This chemical screen showed that a compound known as digoxin — a plant - derived cardiac toxin often used to treat various heart conditions — inhibited
wild type HIV - 1 more than the mutated strain.
These are the same T cell genes inhibited by digoxin, and since replication of integrated HIV - 1 requires transcription of nearby genes, this provides an explanation for why
wild type HIV - 1 is more susceptible to digoxin: digoxin represses the genes that the virus more frequently targets for integration.
Further analysis showed that
wild type HIV - 1 tends to integrate itself into or near genes affecting CD4 + T cell activation and metabolism more frequently than does the mutant strain.
Not exact matches
If it did get into the blood, where normal
HIV thrives, such a virus would not replicate as efficiently as
wild -
type HIV.
In the new study, Alexander Zhyvoloup of University College London, U.K., and colleagues sought to gain more insight into the life cycle of
HIV - 1 by comparing a normal, «
wild type» strain of the virus to a mutated strain.
To determine whether ZFN - mediated disruption of cxcr4 indeed protects CD4 + T cells from an in vitro
HIV challenge, human CD4 + T cells from three different ccr5
wild type donors were stimulated and transduced with AdX4 - ZFNs or an AdR5 - ZFNs control.
In the absence of
HIV infection, the cxcr4 disruption frequency remained stable over time in four independent experiments testing four different ccr5
wild type donors as measured by deep sequencing.
Thus, treatment with X4 - ZFNs of both
wild -
type and ccr5Δ32 CD4 + T cells confers stable cxcr4 disruption and a marked survival advantage in the presence of R5X4 -
HIV and X4 -
HIV in vitro without any detectable effect on cell growth or viability in the absence of
HIV.
They observed a significant decrease in the number of proliferating stem cells in the brains of
HIV / gp120 - mice compared with similar tissue from normal,
wild -
type mice.