BackgroundLeptospirosis is a worldwide zoonotic infection that has been recognized for decades, but the problem of the disease has not been fully addressed, particularly in resource-poor, developing countries, where the major burden of the disease occurs. This paper presents an overview of the current situation of leptospirosis in the region. It describes the current trends in the epidemiology of leptospirosis, the existing surveillance systems, and presents the existing prevention and control programs in the Asia Pacific region.MethodsData on leptospirosis in each member country were sought from official national organizations, international public health organizations, online articles and the scientific literature. Papers were reviewed and relevant data were extracted.ResultsLeptospirosis is highly prevalent in the Asia Pacific region. Infections in developed countries arise mainly from occupational exposure, travel to endemic areas, recreational activities, or importation of domestic and wild animals, whereas outbreaks in developing countries are most frequently related to normal daily activities, over-crowding, poor sanitation and climatic conditions.ConclusionIn the Asia Pacific region, predominantly in developing countries, leptospirosis is largely a water-borne disease. Unless interventions to minimize exposure are aggressively implemented, the current global climate change will further aggravate the extent of the disease problem. Although trends indicate successful control of leptospirosis in some areas, there is no clear evidence that the disease has decreased in the last decade. The efficiency of surveillance systems and data collection varies significantly among the countries and areas within the region, leading to incomplete information in some instances. Thus, an accurate reflection of the true burden of the disease remains unknown.

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a b s t r a c tPharmacological manipulations to purge human immunodeficiency virus (HIV) from latent reservoirs have been considered as an adjuvant therapeutic approach to highly-active antiretroviral therapy for the eradication of HIV. Our novel histone deacetylase inhibitor NCH-51 induced expression of latent HIV-1 with minimal cytotoxicity. Using chromatin immunoprecipitation assays, we observed a reduction of HDAC1 occupancy, histone hyperacetylation and the recruitment of positive transcription factors at the HIV-1 promoter in latently infected-cells under the treatment with NCH-51. Mutation studies of the long terminal repeat (LTR) revealed NCH-51 mediated gene expression through the Sp1 sites. When Sp1 expression was knocked-down by small interfering RNA, the NCH-51-mediated activation of a stably integrated HIV-1 LTR was attenuated. Moreover, the Sp1 inhibitor mithramycin A abolished the effects of NCH-51.

A wide variety of infections, including bacteria, viruses, fungi and protozoa occur in the immunocompromised condition associated with human immunodeficiency virus type 1 (HIV-1) infection and acquired immunodeficiency syndrome (AIDS). Although these opportunistic infections are believed to arise as an effect of the immunodeficiency, these microbes sometimes promote the disease progression of HIV-1 infection by enhancing viral replication or modulating host immune responses. Here we review the experimental and clinical evidence supporting such causal relationships associated with periodontogenic bacteria. Periodontal disease, caused by subgingival infection with oral anaerobic bacteria, typically Porphyromonas gingivalis (P. gingivalis) belonging to the phylum Bacteroidetes, is found worldwide and is one of the most prevalent microbial diseases of mankind. Emerging evidence implicates the involvement of P. gingivalis infection in the progression of HIV-1 infection. We demonstrate that P. gingivalis can induce HIV-1 reactivation via chromatin modification, and that the bacterial metabolite butyric acid produced in anaerobic conditions is responsible for this effect. These findings suggest that periodontal diseases could act as a risk factor for HIV-1 reactivation in infected individuals and might contribute to AIDS progression. Furthermore, it would imply that prevention and early treatment of periodontitis involving P. gingivalis infection could effectively block further clinical progression of AIDS.

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