The gene product Murr1 restricts HIV-1 replication in resting CD4+ lymphocytes

Lakshmanan Ganesh, Ezra Burstein, Anuradha Guha-Niyogi, Mark K. Louder, John R. Mascola, Leo W. J. Klomp, Cisca Wijmenga, Colin S. Duckett and Gary J. Nabel ()
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Lakshmanan Ganesh: Vaccine Research Center, NIAID, National Institutes of Health
Ezra Burstein: Vaccine Research Center, NIAID, National Institutes of Health
Anuradha Guha-Niyogi: Vaccine Research Center, NIAID, National Institutes of Health
Mark K. Louder: Vaccine Research Center, NIAID, National Institutes of Health
John R. Mascola: Vaccine Research Center, NIAID, National Institutes of Health
Leo W. J. Klomp: University Medical Center Utrecht
Cisca Wijmenga: University Medical Center Utrecht
Colin S. Duckett: University of Michigan, Medical Science I
Gary J. Nabel: Vaccine Research Center, NIAID, National Institutes of Health

Nature, 2003, vol. 426, issue 6968, 853-857

Abstract: Abstract Although human immunodeficiency virus-1 (HIV-1) infects quiescent and proliferating CD4+ lymphocytes, the virus replicates poorly in resting T cells1,2,3,4,5,6. Factors that block viral replication in these cells might help to prolong the asymptomatic phase of HIV infection7; however, the molecular mechanisms that control this process are not fully understood. Here we show that Murr1, a gene product known previously for its involvement in copper regulation8,9, inhibits HIV-1 growth in unstimulated CD4+ T cells. This inhibition was mediated in part through its ability to inhibit basal and cytokine-stimulated nuclear factor (NF)-κB activity. Knockdown of Murr1 increased NF-κB activity and decreased IκB-α concentrations by facilitating phospho-IκB-α degradation by the proteasome. Murr1 was detected in CD4+ T cells, and RNA-mediated interference of Murr1 in primary resting CD4+ lymphocytes increased HIV-1 replication. Through its effects on the proteasome, Murr1 acts as a genetic restriction factor that inhibits HIV-1 replication in lymphocytes, which could contribute to the regulation of asymptomatic HIV infection and the progression of AIDS.

Date: 2003
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DOI: 10.1038/nature02171

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