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Parasites
Though not thought about as much as viruses or bacteria, parasites are behind much sickness and suffering in both animals and humans all over the world. Parasites range from microscopic protozoans to insects like ticks and lice and intestinal worms. What they all have in common is that their survival comes at the expense of other living things. This book gives readers a solid introduction to these unpleasant but fascinating organisms, describes how they lead to illness, and discusses preventative measures and cures. Detailed Table of Contents, Full-Color Photographs, Further Information Section, Glossary, Index, Safety Tips, Sidebars, Websites.
Book
What's eating you? : parasites--the inside story
Mites and lice, fleas, ticks, and tapeworms -- most living creatures that have a habitat also are a habitat, including you (are you itchy yet?). Unwelcome guests -- parasites -- are everywhere, from the barnacles hitching a ride on a humpback whale's head to the tiny flies that control a bee's brain and make it literally dig its own grave. Now an expert team returns for an in-depth look at how these insidious critters do it, whether it's leaping aboard moving targets or morphing their body shapes, and what their unwitting hosts have learned to do to fight back and reclaim their space.
Book
Zoom in on body invaders
\"Get an up-close look at some of the creatures that live in and on your body\"--Provided by publisher.
Book
The Antigen-Presenting Potential of Vγ9Vδ2 Cells During Plasmodium falciparum Blood-Stage Infection
During Plasmodium falciparum infections, erythrocyte-stage parasites inhibit dendritic cell maturation and function, compromising effective antimalarial adaptive immunity. Human Vγ9Vδ2 T cells can act in vitro as antigen-presenting cells (APCs) and induce αβ T-cell activation. However, the relevance of this activity in vivo has remained elusive. Because Vγ9Vδ2 T cells are activated during the early immune response against P. falciparum infection, we investigated whether they could contribute to the instruction of adaptive immune responses toward malaria parasites. In P. falciparum–infected patients, Vγ9Vδ2 T cells presented increased surface expression of APC-associated markers HLA-DR and CD86. In response to infected red blood cells in vitro, Vγ9Vδ2 T cells upregulated surface expression of HLA-DR, HLA-ABC, CD40, CD80, CD83, and CD86, induced naive αβ T-cell responses, and cross-presented soluble prototypical protein to antigen-specific CD8⁺ T cells. Our findings qualify Vγ9Vδ2 T cells as alternative APCs, which could be harnessed for therapeutic interventions and vaccine design.
Journal Article
Initiation of gemetocytogenesis at very low parasite density in Plasmodium falciparum infection
The recent focus on the elimination of malaria has led to an increased interest in the role of sexual stages in its transmission. We introduce Plasmodium falciparum gametocyte exported protein-5 (PfGEXP5) transcript analysis as an important tool for evaluating the earliest (ring) stage sexual gametocytes in the blood of infected individuals. We show that gametocyte rings are detected in the peripheral blood immediately following establishment of asexual infections—without the need for triggers such as high-density asexual parasitemia or drug treatment. Committed gametocytes are refractory to the commonly used drug piperaquine, and mature gametocytes reappear in the bloodstream 10 days after the initial appearance of gametocyte rings. A further wave of commitment is observed following recrudescent asexual parasitemia, and these gametocytes are again refractory to piperaquine treatment. This work has implications for monitoring gametocyte and transmission dynamics and responses to drug treatment.
Journal Article
Blood Gene Signatures of Changas Cardiomyopathy With or Without Ventricular Dysfunction
Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, affects 7 million people in Latin American areas of endemicity. About 30% of infected patients will develop chronic Chagas cardiomyopathy (CCC), an inflammatory cardiomyopathy characterized by hypertrophy, fibrosis, and myocarditis. Further studies are necessary to understand the molecular mechanisms of disease progression. Transcriptome analysis has been increasingly used in identify molecular changes associated with disease outcomes. We thus assessed the whole-blood transcriptome of patients with Chagas disease. Microarray analysis was performed on blood samples from 150 subjects, of whom 30 were uninfected control patients and 120 had Chagas disease (1 group had asymptomatic disease, and 2 groups had CCC with either a preserved or reduced left ventricular ejection fraction [LVEF]. Each Chagas disease group displayed distinct gene expression and functional pathway profiles. The most different expression patterns were between CCC groups with a preserved or reduced LVEF. A more stringent analysis indicated that 27 differentially expressed genes, particularly those related to natural killer (NK)/CD8+ T-cell cytotoxicity, separated the 2 groups. NK/CD8+ T-cell cytotoxicity could play a role in determining Chagas disease progression. Understanding genes associated with disease may lead to improved insight into CCC pathogenesis and the identification of prognostic factors for CCC progression.
Journal Article