Case #5: Charlie Xi is a 58-year-old Asian male who is a mechanical engineer at a large telecom company. He has come to your medical office because a week ago he noticed dark colored lesions on his inner thighs, which have increased in number and size. For the last three months he has been feeling weaker and more fatigued than usual; his weight during that period dropped from 170 to 155 pounds. Mr. Xi quit smoking over 20 years ago and is currently a social drinker (one to two drinks with friends). He used to be a heavy drinker (two to three drinks per night), but ten years ago he cut down his alcohol consumption due to a fatty liver diagnosis (>10% fat in liver). Otherwise, he is fairly healthy. He swims for 30 minutes every day during the weekdays and on weekends he goes on two- to three-mile walks with his wife. Charlie’s wife is 54 and has rheumatoid arthritis; they have a healthy 28-year-old son. His father died at age 80 from complications due to Alzheimer’s disease and his mother died at age 68 from intestinal cancer.
Mr. Xi’s blood was drawn and a standardized blood test was conducted. His white-blood cell count was low at 1,000 white-blood cells/mL (normal 3,500–10,500). A biopsy was taken of a lesion and grown in cell culture. After three days of growth the cells were confirmed as coming from malignant cancerous tissue. A magnetic resonance image (MRI) of the area around the skin lesions on Mr. Xi’s inner thigh revealed enlarged lymph nodes, a sign of potential metastasis. DNA sequencing of the lesion biopsy revealed DNA consistent with human herpesvirus 8, also known as Kaposi’s sarcoma-associated herpesvirus, leading to the diagnosis of Kaposi’s sarcoma. His blood tests were indicative of his underlying infection.
-AIDS:- (auto immune defeciency syndrome)
-loss of weight.
-low WBC count
-kaposi sarcoma occurs in HIV infected patients
CD4 less than 200cells/mm3.
-DNA consistent with HHV8
A protein present on the outside of infection-fighting white blood cells. CD4 receptors allow HIV to bind to and enter cells
-the immunity of the patient is decreased
- more than three month,
Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTIs)
NRTIs force the HIV virus to use faulty versions of building blocks so infected cells can't make more HIV.
Non-nucleoside Reverse Transcriptase Inhibitors (NNRTIs)
Binding and Fusion: HIV begins its life cycle when it binds to a CD4 receptor and one of two co-receptors on the surface of a CD4+ T-lymphocyte. The virus then fuses with the host cell. After fusion, the virus releases RNA, its genetic material, into the host cell.
Reverse Transcription: An HIV enzyme called reverse transcriptase converts the single-stranded HIV RNA to double-stranded HIV DNA. Integration: The newly formed HIV DNA enters the host cell's nucleus, where an HIV enzyme called integrase "hides" the HIV DNA within the host cell's own DNA. The integrated HIV DNA is called provirus. The provirus may remain inactive for several years, producing few or no new copies of HIV.
NRTIs inhibits reverse transcriptase and helps in chain termination.
Transcription: When the host cell receives a signal to become active, the provirus uses a host enzyme called RNA polymerase to create copies of the HIV genomic material, as well as shorter strands of RNA called messenger RNA (mRNA). The mRNA is used as a blueprint to make long chains of HIV proteins.
Assembly: An HIV enzyme called protease cuts the long chains of HIV proteins into smaller individual proteins. As the smaller HIV proteins come together with copies of HIV's RNA genetic material, a new virus particle is assembled. Budding: The newly assembled virus pushes out ("buds") from the host cell. During budding, the new virus steals part of the cell's outer envelope. This envelope, which acts as a covering, is studded with protein/sugar combinations called HIV glycoproteins. These HIV glycoproteins are necessary for the virus to bind CD4 and co-receptors. The new copies of HIV can now move on to infect other cells.
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