Varicella Zoster Virus gpI Inhibitors, in this context, refer to a class of antiviral chemicals that inhibit the functionality of VZV gpI by targeting various aspects of the viral replication cycle. These inhibitors primarily function by interfering with the viral DNA synthesis or the activity of viral enzymes crucial for replication. The mechanism of action of these inhibitors can be broadly classified into two categories: nucleoside analogues and viral enzyme inhibitors. Nucleoside analogues, such as Acyclovir, Valacyclovir Hydrochloride, Famciclovir, Penciclovir, Cidofovir, Idoxuridine, Vidarabine, Sorivudine, and Trifluridine, mimic the structure of nucleotides, the building blocks of DNA. Once incorporated into the viral DNA during replication, these analogues lead to premature termination of the DNA strand or cause errors in the DNA sequence, thereby inhibiting viral replication. Since gpI is a glycoprotein involved in viral entry and cell-to-cell spread, its functional impact is indirectly diminished due to the reduced replication efficiency of the virus. Acyclovir and Valacyclovir are particularly notable for their high selectivity and low cytotoxicity, making them widely used for VZV infections.
Viral enzyme inhibitors, such as Foscarnet and Tenofovir Disoproxil Fumarate, target specific enzymes required for viral replication. Foscarnet sodium directly inhibits viral DNA polymerase without requiring activation by viral enzymes, which disrupts DNA synthesis. Tenofovir Disoproxil Fumarate is a nucleotide analogue that undergoes conversion to an active form within the host cells and then inhibits the action of viral replication enzymes. By targeting these enzymes, these inhibitors reduce the ability of VZV to replicate, indirectly affecting the role of gpI in the viral lifecycle. Overall, while these inhibitors do not target VZV gpI directly, their impact on viral replication significantly affects the functionality of gpI, thus playing a crucial role in controlling VZV infections.
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