Acyclovir

Chickenpox is a highly infectious disease caused by the varicella-zoster virus. Acyclovir (ACV) is an antiviral drug that has been concomitantly used with paracetamol (PA) for its analgesic effect in the management of chicken pox infections. However, the simultaneous pharmacokinetic interaction study for ACV and PA has not yet been reported. A simple high-performance liquid chromatography assay was developed and validated for their simultaneous analysis in human urine. The proposed method presents a pharmacokinetic study for ACV with/without co-administration of PA in human urine with high precision, accuracy and sensitivity in a short time not more than 10 minutes.

The herpesviruses continue to produce considerable morbidity in man. Once infected with herpes simplex (HSV), the virus remains dormant within the nervous system and may reactivate if provoked by stress, trauma and/or other factors. To date, there is no cure, but antiviral medication can reduce duration and severity of symptoms and prophylaxis can suppress recurrent episodes of disease. The second-generation guanosine nucleosides, acyclovir and penciclovir, are effective inhibitors with low toxicity; both, however, have relatively low oral bioavailability. Subsequently, the orally bioavailable prodrugs valaciclovir and famciclovir have been introduced. These compounds offer high oral bioavailabilty and deliver acyclovir and penciclovir, respectively, to the target cells by means of more convenient dosing schedules. This short review points to recent experience with famciclovir in the management of HSV and varicella-zoster virus.

As in the case of other CNS infectious agents claimed to cause Alzheimer's disease [AD], the theory that Herpes Simplex Virus or any other herpes virus causes AD is still controversial. In their 2013 review, Mawanda and Wallace's Can Infections Cause Alzheimer's Disease [1] gave seven annotated references as to why HSV-1 "remains questionable" as a cause for Alzheimer's. Some say that Herpes simplex virus type 1 in conjunction with APOE-epsilon 4 allele is a strong risk factor for AD, though either of these features alone do not increase the risk for AD. It is claimed that people who have symptoms of late onset Alzheimer's disease (AD) and have one or more APOE-ε4 gene copies are more likely to have AD. However, APOE-ε4 is not diagnostic of AD and should not be used to screen people or their family members. Furthermore, many of those who have ε4 alleles will never develop AD. And even in symptomatic people, only about 60% of those with late onset AD will have APOE-ε4 alleles [2, 3]. Not only is the APOE gene not a clinical diagnosis, but just as importantly, "negative" results do not confer later protection. Beyond APOE, there are at least 20 other genetic factors which have been shown to have a small but significant role in determining Alzheimer risk [4]. And true understanding of genetic test results also requires attention to potential inaccurate results. For example, APOE-ε4 alleles themselves are known to show a distinct increase in tuberculosis [5]. Before widespread institution of anti-herpetics on the general population, this is an area which requires further research. In the case of Herpes Simplex Virus type 1-an estimated 80 percent of the U.S. population has HSV-1. To Alzheimer's specialist Jagan Pillae of the Cleveland Clinic, the connection between HSV-1 and Alzheimer's is still murky and "The research does not say, nor does it tell us if herpes simplex 1 virus caused Alzheimer's. The studies show that for some as-yet unclear reason, immune changes related to herpes simplex 1 appear to be more common in older individuals (meaning older than age 60) with Alzheimer's. The research does not say, nor does it tell