Introduction: is the protozoan parasite causing Chagas disease, a Neglected Tropical Disease that affects 8 million people and causes 12,000 deaths per year, primarily because of cardiac pathology. Effective vaccination for remains an elusive goal. The use of a live vaccine vector, especially one that mimics the pathogen target, may be superior to the use of recombinant protein or DNA vaccine formulations.
View Article and Find Full Text PDFis a micro-organism well known to cause pseudomembranous colitis with rare extraintestinal manifestations. We present the case of an elderly male with multiple comorbidities who presented with acute onset of fever/chills and hypotension, found to have polymicrobial bacteraemia with and He was treated with piperacillin/tazobactam for bacteraemia, oral vancomycin for colitis and intravenous, followed by oral metronidazole for bacteraemia. cleared after 1 day, and cleared after 4 days.
View Article and Find Full Text PDFBackground: Cytomegalovirus (CMV) end-organ disease (EOD) continues to pose a significant risk to patients with advanced HIV disease despite decreased incidence with combination anti-retroviral therapy (ART) and lower mortality with effective -CMV therapy. Subclinical CMV shedding may also contribute to ongoing inflammation and non-infectious comorbidities.
Methods: We examined the occurrence of CMV EOD and CMV shedding in a cohort of patients participating in a prospective observational study of severely immunosuppressed (CD4 ≤100 cells/μl), ART-naïve, HIV-1 infected adult participants.
Trypanosoma cruzi is the intracellular parasite of Chagas disease, a chronic condition characterized by cardiac and gastrointestinal morbidity. Protective immunity requires CD4 T cells, and Th1 cells and gamma interferon (IFN-γ) are important players in host defense. More recently, Th17 cells and interleukin 17A (IL-17A) have been shown to exert protective functions in systemic T.
View Article and Find Full Text PDFThe usage of combination antiretroviral therapy in people with HIV (PWH) has incited profound improvement in morbidity and mortality. Yet, PWH may not experience full restoration of immune function which can manifest with non-AIDS comorbidities that frequently associate with residual inflammation and can imperil quality of life or longevity. In this review, we discuss the pathogenesis underlying chronic inflammation and residual immune dysfunction in PWH, as well as potential therapeutic interventions to ameliorate them and prevent incidence or progression of non-AIDS comorbidities.
View Article and Find Full Text PDFPersistent viral activity may cause enduring seropositivity and inflammation in treated people with HIV (PWH). We compared inflammatory biomarkers between early treated PWH who remained seronegative or seroconverted and found similar levels of D-dimer, soluble cluster of differentiation 14, C-reactive protein, and interleukin-6, indicating that seronegativity does not affect chronic inflammation in early treated PWH.
View Article and Find Full Text PDFCell Mol Gastroenterol Hepatol
January 2018
Background & Aims: Atrophic gastritis caused by chronic inflammation in the gastric mucosa leads to the loss of gastric glandular cells, including acid-secreting parietal cells. Parietal cell atrophy in a setting of chronic inflammation induces spasmolytic polypeptide expressing metaplasia, a critical step in gastric carcinogenesis. However, the mechanisms by which inflammation causes parietal cell atrophy and spasmolytic polypeptide expressing metaplasia are not well defined.
View Article and Find Full Text PDFTh17 cells are a subset of CD4+ T cells known to play a central role in the pathogenesis of many autoimmune diseases, as well as in the defense against some extracellular bacteria and fungi. However, Th17 cells are not believed to have a significant function against intracellular infections. In contrast to this paradigm, we have discovered that Th17 cells provide robust protection against Trypanosoma cruzi, the intracellular protozoan parasite that causes Chagas disease.
View Article and Find Full Text PDFNucleos(t)ide analog drugs profoundly suppress Hepatitis B virus (HBV) replication but rarely cure the infection, so therapy is usually life-long. The nucleos(t)ide analogs inhibit the viral DNA polymerase and often push HBV to the brink of extinction, so it may be possible to eradicate HBV by suppressing HBV replication further. The HBV ribonuclease H (RNaseH) is a logical new drug target because it is the second of only two viral enzymes essential for viral replication.
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