Although mammalian studies have not been conducted, there is potential for a manganese transporter gene to be a therapeutic strategy for human immunodeficiency virus (HIV) in the prevention of AIDS. Bolton etal. reported that increasing the cellular content of manganese in yeast blocks the activity of reverse transcriptase (RT).65 This key enzyme is the basis by which HIV and other retroviruses transcribe DNA from RNA when they infect normal cells. In HIV, the transcription process is the reverse of the usual copying of RNA from DNA; hence, the enzyme is named 'reverse transcriptase'. The RTs that were investigated each had docking places for two metals magnesium and manganese. Failure of these metals to dock or attach at these specific sites disrupted the functional ability of the RT. Ordinarily the cellular concentrations of magnesium are several thousand times that of manganese, but raising the manganese content only three times to that of normal reduced the activity of the RT by 50%. The elevated manganese levels were due to a defect in the gene
PMR1, a P-type ATPase that codes for the protein that transports manganese (and calcium) out of cells. Adding trace amounts of Mn2+ also inhibited the HIV-1 RT in vitro in the presence of magnesium cations. Thus, targeting this gene or its transporter protein to increase intracellular manganese could be a novel and safe approach for anti-retroviral therapy for diseases such as AIDS.
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