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A key distinction of natural SIV infections is a rapidly developing anti-inflammatory milieu that prevents chronic activation, apoptosis and proliferation of T cells and preserves the function of other immune cell subsets, thus contributing to the integrity of the mucosal barrier and the lack of microbial translocation from the gut to the peritoneum.
Microbial translocation from a leaky gut may contribute to immune activation during chronic HIV infection [11] [15].
Elevated plasma lipopolysaccharide (LPS), an indicator of microbial translocation from the gut, is a likely cause of systemic immune activation in chronic HIV infection.
These findings also suggest that measurements of microbial translocation from peripheral blood are likely to be both underestimates of intestinal translocation and significantly confounded by liver disease.
Increased microbial translocation from the gut during periods of viral rebound may contribute to increased concentrations of inflammatory markers (i.e. tumour necrosis factor alpha and interleukin-6) within the liver parenchyma contributing to increased fibrosis progression 45.
Plasma lipopolysaccharides (LPS), indicators of microbial translocation from the gut, induce monocyte activation in HIV infection and may contribute to HIV-associated dementia (HAD) by increased trafficking of activated monocytes into the brain [ 65].
Similar(49)
Amongst numerous causes, microbial translocation (MT) from the gut has been shown to substantially contribute to liver disease in several clinical settings such as alcoholic liver disease, and other enteric processes [ 1- 4].
Such material may be derived from microbial translocation, as well as from HIV virions.
Also referred to as "leaky gut," microbial translocation can result from reduced host immunity and/or increased permeability of the intestinal lining and has been shown in a number of infectious and noninfectious chronic inflammatory diseases, including celiac disease, inflammatory bowel disease, and hepatitis B and hepatitis C [ 197– 197].
'Microbial translocation' of bacterial products from a disturbed gastrointestinal tract has been proposed as a driver of HIV-associated chronic immune activation[2], which in turn predicts progression to AIDS[16].
We enrolled a subset of trial participants from Zambia into a prospective cohort to evaluate markers of intestinal permeability, microbial translocation, and systemic inflammation from recruitment through the first 12 weeks of ART (inclusive of nutritional supplementation from enrollment to 6 weeks after starting ART).
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