NSC2500: HIV-AIDS Abstract Exploring Pathophysiology and Pharmacology

This assignment presents an abstract on HIV-AIDS, detailing the disease's nature as caused by an RNA virus targeting helper T-cells, leading to immune deficiency. It discusses the role of antiretroviral drugs, particularly Zidovudine (ZDV), and their mechanism of action, along with associated side effects like hepatic toxicity and mitochondrial damage. The abstract emphasizes the importance of patient education for prevention and references relevant studies. The assignment is based on the NSC2500 course, focusing on understanding the pathophysiology of a disease and the pharmacology used to address it, aiming to improve knowledge of homeostasis, drug therapies, and communication skills.

HIV-AIDS
Abstract
HIV/AIDS: Human Immunodeficiency Virus: Acquired Immunodeficiency
Syndrome. This fatal disease is caused by RNA virus. The virus target the helper T-cells
(CD4+ T-cells) leading to rapid cell lysis and generation of immune-deficiency. The viral
target to Th cells hampers the cell-mediated immunity. The failure in the development of the
cell-mediated immunity hampers the humoral immune response and thereby causing
complete paralysis of the immune-system and making the infected person immune-
compromised (Punt et al., 2019). According to Australian Federation of AIDS Organisations
(2017), in 2017 there are 27,545 in Australia who are infected with HIV-AIDS and the
majority of which occur as a result of sexual contacts and mother to child transfusion.
The main target for the anti-retroviral drug for the treatment of HIV-AIDS is
inhibitions of the reverse transciptase (RT) that acts in conversion of viral RNA to c-DNA or
provirus. One of the popular drug (anti-retroviral drug) used for the treatment for HIV-AIDs
is Zidovudin (ZDV) or Retrovir (AZT). ZDV is a nucleoside analogue inhibits viral reverse
transcription. It is activated by intra-cellular phosphorylation. ZDV is either administered
orally or given intravenously (Chen et al., 2018). However, ZDV is associated with numerous
side effects. ZDV leads to the generation or reactive oxygen species leading to oxidative
stress and thus hampering the activity of hepatic cells and mitochondrial respiration. Hamper
in the mitochondrial respiration causes destruction in ATP followed by anaerobic respiration
and lactic acidosis. The increase in the acidic content of the body leads to cell death,
hematological toxicity along with myopathy ((Liu et al., 2019). In order to overcome hepatic
toxicity, ZDV at times is administered with silibinin, a hepato-protective drug (Raghu &
Karthikeyan, 2016).

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HIV-AIDS
For comprehensive prevention of the HIV-AIDS proper patient education is
important. Patient education will be directed towards education about safe sex, sex with
multiple partners and mother to child transmission. Proper education must also be given in
order to eradicate the myths about HIV-AIDS pathogenesis (Landefeld et al., 2018).

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HIV-AIDS
References
Australian Federation of AIDS Organisations (2017). HIV AIDS. Access date: 17th April
2019. Retrieved from: https://www.afao.org.au/australia/
Chen, S., Wang, X., Zhu, H., Tang, Q., Du, W., Cao, H., ... & Lu, W. (2018). Zidovudine-
Based Treatments Inhibit the Glycosylation of ADAM17 and Reduce CD163
Shedding From Monocytes. JAIDS Journal of Acquired Immune Deficiency
Syndromes, 79(1), 126-134.
Landefeld, C. C., Fomenou, L. A., Ateba, F., & Msellati, P. (2018). Prevention of Mother-to-
Child Transmission of HIV in Yaounde: Barrier to Care. AIDS care, 30(1), 116-120.
Lin, H., Stankov, M. V., Hegermann, J., Budida, R., Panayotova-Dimitrova, D., Schmidt, R.
E., & Behrens, G. M. N. (2019). Zidovudine-mediated autophagy inhibition enhances
mitochondrial toxicity in muscle cells. Antimicrobial agents and chemotherapy, 63(1),
e01443-18.
Punt, J., Stranford, S., Jones, P. P., & Owen, J. A. (2019). Kuby immunology. WH Freeman.
Raghu, R., & Karthikeyan, S. (2016). Zidovudine and isoniazid induced liver toxicity and
oxidative stress: Evaluation of mitigating properties of silibinin. Environmental
toxicology and pharmacology, 46, 217-226.