Week 2: Allison [Following the Story of HIV]

 Did it start when a chimpanzee bit a human hunter in the forests of West Africa? Or perhaps when a butcher some day cut himself while preparing bushmeat of primate origin in the blazing heat? Either way or infinite ways, at some point a version of Simian Immunodeficiency Virus (SIV) jumped the species barrier from chimp to human where it mutated from a non-pathogenic virus into HIV-1 which would then go on to infect an estimated 1.1 million people in the United States. 

Fast forward to last week shadowing clinical rounds at Lower Manhattan Hospital with Dr. Carrie Johnston. A hypothetical patient of hers with uncontrolled HIV, diagnosed AIDs, substance addiction and abuse is at the ICU. Every doctor congregating to talk about their case - cardiologists, nurses, physician assistants, and now an infectious disease specialist- acknowledges that this patient is in bad shape. They came in with a high fever, pneumonia that had spread into the bloodstream - sepsis- and tachycardia -low heart rate- possibly due to the methadone they take to help manage their substance abuse. Their CD4 T-cell count was in the 100s range instead of the preferable higher range of 800 to 1000. Several IVs bags were hung off to the side, their contents full of antibiotics slowly being injected into their bloodstream. 


Dr. Johnston disinfected her hands and walked in.

“Hello, It’s me, Dr. Johnston. How are you feeling? Is anything better than it was when we last saw you? What happened? “Do you have anyone you would feel comfortable calling right now? You’re in bad shape right now, but we are going to do our best to make you healthy again, okay?”

Dr. Johnston empathetically repeated the series of questions again and the patient, overwhelmed and exhausted, began to cry.

“I just want to be better.”


On Wednesday, Dr. Glesby explained to me the mechanism of action of HIV, the disease I’ve been observing all this time in patients with controlled viral loads, uncontrolled viral load, the elderly, the young, and the very sick. It starts when an HIV virus in the human bloodstream encounters a CD4 T-cell. Interactions between receptors on the cell surface and the virus glycoproteins allow for the endocytosis of the virus into the immune cell where it uses reverse transcriptase to turn it’s viral RNA into DNA that can integrate with the host genome. Everytime the genetic code of the infected cell is activated, it produces in turn more and more of the virus , making this a permanent genetic change by viral nucleic acid integration. As the viral load increases, the t-cell count decreases, making patients like the hypothetical example above at risk for opportunistic infections and cancers in the face of a failing immune system.


Tune in next time to learn more about the antiretroviral medications used to intervene in HIV and prevent AIDS.

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