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Review
. 2016 Mar 30;8(1):1-6.
doi: 10.1038/ijos.2016.3.

New strategies against drug resistance to herpes simplex virus

Yu-Chen Jiang  1 , Hui Feng  2 , Yu-Chun Lin  1 , Xiu-Rong Guo  3   4
Affiliations
Review

New strategies against drug resistance to herpes simplex virus

Yu-Chen Jiang et al. Int J Oral Sci. .

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.

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Figures

Figure 1
Figure 1
The anti-HSV mechanism of ACV. ACV, acyclovir; HSV, herpes simplex virus.
Figure 2
Figure 2
The chemical structures of two potent HPI active compounds against HSV. HPI, helicase-primase inhibitor; HSV, herpes simplex virus.
Figure 3
Figure 3
The lethal mutagenesis mechanism of ribavirin. The ribavirin cis conformer can pair with uridine by mimicking adenosine, and the trans conformer can pair with cytidine by mimicking guanosine.
Figure 4
Figure 4
The potential mutagenic molecule. Janus nucleoside analogues (for example, J-GC) can pair with guanosine and cytidine by rotating around the glycosyl bond. J-GC, Janus-type pyrimido[4,5-d]pyrimidine guanosine–cytosine.
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