Respond to this post Share insights on how the factor you selected impacts the pathophysiology of the disorder your colleague analyzed.

  • Suggest alternative recommendations for drug treatments.
  • Expand on your colleague’s posting by providing additional insights or contrasting perspectives based on readings and evidence.


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Pathophysiology of HIV

           Human Immunodeficiency Virus (HIV) is a blood borne pathogen passed through bodily fluid and is usually transmitted through blood, sexual activity, used needles and maternal – child transmission. HIV is a part of the retrovirus family. The person becomes infected by HIV in. someway, other than a dirty needle, most likely sexual contact. The dendritic cell picks up the HIV off the surface of the mucus membrane and test it and takes it to the lymph node to the T cell. Which is where CD4 is on of the cells that is mainly effected by HIV. This is where HIV either uses the dendritic cell to transport it to the lymph node. OR the dendritic cell is infected with HIV and then starts reproducing copy after copy of HIV.

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On the outside of the capsule there is two viral proteins (pg41 and gp120) that react or are the key to opening the CD4 and CCR5 receptor locks. HIV only has to unlock one to infect and it is pulled in and fusion with the plasma membrane happens. Now the release its capsule filled with HIV RNA into the T cell happens, now the reverse transcriptase takes the RNA and transforms with help from nucleotides to make a single and then a double strand of DNA. Because the DNA was made by reverse transcriptase it makes error which then allow the HIV DNA to become resistant to a lot of viral medication. The HIV also brings integrase with the capsule, integrase will take the double DNA and go into the nucleus and cut the original DNA and integrate the viral DNA strand and then is when it become a life long infection.

           The cell now can remain dormant which is called latent infection or MRNA is made from the infected cell to make a new T cell. These T cell will continue to repeat the process and keep making infected T cells.

Clinical Manifestation

           The manifestation of symptoms can happen in the first two to four weeks (, 2020). These symptoms may be fever, headache, joint pain, and swollen lymph glands to name a few (, 2020). Even though the viral amount is extremely high in the first few weeks the symptoms remain quite mild (, 2020).

The latent infection can last for an extended period and may not have any symptoms (, 2020). If untreated this stage can last for years but they will develop a severe disease at some point (, 2020). The reason a severe disease come on is because there are little amount of T cells.

           Symptomatic HIV infection is when the virus has killed off your immune cells and you develop more chronic signs such as diarrhea, pneumonia, and thrush (, 2020). Due to antiviral treatment most HIV does not progress into AIDS (, 2020).

Medication to Treat Symptoms of HIV

           There are nine different drug classes for medications to help treat HIV, these drugs are called antiretroviral therapy (ART) (, 2021). Even though there are nine different drug class they are all inhibitors (, 2021). They inhibit the virus from reproducing some where during its cell life (, 2021). There are nucleoside reverse transcriptase inhibitors (NRTIs), it blocks the reverse transcriptase from replicating (, 2021). Non- nucleoside reverse transcriptase inhibitors (NNRTIs), this drug alters the reverse transcriptase so it can not replicate (, 2021). Protease Inhibitor (PIs), blocks the enzyme in the release of making more cells (, 2021). Fusion inhibitors complete block HIV from even entering the CD4 cells (, 2021). CCR5 antagonist blocks the receptor so the HIV can not be pulled into the cell (, 2021) There are two receptors that can pull the cell in and this medication only blocks the main receptor not the other. Integrase strand transfer inhibitors (INSTIs), block intrgrase from cutting the original DNA, so it can but in the viral DNA (, 2021). Attachment inhibitors bind to the gp120 on the outside of the HIV capsule and prevents it from attaching to the CD4 cells plasma membrane. (, 2021). Post attachment inhibitors blocks the receptor on the cd4 surface, so HIV can’t bind (, 2021). Pharmacokinetics enhances will increase the use of one drug (, 2021). The also prescribe a combination of drugs to help fight it in multiple different areas (, 2021).

Patient’s Factors

           The patient I have chosen is a 28 year old female had a single sexual partner for eight years and was not sexually active before her partner. She is highly educated and has a good career. She is a nurse in the ICU. She came into contact with HIV when and unruly trauma patient with open wounds attacked her. She had the patient blood on her face and hands. She was unaware the patient had HIV which was found when they tested both the patient and herself. She was seen by employee health who immediately but her on an antiretroviral therapy. She is also in the process of trying to start a family, this complicates medication she can take. She was prescribed dolutegravir as well as emtricitabine These drug were also picked the dolutegravir is a integrase inhibitor so the HIV DNA can never be transcribe into a cell and the cell would self destruct. Emtricitabine is blocks the reverse transcriptase so the RNA can never be transformed into even a single strand of RNA. The side effects from these medications are headaches, back pain, and insomnia. She receives test weekly to test her CD4 count and watch for HIV. 


Khan Academy Medicine (Director). (A). (2015, June 26).How hiv infects us: Cd4 (t-helper) lymphocyte infection | nclex-rn | khan academy[Video file]. Retrieved March 24, 2021, from

Khan Academy Medicine (Director). (B). (2015

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