CMV gH Inhibitors

The chemical class of CMV gH inhibitors consists of compounds that indirectly modulate the function of CMV gH, primarily through their action on various stages of viral replication and entry processes. These inhibitors target different components of viral replication machinery, thereby influencing the need for or efficiency of gH-mediated viral entry. Compounds such as Ganciclovir, Valganciclovir, Foscarnet, Cidofovir, and Letermovir are well-known for their effectiveness against CMV by targeting viral DNA synthesis and processing. For example, Ganciclovir and its prodrug Valganciclovir inhibit CMV DNA polymerase, thereby reducing viral replication, which indirectly impacts the requirement for gH in the viral entry process. Similarly, Foscarnet and Cidofovir inhibit viral DNA synthesis, affecting the replication cycle where gH plays a role. Letermovir, which targets CMV DNA terminase, indirectly affects viral replication processes that involve gH.

Additionally, compounds like Maribavir, Docosanol, Amantadine, Oseltamivir, Rimantadine, Acyclovir, and Famciclovir, though not primarily targeted against CMV, demonstrate mechanisms that could influence CMV gH function. Maribavir inhibits CMV UL97 kinase, affecting viral maturation. Docosanol and Amantadine inhibit viral fusion and uncoating, respectively, which are processes where gH might be involved. Oseltamivir and Rimantadine, known for their action against influenza viruses, along with Acyclovir and Famciclovir, which target herpes simplex virus DNA polymerase, could offer insights into indirect mechanisms affecting CMV gH.