Cells and their membrane-the lock and key

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SUMMARY

This discussion centers on the mechanisms of HIV infection and the unique case of an individual who carries the virus without developing AIDS due to a lack of functional protein channels in his cells. The conversation highlights the role of the CD4 receptor in T-lymphocytes, which HIV targets to inject its genetic material. It concludes that the individual’s resistance to AIDS may stem from a mutation in the receptor, preventing the virus from hijacking the immune system's cellular machinery. The discussion raises questions about alternative transport mechanisms for larger molecules in the absence of integral membrane proteins.

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  • Understanding of cell membrane structure and function
  • Knowledge of HIV infection mechanisms and retroviral biology
  • Familiarity with T-lymphocyte roles in the immune system
  • Basic concepts of exocytosis and endocytosis
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  • Research the role of CD4 receptors in HIV infection
  • Explore genetic mutations that confer resistance to HIV
  • Study the processes of exocytosis and endocytosis in cellular transport
  • Investigate the implications of retroviruses on immune system function
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Biologists, immunologists, medical researchers, and anyone interested in the mechanisms of viral infections and cellular biology.

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Cells and their membranes-the lock and key

So in biology we were discussing cell membranes and the effects and processes viruses impose on the cell. Take lytic infection for example-in basic terms attaching to the cell, using one of the cells protein channels in the phospholipid bilayer and injecting its genetic material thus using the cell as a factory to make copies. Well this one man, whose name I shall not mention mainly because I do not remember, had the HIV virus but never got AIDS. The reason being because the man had no protein channels in his cells. Therefore there was no way of getting the genetic material into the cell. Leave diffusion across the membrane out of the question since RNA and DNA are not selectively permeable to it. And more interesting is how he lived. How were larger molecules and such transported in and out of the cell without the integeral membrane proteins? Maybe proteins and larger molecules could be exported and imported through exo and endo cytosis but other than that I could not see how he lived. That, if anyone is willing to answer, is an answer I am still looking for.
 
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You're right, this is absurd. I'm not familiar with specific HIV recognition sites or channels but perhaps the one targeted by it was sufficiently mutated in this person to block it. I am not sure how it would do that and not block whatever it was supposed to do though.
 
HIV is a retrovirus that hijacks your immune system's cellular machinery. On the HIV viron are specific glycoproteins that bind to receptor proteins (eg. CD4 receptor) on T-lymphocytes. After the binding of the glycoprotein and receptor occures, penetration occurs and the HIV loads all of its cellular contents into the T-cell (viral RNA, reverse transcriptase, integrase). The reverse transcriptase starts to make a cDNA template from the viral RNA, and integrase integrates the viral DNA into the DNA of the T-cell. The infected T-cell that reproduces its DNA as if nothing happened, hence replicating viral DNA. After transcription we get more viral RNA and they pinch off the T-cell as new virons and start to affect other cells.

AIDS develops when the HIV virons affect a critical level of T-cells in your body, compromising your immune system and causing it to collapse. The man who didn't get AIDS from HIV could have a mutated receptor on his T-cells, or not have a receptor at all (latter not likely). The man could still have normal transportation of stuff in and out of his cells, but HIV could not affect his immune system because of a faulty receptor.

K.
 

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