RESEARCH ARTICLE Synergistic effects of acyc h

rd ogens that cause herpes labialis, herpes genitalis, kera-titis and encephalitis. According to epidemiological compromised individuals such as HIV-infected patients and transplant recipients. Resistance of HSV to ACV has Priengprom et al. BMC Complementary and Alternative Medicine (2015) 15:56 DOI 10.1186/s12906-015-0591-xgenome replication by a chain-termination mechanism. In accordance with this mechanism of action, viral Kaen, Thailand Full list of author information is available at the end of the articlesurveys, the HSV infection rate has continuously in-creased in most countries [1]. Nucleoside analogs, acyclovir (ACV) and others such as penciclovir, valaci-clovir, and famciclovir, have been approved for treatment of HSV infections worldwide, but severe side effects may occur [2-4]. Moreover, long-term prophylactic and been reported in 5-30 % of cases, mainly among im-munocompromised patients and particularly in allogen-eic bone marrow transplant patients [5]. ACV is an analogue of guanosine that requires activation through triphosphorylation. The first phosphorylation is mainly achieved by HSV thymidine kinase (TK), encoded by the UL23 gene, whereas subsequent phosphorylations are carried out by host cellular kinases [6]. The ACV active form is then incorporated by the viral DNA polymerase, encoded by the UL30 gene, and finally disrupts vira