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Page #27



MA: And so it went. The decades have past and we have made great strides in many medical fields but this deadly HIV virus has thrived in our midst.

But that is not surprising considering that it lives to destroy our immune system and kill human beings.

I understand that bugs have no drive and no destiny, but this deadly bit of RNA frightens me.

What we have learned is not good. It hides out for years in long term memory cells multiplying and waiting for an opportunity to re-emerge and ravage the carrier.

It has actually developed numerous strategies for eluding the body's defenses and our best medications. We also know that HIV modifies the cell structure system of the host cells enabling them to enter the cells more easily.

HIV especially attacks immune cells of the T-helper type. These cells support not only direct defense against the bugs, but are also necessary for building sufficient antibodies against the invader. For this, they must rely on their mobility.

The cell structure element actin, which also gives muscles their mobility, aids in the motility of immune cells. This is necessary for immune cells to be able to establish contact with each other and combat the virus.

And now we discover that cell mobility is inhibited by the HIV Nef protein.

Nef causes an enzyme that normally has nothing to do with cell mobility to deactivate a regulator for actin regeneration. Nef therefore causes a short-circuit of two cellular mechanisms, thus inhibiting the reorganization of the cell structure element actin and the cell's ability to move. Thus, the affected immune cells can no longer fulfill their function.

MA: Do you understand how important that is?

Q: I guess that by short-circuiting the method that the immune cell uses to have good mobility the HIV virus prevents the body from mounting a good defense.

MA: Well yes, but the negative effect of Nef on the mobility of T-helper cells also has far reaching consequences for the efficient formation of antibodies by B-lymphocytes in the patient.

We often see a malfunction of B-lymphocytes in AIDS patients and now we understand why.

It is not this one extraordinary thing about HIV but the multitude of functions and abilities that gives me great pause and eventually intrigued me enough to study the mechanism of HIV virulence.

Q: I see Ė and that is going to bring us around to your theory on Neuraminidase isnít it?

MA : Yes it is.






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