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In untreated HIV/AIDS, the highest degree of microbial translocation has been shown in patients with severe immune depression [1], [4].

However, while patients starting HAART with high CD4+ counts present a substantial LPS/sCD14 plasma reduction that is inversely correlated with the magnitude of CD4+ recovery [1], [4], a less efficient containment of microbial translocation has been shown in naïve patients starting therapy with low CD4+ [16], [16].

Among HIV-infected patients, microbial translocation has also been found to be associated with sluggish CD4+ T-cell reconstitution in the context of HAART [ 15, 18].

In studies of predominantly well-nourished individuals, microbial translocation has been proposed as an etiology of the persistent immune activation observed in patients with both untreated and treated HIV.

In HIV-infected patients, microbial translocation has characteristic features: thus, generalized immune activation is associated with preferential loss of cell subsets involved in maintaining epithelial integrity at mucosal surfaces and antimicrobial immunity, such as the CD4+ T cells secreting IL-17 and IL-22 [ 53, 54].

Similar(55)

Sevelamer administration to acutely SIV-infected NHPs improved the levels of immune activation and coagulation [ 36]; in chronically HIV-infected patients, sevelamer did not reduce microbial translocation but had a statistical effect on soluble tissue factor, low-density lipoprotein (LDL) cholesterol, and oxidized LDL cholesterol [ 65].

Increased levels of soluble CD14, which is expressed mainly by macrophages and may be a consequence of microbial translocation [ 27], have also been related to mortality in HIV-1-infected patients [ 28].

The thermodynamic generalized forces governing the translocation have been calculated.

Surgical translocation had no apparent untoward effect on ovarian function.

Mothers carrying a translocation have a 10 12 percent risk of transmitting the genetic rearrangement to their offspring, whereas fathers carrying a translocation have a 3percentt risk of transmission.

Accumulated literatures [ 26- 29] have demonstrated that microbial translocation is a cause of systemic immune activation in chronic HIV infection, which characterized by higher levels of plasma bacterial DNA and LPS in HIV-infected patients compared to healthy controls.

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