and Malaria. In spite of this, people who inject drugs continue to have poor and inequitable access to these services and face widespread stigma and discrimination. In 2013, the Global Fund launched a new funding model-signalling the end of the previous rounds-based model that had operated since its founding in 2002. This study updates previous analyses to assess Global Fund investments in harm reduction interventions for the duration of the rounds-based model, from 2002 to 2014. Methods: Global Fund HIV and TB/HIV grant documents from 2002 to 2014 were reviewed to identify grants that contained activities for people who inject drugs. Data were collected from detailed grant budgets, and relevant budget lines were recorded and analysed to determine the resources allocated to different interventions that were specifically targeted at people who inject drugs. Results: 151 grants for 58 countries, plus one regional proposal, contained activities targeting people who inject drugs-for a total investment of US 620. million. Two-thirds of this budgeted amount was for interventions in th

    The promise of treatment as prevention for hepatitis C: Meeting the needs of people who inject drugs?

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    Treatment as prevention (TasP) is a concept common to the HIV sector. In this commentary we draw on the literature addressing HIV and HCV TasP, alongside qualitative HCV research, to critically appraise the promise of TasP for HCV and assess the needs of PWID in the future of HCV care. With the advent of highly effective direct-acting antiviral HCV treatments, TasP is now under consideration for HCV. A growing body of literature documents numerous social structural barriers to HCV treatment access and uptake for PWID, among whom HCV is highly prevalent. Yet these barriers - and suggestions for surmounting them - are rarely included in emergent literature on HCV TasP. Although HCV TasP has important advocacy potential for increasing treatment access among PWID, critical reflection on its implications are warranted. We outline potential limitations of TasP for HCV and the conditions under which it might be optimised. We argue that HCV treatment as a prevention strategy can only be realisable in a context of enhanced harm reduction access, meaningful community engagement, and enabling environment interventions informed by the needs and perspectives of PWID

    The Legionella Autoinducer Synthase LqsA Produces an α-Hydroxyketone Signaling Molecule*S⃞

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    The opportunistic pathogen Legionella pneumophila replicates in human lung macrophages and in free-living amoebae. To accommodate the transfer between host cells, L. pneumophila switches from a replicative to a transmissive phase. L. pneumophila harbors a gene cluster homologous to the Vibrio cholerae cqsAS quorum sensing system, encoding a putative autoinducer synthase (lqsA) and a sensor kinase (lqsS), which flank a response regulator (lqsR). LqsR is an element of the L. pneumophila virulence regulatory network, which promotes pathogen-host cell interactions and inhibits entry into the replicative growth phase. Here, we show that lqsA functionally complements a V. cholerae cqsA autoinducer synthase deletion mutant and, upon expression in L. pneumophila or Escherichia coli, produces the diffusible signaling molecule LAI-1 (Legionella autoinducer-1). LAI-1 is distinct from CAI-1 (Cholerae autoinducer-1) and was identified as 3-hydroxypentadecan-4-one using liquid chromatography coupled to high resolution tandem mass spectrometry. The activity of both LqsA and CqsA was abolished upon mutation of a conserved lysine, and covalent binding of the cofactor pyridoxal 5′-phosphate to this lysine was confirmed by mass spectrometry. Thus, LqsA and CqsA belong to a family of pyridoxal 5′-phosphate-dependent autoinducer synthases, which produce the α-hydroxyketone signaling molecules LAI-1 and CAI-1
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