Hepatitis B and C in dialysis units in Kosova |
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Authors: | Skender Telaku Hajrullah Fejza Ymer Elezi Teuta Bicaj |
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Institution: | 1. Academy of Military Medical Science, Institute of Disease Control and Prevention, 100071, Beijing, PR China 2. 302 Hospital of People's Liberation Army, 100039, Beijing, PR China 3. Department of Epidemiology, Chinese Center for Disease Control and Prevention, 100050, Beijing, PR China 4. State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, 100071, Beijing, PR China
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Abstract: | Background The complement system is one of the most potent weapons of innate immunity. It is not only a mechanism for direct protection against invading pathogens but it also interacts with the adaptive immunity to optimize the pathogen-specific humoral and cellular defense cascades in the body. Complement-mediated lysis of HIV is inefficient but the presence of HIV particles results in complement activation by the generation of many C3-fragments, such as C3dg and C3d. It has been demonstrated that activation of complement can enhance HIV infection through the binding of special complement receptor type 2 expression on the surface of mature B cells and follicular dendritic cells. Presentation of the hypothesis Previous studies have proven that the complement-mediated antibody-dependent enhancement of HIV infection is mediated by the association of complement receptor type 2 bound to the C3 fragment and deposited on the surface of HIV virions. Thus, we hypothesize that a new activator of complement, consisting of a target domain (C3-binding region of complement receptor type 2) linked to a complement-activating human IgG1 Fc domain (CR2-Fc), can target and amplify complement deposition on HIV virions and enhance the efficiency of HIV lysis. Testing the hypothesis Our hypothesis was tested using cell-free HIV-1 virions cultivatedin vitro and assessment of virus opsonization was performed by incubating appropriate dilutions of virus with medium containing normal human serum and purified CR2-Fc proteins. As a control group, viruses were incubated with normal human serum under the same conditions. Virus neutralization assays were used to estimate the degree of CR2-Fc-enhanced lysis of HIV compared to untreated virus. Implications of the hypothesis The targeted complement activator, CR2-Fc, can be used as a novel approach to HIV therapy by abrogating the complement-enhanced HIV infection of cells. |
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