Human Immunodeficiency Virus (HIV) and Systemic lupus erythematosus are disorders of the immune system that trigger responses that promote their progression. This paper aims at discussing the two disorders with reference to their pathophysiology and responses triggered.
HIV is a retrovirus that impinges on the immune system by destroying the CD4+T cells. There are three phases of HIV: primary HIV acute infection, latency phase and AIDS. In the three stages, the CD4+T cells gradually reduce, giving way to opportunistic infections (Porth, 2011). The virus destroys the CD4+T cells by attaching to the CD4+T cells receptors and fusing with these cells so that it becomes easy to enter. Subsequently, it introduces its RNA into the DNA of the CD4+T cells and uses this DNA to replicate itself in large numbers.
Systemic lupus erythematosus (SLE) entails immune responses against endogenous nuclear antigens (Porth, 2011, p. 479). Apoptotic cells (dendritic cells in the figure below) release autoantigens to T cells, thereby activating the T cells. The activated T cells trigger the B cells to release antibodies by producing cytokines, for example, interleukin 10 and 23. In addition, cell surface molecules including CD40L and CTLA-4 release antibodies.
The HIV virus destroys the CD4+T cells by attaching to the CD4+T cells receptors and fusing with these cells so that it becomes easy to enter. Subsequently, it introduces its RNA into the DNA of the CD4+T cells and uses this DNA to replicate itself in large numbers (Porth, 2011). The RNA of the HIV virus escapes action from antiviral RNAi action. Elevated production of apoptosis-related endogenous nucleic acids triggers the release of IFNα and foster autoimmunity in SLE.
This increased apoptosis action subsequently interferes with self-tolerance by activating antigen-presenting cells as shown in the figure below. Normally, in healthy tissue, this increase in the amount of immune reactants and complexes is usually cleared by Fc and complement responses. However, in the case of SLE, the body is not able to clear these reactants resulting in tissue deposition and injury. Tissue damage is catalyzed by various processes that entail “modulation of the coagulation cascade, production of inflammatory cytokines, recruitment of inflammatory cells, and reactive oxygen intermediates” (Bertsias, Cervera, Boumpas, 2012, p. 480).
HIV proliferates within the body through incorporation of its RNA into the DNA of the CD4+T cells. On the other hand, inflammation is enabled in SLE through increased production of immune reactants
Two genetic forms of HIV prevail: HIV-1 and HIV-2. The HIV-1 is prevalent in US, central Africa, and Europe, while HIV-2 is the principal HIV type in western Africa. Unlike SLE, HIV is not genetically determined. Children born to parents with SLE are 30-fold more susceptible to SLE than individuals born to parents without SLE.
Both HIV-1 and HIV-2 are transmitted in the same way, and their pathogenesis is the same, but the spread of HIV-2 is slower compared to that of HIV-1 (Porth, 2011, p. 365). Despite the fact that the origin of HIV is puzzling, it circulates within the human species through sexual contact, blood transfusion and mother-to-child (U. S. National Library of Medicine, 2014).
Both the HIV and SLE are detrimental diseases that interfere with the gear of the body, which is the immune system. The HIV disease is initiated by a virus whereas SLE is triggered by antigens.
Bertsias, G., Cervera, R., Boumpas, D. (2012). Systemic Lupus Erythematosus: Pathogenesis and Clinical Features. In J. Bijlsma (Ed.). EULAR Textbook of Rheumatic Diseases (476-505). London: BMJ Group.
Porth, C. (2011). Essentials of Pathophysiology: Concepts of Altered Health States. Philadephia: Lippincott Williams & Wilkins.
U. S. National Library of Medicine. (2014). Hiv infection. Web.