BackgroundHTLV-1 and HTLV-2 are retroviruses linked etiologically to various human diseases, and both of them can be transmitted by vertical route, sexual intercourse, blood transfusion and intravenous drug use. Recently, some HTLV-infected cases have been reported and this virus is mainly present in the Southeast coastal areas in China, but has not been studied for the people in Central China.ObjectivesTo know the epidemiologic patterns among different population samples in Central China and further identify risk factor for HTLV-1 and HTLV-2 infection.MethodsFrom January 2008 to December 2011, 5480 blood samples were screened for HTLV-1/2 antibodies by using enzyme immunoassay, followed by Western Blot.ResultsThe prevalence of HTLV-1 and HTLV-2 was found with infection rates 0.13% and 0.05% among all population samples for HTLV-1 and HTLV-2, respectively. The highest percentages of infection, 0.39% and 0.20%, were found in the high risk group, while only 0.06% and 0.03% in the blood donor group. There was only one case of HTLV-1 infection (0.11%) among patients with malignant hematological diseases. Of seven HTLV-1 positive cases, six were co-infected with HBV, two with HCV and one with HIV. Among three HTLV-2 positive individuals all were co-infected with HBV, one with HCV.ConclusionsHTLV-1 and HTLV-2 have been detected in the Central China at low prevalence, with the higher infection rate among high risk group. It was also found that co-infection of HTLV-1/2 with HIV and HBV occurred, presumably due to their similar transmission routes. HTLV-1/2 antibody screen among certain population would be important to prevent the spread of the viruses.
The development of acute liver failure (ALF) is dependent on its local inducer. Inflammation is a high‐frequency and critical factor that accelerates hepatocyte death and liver failure. In response to injury stress, the expression of the transcription factor hypoxia‐inducible factor‐1α (HIF‐1α) in macrophages is promoted by both oxygen‐dependent and oxygen‐independent mechanisms, thus promoting the expression and secretion of the cytokine interleukin‐1β (IL‐1β). IL‐1β further induces hepatocyte apoptosis or necrosis by signaling through the receptor (IL‐1R) on hepatocyte. HIF‐1α knockout in macrophages or IL‐1R knockout in hepatocytes protects against liver failure. However, whether HIF‐1α inhibition in macrophages has a protective role in ALF is unclear. In this study, we revealed that the small molecule HIF‐1α inhibitor PX‐478 inhibits the expression and secretion of IL‐1β, but not tumor necrosis factor α (TNFα), in bone marrow‐derived macrophages (BMDMs). PX‐478 pretreatment alleviates liver injury in LPS/D‐GalN‐induced ALF mice by decreasing the hepatic inflammatory response. In addition, preventive or therapeutic administration of PX‐478 combined with TNFα neutralizing antibody markedly improved LPS/D‐GalN‐induced ALF. Taken together, our data suggest that PX‐478 administration leads to HIF‐1α inhibition and decreased IL‐1β secretion in macrophages, which represents a promising therapeutic strategy for inflammation‐induced ALF.
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