HIV-1 Vpu protein

A summary of an article on PLoS:

Mutations of Vpu that confer resistance to this degradation process enhance viral particle release, whereas the determinant of Vpu turnover is paradoxically well conserved among HIV-1 isolates. These results suggest that the virus is constrained to limit its own production for long-term persistence.

Further on:

This may in turn reflect that long-term persistence of the virus requires the optimal balance between efficient viral production and host cell viability. In light of our present study, the regulated degradation process of Vpu is expected to be lost in the viral strains naturally mutated at the relevant phosphorylation site. Whether these strains show higher pathogenicity will be interesting to address for our better understanding of the constraints that govern the relation between HIV-1 and the human organism.

I look forward to reading the next article studying if HIV becomes more pathogenic by losing the ability to regulate the degradation of Vpu through natural mutation.