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10.1128/AAC.01114-13 http://scihub22266oqcxt.onion/10.1128/AAC.01114-13 C3837890!3837890!24018260     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24018260&cmd=llinks): Failed to open stream: HTTP request failed! 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Rapid Viral Expansion and Short Drug Half-Life Explain the Incomplete Effectiveness of Current Herpes Simplex Virus 2-Directed Antiviral Agents |pdf=|usr=}}{{24018260}} gab.com Text Rapid Viral Expansion and Short Drug Half-Life Explain the Incomplete Effectiveness of Current Herpes Simplex Virus 2-Directed Antiviral Agents JO: Antimicrob Agents Chemother http://www.kidney.de/pget.php?&tw=1&pmid=24018260 #FOAvip The nucleoside analogues acyclovir (ACV) and famciclovir (FCV) reduce the frequency and severity of herpes simplex virus 2 (HSV-2) genital shedding, yet despite their high potency in vitro and a lack of induced drug resistance, frequent episodes of breakthrough mucosal shedding occur. We tested a published stochastic, spatial mathematical model of HSV-2 replication and spread, in concert with pharmacokinetic and pharmacodynamic equations, against virologic data from clinical trials of twice-daily acyclovir and famciclovir suppression. The model reproduced the key features of clinical trial data, including genital shedding episode rate, expansion and decay dynamics, and heterogeneous peak viral production and duration. In simulations, these agents shortened episode duration by limiting the extent of viral production by 1 to 2 log units and limiting the formation of secondary ulcers by ?50%. However, drug concentrations were noninhibitory during 42% of the dosing cycle. Even if drug concentrations were high at episode initiation, prolonged episodes often ensued due to drug decay over ensuing hours and subsequent rebound of rapidly replicating HSV-2. The local CD8+ T-cell density was more predictive of episode viral production (R2 = 0.42) and duration (R2 = 0.21) than the drug concentration at episode onset (R2 = 0.14 and 0.05, respectively), though the model projected that an agent with an equivalent potency but a two times longer half-life would decrease shedding by 80% compared to that of standard twice-daily regimens. Therefore, long half-life is a key characteristic of any agent that might fully suppress HSV-2 reactivations. Twit Text FOAVip Rapid Viral Expansion and Short Drug Half-Life Explain the Incomplete Effectiveness of Current Herpes Simplex Virus 2-Directed Antiviral Agents ????Antimicrob Agents Chemother http://www.kidney.de/pget.php?&tw=1&pmid=24018260 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24018260 #FOAvip English Wikipedia <ref>{{Cite pmid|24018260}}</ref> Rapid Viral Expansion and Short Drug Half-Life Explain the Incomplete Effectiveness of Current Herpes Simplex Virus 2-Directed Antiviral Agents #MMPMID24018260 Schiffer JT; Swan DA; Corey L; Wald A Antimicrob Agents Chemother 2013[Dec]; 57 (12): 5820-9 PMID24018260show ga The nucleoside analogues acyclovir (ACV) and famciclovir (FCV) reduce the frequency and severity of herpes simplex virus 2 (HSV-2) genital shedding, yet despite their high potency in vitro and a lack of induced drug resistance, frequent episodes of breakthrough mucosal shedding occur. We tested a published stochastic, spatial mathematical model of HSV-2 replication and spread, in concert with pharmacokinetic and pharmacodynamic equations, against virologic data from clinical trials of twice-daily acyclovir and famciclovir suppression. The model reproduced the key features of clinical trial data, including genital shedding episode rate, expansion and decay dynamics, and heterogeneous peak viral production and duration. In simulations, these agents shortened episode duration by limiting the extent of viral production by 1 to 2 log units and limiting the formation of secondary ulcers by ?50%. However, drug concentrations were noninhibitory during 42% of the dosing cycle. Even if drug concentrations were high at episode initiation, prolonged episodes often ensued due to drug decay over ensuing hours and subsequent rebound of rapidly replicating HSV-2. The local CD8+ T-cell density was more predictive of episode viral production (R2 = 0.42) and duration (R2 = 0.21) than the drug concentration at episode onset (R2 = 0.14 and 0.05, respectively), though the model projected that an agent with an equivalent potency but a two times longer half-life would decrease shedding by 80% compared to that of standard twice-daily regimens. Therefore, long half-life is a key characteristic of any agent that might fully suppress HSV-2 reactivations. äRapid Viral Expansion and Short Drug Half-Life Explain the Incomplete (epmc).pdf DeepDyve Pubget Overpricing