Varicella-Zoster Virus (VZV) Inhibitors

Varicella-zoster virus (VZV) is a human herpesvirus that causes two distinct manifestations: primary varicella (chickenpox) and reactivation as herpes zoster (shingles). The virus enters the body through the respiratory tract, initially infecting respiratory epithelial cells. It then disseminates through the bloodstream to the skin, where it causes characteristic vesicular lesions. VZV establishes latency in sensory ganglia, and reactivation from latency can lead to herpes zoster, characterized by painful dermatomal rash. VZV employs a complex and well-coordinated signaling network to regulate its replication, immune evasion, and latency establishment. This includes interactions with host cell factors, immune evasion strategies, and modulation of cellular pathways to ensure its survival and dissemination within the host. Targeting VZV signaling is essential to develop effective antiviral strategies, especially considering the potential for severe complications in immunocompromised individuals and the elderly, where herpes zoster can lead to persistent pain (post-herpetic neuralgia) and other serious conditions.

The significance of Varicella-zoster virus inhibitors lies in their potential to mitigate the impact of VZV infections. By specifically targeting key viral enzymes, proteins, or processes involved in viral replication and dissemination, these inhibitors can limit the progression of varicella and herpes zoster and reduce associated complications. Antiviral inhibitors have shown efficacy in suppressing viral replication and preventing the establishment of latency. For example, nucleoside analogues like acyclovir and its derivatives interfere with viral DNA replication, reducing the severity and duration of VZV infections.