HIV is still a major health problem in developing countries. Even though high HIV-risk-taking behaviors have been reported in African fishing villages, local distribution patterns of HIV infection in the communities surrounding these villages have not been thoroughly analyzed. The objective of this study was to investigate the geographical distribution patterns of HIV infection in communities surrounding African fishing villages. In 2011, we applied age- and sex-stratified random sampling to collect 1,957 blood samples from 42,617 individuals registered in the Health and Demographic Surveillance System in Mbita, which is located on the shore of Lake Victoria in western Kenya. We used these samples to evaluate existing antibody detection assays for several infectious diseases, including HIV antibody titers. Based on the results of the assays, we evaluated the prevalence of HIV infection according to sex, age, and altitude of participating households. We also used Kulldorff’s spatial scan statistic to test for HIV clustering in the study area. The prevalence of HIV at our study site was 25.3%. Compared with the younger age group (15–19 years), adults aged 30–34 years were 6.71 times more likely to be HIV-positive, and the estimated HIV-positive population among women was 1.43 times larger than among men. Kulldorff’s spatial scan statistic detected one marginally significant (P = 0.055) HIV-positive and one significant HIV-negative cluster (P = 0.047) in the study area. These results suggest a homogeneous HIV distribution in the communities surrounding fishing villages. In addition to individual behavior, more complex and diverse factors related to the social and cultural environment can contribute to a homogeneous distribution pattern of HIV infection outside of African fishing villages. To reduce rates of transmission in HIV-endemic areas, HIV prevention and control programs optimized for the local environment need to be developed.
Strongyloidiasis is caused by the nematode Strongyloides stercoralis which has the unique ability to reproduce and complete its entire life cycle within the human host through its autoinfection cycle. Diagnosis of this infection is important because of its potential to cause fatal hyperinfection syndrome or disseminated infections in those with defective cellular immunity. Parasitological methods based on faecal microscopy and culture often fail to detect low-intensity infections. A multiplex polymerase chain reaction (PCR) assay was developed for the detection of S. stercoralis, Ascaris lumbricoides, and Enterobius vermicularis by designing primers specific for the ITS1 region of ribosomal DNA of S. stercoralis and A. lumbricoides and 18S region of rRNA of E. vermicularis. A 61-year-old patient presented with chronic gastrointestinal and respiratory symptoms and weight loss with a stool microscopy positive for helminth larvae. Stool cultures with the Harada–Mori technique yielded L3 larvae which were identified as S. stercoralis based on morphology. The multiplex PCR performed on DNA extracted from stool elicited the expected band at 129 bp on gel electrophoresis of the PCR yield providing molecular evidence of intestinal strongyloidiasis. The patient’s gastrointestinal symptoms improved with a six-day course of albendazole (400 mg twice daily). Negative posttreatment stool microscopy, culture, and PCR confirmed successful clearance of infection. Molecular-based PCR assay is a promising tool to diagnose and assess the therapeutic efficacy of anthelmintics in intestinal helminthiases such as strongyloidiasis.
The phagocyte NADPH oxidase catalyzes the production of superoxide, the precursor to microbicidal oxidants that are essential for normal host defense. The active enzyme complex includes a membrane-bound flavocytochrome b along with p47−phox, p67phox, and Rac-GTP, which translocate from the cytosol to the membrane to activate electron transport through the flavocytochrome upon cellular stimulation with soluble or particulate agonists. Translocation of p67phox is mediated by p47phox, which can be isolated from the cytoplasm prior to oxidase activation as a complex along with a third protein, p40phox. Although p40phox also translocates to the membrane of activated cells, its role in regulation of the NADPH oxidase has been unclear. p40phox is not required for reconstitution of high-level NADPH oxidase activity in cell-free systems or in heterologous whole cell models based in COS7 or K562 cell lines. It has recently been recognized that p40phox binds phosphatidylinositol-3-phosphate (PI(3)P), a product of type III phosphatidylinositol 3-kinase, via an N-terminal PX domain, and that PI(3)P is generated in high levels in the phagosomal membrane, where it recruits proteins important for phagosomal maturation. To examine whether p40phox might play a role in NADPH oxidase activation during phagocytosis, we introduced a cDNA for the human FcγIIA receptor via retroviral-mediated gene transfer into COS7 cells expressing the phagocyte flavocytochrome b, p47phox, and p67phox from stable transgenes. As previously shown by a number of groups for parental COS7 cells, heterologous expression of FcγIIA enabled “COSphox” cells to ingest IgG-coated sheep red blood cells (IgG-SRBC). However, NADPH oxidase activity was not detected, using nitroblue tetrazolium as a probe to detect superoxide production, which is otherwise evident by the accumulation of intraphagosomal formazan deposits in macrophages and neutrophils undergoing phagocytosis. However, numerous NBT-positive (formazan-stained) phagosomes were seen in COSphoxFcγR cells upon transient or stable transfection of an expression plasmid for p40phox. NBT-positive phagosomes were detected within five minutes in a synchronized phagocytosis assay. Upon transient expression of derivatives of p40phox which had point missense mutations in the PX domain predicted to prevent binding of PI(3)P, only rare NBT-positive phagosomes were detected in COSphoxFcγR cells ingesting IgG-SRBC. Transient expression of p40phox derivatives with point mutations in the SH3 domain, which disrupts a potential binding site for p47phox, or in the PC motif, which should disrupt binding to p67phox, resulted in a ~2-fold reduction in the numbers of NBT-positive phagosomes. Introduction of both the SH3 and PC mutations into p40phox resulted in only rare NBT-positive phagosomes following transient transfection of the double mutant and subsequent phagocytosis of IgG-SRBC. Thus, this study identifies a role for p40phox in coupling NADPH oxidase activation to phagocytosis of IgG-coated particles. Results of experiments using mutant derivatives of p40phox suggest that its ability to interact with both PI(3)P and p47phox/p67phox are critical determinants in this process.
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