Evidence for non‐adaptive immune response in HIV infection

Abstract

Increased levels of soluble forms of adhesion molecules such as intercellular adhesion molecule 1 (ICAM-1) and E-selectin have been found in the sera of HIV-infected patients and have been associated with disease progression. The aim of the present study was to investigate whether this phenomenon reflects activation of the non-adaptive immune response in HIV infection. Fifty-one patients with HIV infection (42 men, nine women) were classified into two subgroups: those with HIV infection but without evidence of AIDS indicator conditions (HIV infected non-AIDS cases, n = 27) and those with AIDS (AIDS cases, n = 24). The activation of non-adaptive immune response was evaluated as the production of reactive oxygen species that cause lipid peroxidation, which was assessed by measuring thiobarbituric reactive substances (TBARS) using the thiobarbituric acid assay (TBA). Plasma levels of von Willebrand factor (vWF), measured by rocket immunoelectrophoresis, were used to show activation of endothelial cells even in the absence of any other causative agent, in these patients. TBARS levels in non-AIDS cases were significantly higher than in control subjects (n = 17) or AIDS cases (P < 0.001). The mean vWF levels were higher in AIDS cases than in non-AIDS cases or normal subjects (P < 0.05). TBARS levels remained significantly higher in non-AIDS cases after adjusting for age, CD4 T-cell and neutrophil counts, antiretroviral therapy and vWF plasma levels. The above findings indicate that in HIV infection, the virus per se is responsible for the increased oxidative stress that in turn activates various transduction pathways, may be leading to endothelial cell activation and shedding of adhesion molecules from the cell surface.

Infection as a cause of early relapse in patients recovering from thrombotic thrombocytopenic purpura

“…It is postulated that bacterial endotoxins, cytokine release, and antibodies to the bacteria may induce recurrence. Increased plasma levels of von Willibrand factor have been reported in a wide variety of disease states including bacterial or viral infection [19,20]. In addition, a study by Bernado et al showed that inflammatory cytokines such as tumour necrosis factor a (TNF a) and interleukin 8 (IL-8) may stimulate ULVWF release, while interleukin 6 (IL-6) inhibited ULVWF cleavage resulting in the accumulation of hypereactive ULVWF in plasma and on the surface of endothelial cells [21].…”

Anti-phospholipid Antibodies in HIV Infection and SLE With or Without Anti-phospholipid Syndrome: Comparisons of Phospholipid Specificity, Avidity and Reactivity with β2-GPI

“…The aCL antibodies in particular, recognize oxidized CL more strongly than reduced CL. This finding, in conjunction with the increased oxidative stress found in HIV-infected individuals [42], may further explain the aPL antibody generation as the result of neoepitope formation by oxidized PLs [43,44].…”

ADAMTS13: a new link between thrombosis and inflammation

“…Increased plasma VWF levels have been reported in diseases implicating infl ammation, such as rheumatoid arthritis ( 36 ), viral and bacterial infections ( 37,38 ), coronary artery disease ( 39 ), and ischemic stroke ( 40 ). In addition, several studies suggest that infl ammation is accompanied by a decrease in ADAMTS13 activity ( 41 ).…”