Human Immunodeficiency Virus (HIV) is a sexually transmitted virus. It attaches itself and penetrates its host cells known as the T-cells thereby releasing enzymes and HIV RNA into T cells. The reverse transcriptase further replicates itself into proviral DNA which also integrates itself in the host cells and thus duplicated along the DNA that hosts the proviral DNA. The integration produces HIV proteins and HIV RNA. The HIV proteins assemble into HIV virions and later budded from the surface of the cell. Viral proteins after cleaving with HIV protease converts immature virion into an infectious disease. The pathophysiology of SLE involves activation of autoreactive B cells and CD4 T cells leading to the production of autoantibodies pathogenic in nature and thus the resultant end-organ injury.

Unlike HIV which suppresses the immune response against itself, the SLE forms its autoantibodies thus forming resistant components. Moreover, the stress of being infected by HIV disorder is perceived to be a norm that helps in the prevention of the virus. On the other hand, the maladaptive response to SLE is not always adverse as the virus forms its autoantibodies that lead to a resultant end-organ injury. Besides, significant advancements have been made to help people living with HIV to adapt to the situation through the provision of medical treatments and caring for the sick.

Genetics is among the different factors that affect the pathophysiology of both HIV and systemic lupus E disorders. In HIV disorder, the variability to the HIV infection and responsiveness is controlled by the available genetic host factors including chemokines and cytokines amongst other receptors. These might cause variability in the responsiveness to ART. On the hand, the risk of developing SLE in humans is mostly contributed by various genetic factors. For instance, SLE is at times developed due to the mutations of different single genes. Besides, the genetic factors lead to heterogeneity of SLE.

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