Abstract
Herpes simplex virus (HSV), a member of the Herpesviridae family, is a significant human pathogen that results in mucocutaneous lesions in the oral cavity or genital infections. Acyclovir (ACV) and related nucleoside analogues can successfully treat HSV infections, but the emergence of drug resistance to ACV has created a barrier for the treatment of HSV infections, especially in immunocompromised patients. There is an urgent need to explore new and effective tactics to circumvent drug resistance to HSV. This review summarises the current strategies in the development of new targets (the DNA helicase/primase (H/P) complex), new types of molecules (nature products) and new antiviral mechanisms (lethal mutagenesis of Janus-type nucleosides) to fight the drug resistance of HSV.
Highlights
This review summarises the current strategies in the development of new targets (the DNA helicase/primase (H/P) complex), new types of molecules and new antiviral mechanisms to fight the drug resistance of Herpes simplex virus (HSV)
HERPES SIMPLEX VIRUS AND DRUG RESISTANCE Herpes virus detection and risk Viral diseases are the primary cause of death among human infectious diseases worldwide.[1]
Researchers have developed a series of anti-HSV nucleoside drugs, such as VCV, famciclovir, and ganciclovir, which are firstline drug treatments for HSV infections
Summary
Herpes simplex virus (HSV), a member of the Herpesviridae family, is a significant human pathogen that results in mucocutaneous lesions in the oral cavity or genital infections. Current drug and antiviral mechanisms There are three classes of drugs approved for treatment of HSV infections, and all of which target viral DNA replication: acyclic guanosine analogues,[24,25,26,27,28,29,30,31,32] acyclic nucleotide analogues,[33,34,35] and pyrophosphate analogues[36,37] (Table 1). Typical drugs from these three categories include valacyclovir (VCV), cidofovir, and foscarnet. ACV-TP incorporates into the replicating DNA because of the absence of 3ʹ prime hydroxyl, which terminates the replication of viral DNA (refs. 2,38–39) (Figure 1)
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