Since the virus incorporates its genome into the host cell, I think inhibiting all or some of host cell transcription factors could be a potential target for HIV proliferation.
Does it mean you are trying to curtail HIV replication by curtailing T-cell proliferation or activity. This for me is like keeping HIV in dormant stage, I don't think HIV to be susceptible to such cellular inactivity. They still persist in them and spill out on the death of the cell. Once the virus has integrated I don't think curtailing the cell response can bring virus proliferation to a halt. The tactics needed if at all one can curtail them, is even before one round of protein synthesis post-integration, ie., formation of mature viruses in the cell. The cell has to be killed before such production after the virus integrates. Here the genome(viral) dies with cell.
I was hoping that halting the transcriptional ability of T-cells to make its needed proteins will subsequently destroy the cell together with incorporated viral genome. Then after, the thymus can be induced to produce more T-cells
That is a good idea but how can one differentiate the infected and uninfected T-cell before halting transcription.
Else u will be inactivating all T cells.
Leading to loss of immunity and making the host susceptible rather than the virus.
I think differentiating such cells is the challenge (targeting cells), than identifying drug target.
That's is correct. Thank you so much for your responses. I appreciate it
The secret lies in inhibiting Nuclear factor kappa b, which activates the HIV transcription in the CD4 T-Cells
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