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The HIV nucleocapsid protein (NC), particularly from HIV-1, contains two highly conserved zinc finger domains, each with a CCHC motif. These domains are essential for viral replication, acting as nucleic acid chaperones, and are considered prime antiviral targets due to their mutational intolerance and requirement throughout infection. Small molecules that disrupt these domains can inhibit multiple steps in HIV replication simultaneously.
Disruption of zinc binding, leading to structural instability and loss of function in viral replication
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