title: Differential decay kinetics of human cytomegalovirus glycoprotein B genotypes following antiviral chemotherapy.
abstract: BACKGROUND
  The impact of different cytomegalovirus (HCMV) glycoprotein B (gB) genotypes on pathogenesis remains controversial.
  
  
  OBJECTIVE
  To investigate the effect of gB genotypes either as single infections or as part of multiple infections on the early kinetics of response to ganciclovir therapy.
  
  
  METHODS
  Patients (n=239) enrolled in a study of intravenous ganciclovir or valganciclovir for the treatment of HCMV disease were analysed by a gB genotype specific PCR to quantify the amount of each gB genotype present at initiation of therapy (baseline, day 0) and at days 3, 7, 14 and 21 post therapy.
  
  
  CONCLUSIONS
  In all gB groups (individual gB genotype infections and mixed genotype infections) there was a biphasic decline in viral load after therapy. The first phase half life (days 0-3) was ≤1 day and was followed over the next 18 days by a slower second phase decline with half lives ranging from 3.4 to 4.4 days. The 1st phase rapid decline in viral load was dependent upon gB genotype whereas the ultimate viral load reduction at day 21 was relatively insensitive to gB genotype. A strong correlation between 1st phase decline and extent of viral load reduction at day 21 was observed (r=0.37; p=0.002). These data imply that early reductions in HCMV load after therapy may be useful in predicting the duration of drug therapy needed to control HCMV replication.
authors.affiliation: Centre for Virology, Department of Infection, University College Medical School, London, United Kingdom.
authors.forename: Vincent C
authors.initials: VC
authors.lastname: Emery
authors.forename: Oriol
authors.initials: O
authors.lastname: Manuel
authors.forename: Anders
authors.initials: A
authors.lastname: Asberg
authors.forename: Xiaoli
authors.initials: X
authors.lastname: Pang
authors.forename: Deepali
authors.initials: D
authors.lastname: Kumar
authors.forename: Anders
authors.initials: A
authors.lastname: Hartmann
authors.forename: Jutta K
authors.initials: JK
authors.lastname: Preiksaitis
authors.forename: Mark D
authors.initials: MD
authors.lastname: Pescovitz
authors.forename: Halvor
authors.initials: H
authors.lastname: Rollag
authors.forename: Alan G
authors.initials: AG
authors.lastname: Jardine
authors.forename: Christoph G
authors.initials: CG
authors.lastname: Gahlemann
authors.forename: Atul
authors.initials: A
authors.lastname: Humar
mesh_terms: D000998:Antiviral Agents / Q000008:administration & dosage*; D003587:Cytomegalovirus / Q000235:genetics / Q000302:isolation & purification*; D003586:Cytomegalovirus Infections / Q000188:drug therapy* / Q000821:virology*; D004279:DNA, Viral / Q000235:genetics; D015774:Ganciclovir / Q000008:administration & dosage / Q000031:analogs & derivatives; D005838:Genotype; D006801:Humans; D007262:Infusions, Intravenous; D016133:Polymerase Chain Reaction; D013997:Time Factors; D016896:Treatment Outcome; D000077562:Valganciclovir; D014759:Viral Envelope Proteins / Q000235:genetics*; D019562:Viral Load
chemical_list: D000998:Antiviral Agents; D004279:DNA, Viral; D014759:Viral Envelope Proteins; C040495:glycoprotein B, Simplexvirus; D000077562:Valganciclovir; D015774:Ganciclovir