Abstract:
:The acyclic analogue of guanosine acyclovir (ACV) constitutes the first-line drug for the treatment of herpes simplex virus (HSV) infections. ACV activation requires primophosphorylation by virus-encoded HSV thymidine kinase (TK). In 95% of cases, HSV resistance to ACV is associated with mutations located in TK. The aim of this work was to address the question of the potential involvement of novel HSV-1 and HSV-2 TK mutations in reduced susceptibility to ACV using a novel nonradioactive method, based on luminescent quantitation of ADP, for the evaluation of in vitro phosphorylation activity of TK. All recombinant TKs tested exhibited significantly lower ACV phosphorylation activities in comparison with those of reference KOS or gHSV-2 TKs (p<0.015), therefore indicating that amino acid changes Y53D, L170P, R176W, A207P (HSV-1) and S66P, A72S, I101S, M183I (HSV-2) were likely to be involved in HSV resistance to ACV.
journal_name
Antiviral Resjournal_title
Antiviral researchauthors
Burrel S,Bonnafous P,Hubacek P,Agut H,Boutolleau Ddoi
10.1016/j.antiviral.2012.09.016subject
Has Abstractpub_date
2012-12-01 00:00:00pages
386-90issue
3eissn
0166-3542issn
1872-9096pii
S0166-3542(12)00223-9journal_volume
96pub_type
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