Pathophysiology. Age and the Pathophysiology of HIV and SLE

Pathophysiology
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Age and the Pathophysiology of HIV and SLE
Human immunodeficiency virus (HIV) is a viral infection caused by a retroviral of the family retroviridae. The causative agent of HIV attaches itself to the epithelial and macrophage cell surface glycoproteins (Honeycutt et al., 2016). Afterward, the virus penetrates the cell and takes advantage of the host cellular respiratory and metabolic mechanisms to replicate. In particular, the virus uses the transcription and translation pathways in the host cells to make proteins that allow its further replication. Once the proteins are produced, the virus reassembles itself, kills the host cell and enters the bloodstream to infect other cells. HIV infects and kills T helper cells of the body. Since these cells are in the frontline in the fight against diseases, body immunity is compromised, and the patient becomes more susceptible to multiple opportunistic infections (Honeycutt et al., 2016).
Systemic Lupus Erythromatosus (SLE) is an autoimmune disorder where the body produces antibodies against its proteins. The antibody-antigen complexes formed from this autoimmune process are deposited in many areas of the body causing widespread systemic organ damage. In the kidneys, the complexes damage the nephrons causing lupus nephrosis (Bomback, Appel & Pisetsky, 2017).
In HIV, maladaptive responses include depression, school dropout, drug and substance abuse, and enhanced chances of dise...