title: Acute cytomegalovirus infection in Kenyan HIV-infected infants.
abstract: OBJECTIVE
  Cytomegalovirus (CMV) coinfection may influence HIV-1 disease progression during infancy. Our aim was to describe the incidence of CMV infection and the kinetics of viral replication in Kenyan HIV-infected and HIV-exposed uninfected infants.
  
  
  METHODS
  HIV-1 and CMV plasma viral loads were serially measured in 20 HIV-exposed uninfected and 44 HIV-infected infants born to HIV-infected mothers. HIV-infected children were studied for the first 2 years of life, and HIV-exposed uninfected infants were studied for 1 year.
  
  
  RESULTS
  CMV DNA was detected frequently during the first months of life; by 3 months of age, CMV DNA was detected in 90% of HIV-exposed uninfected infants and 93% of infants who had acquired HIV-1 in utero. CMV viral loads were highest in the 1-3 months following the first detection of virus and declined rapidly thereafter. CMV peak viral loads were significantly higher in the HIV-infected infants compared with the HIV-exposed uninfected infants (mean 3.2 versus 2.7 log10 CMV DNA copies/ml, respectively, P = 0.03). The detection of CMV DNA persisted to 7-9 months post-CMV infection in both the HIV-exposed uninfected (8/17, 47%) and HIV-infected (13/18, 72%, P = 0.2) children. Among HIV-infected children, CMV DNA was detected in three of the seven (43%) surviving infants tested between 19 and 21 months post-CMV infection. Finally, a strong correlation was found between peak CMV and HIV-1 viral loads (rho = 0.40, P = 0.008).
  
  
  CONCLUSIONS
  Acute CMV coinfection is common in HIV-infected Kenyan infants. HIV-1 infection was associated with impaired containment of CMV replication.
authors.affiliation: MRC Human Immunology Unit, Oxford University, Oxford, UK. jslyker@u.washington.edu
authors.forename: Jennifer A
authors.initials: JA
authors.lastname: Slyker
authors.forename: Barbara L
authors.initials: BL
authors.lastname: Lohman-Payne
authors.forename: Grace C
authors.initials: GC
authors.lastname: John-Stewart
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Maleche-Obimbo
authors.forename: Sandra
authors.initials: S
authors.lastname: Emery
authors.forename: Barbra
authors.initials: B
authors.lastname: Richardson
authors.forename: Tao
authors.initials: T
authors.lastname: Dong
authors.forename: Astrid Kn
authors.initials: AK
authors.lastname: Iversen
authors.forename: Dorothy
authors.initials: D
authors.lastname: Mbori-Ngacha
authors.forename: Julie
authors.initials: J
authors.lastname: Overbaugh
authors.forename: Vincent C
authors.initials: VC
authors.lastname: Emery
authors.forename: Sarah L
authors.initials: SL
authors.lastname: Rowland-Jones
mesh_terms: D017088:AIDS-Related Opportunistic Infections / Q000150:complications / Q000453:epidemiology / Q000821:virology*; D002675:Child, Preschool; D003587:Cytomegalovirus / Q000235:genetics / Q000302:isolation & purification*; D003586:Cytomegalovirus Infections / Q000151:congenital / Q000453:epidemiology / Q000276:immunology*; D004279:DNA, Viral / Q000097:blood; D018450:Disease Progression; D005260:Female; D015658:HIV Infections / Q000150:complications / Q000453:epidemiology / Q000276:immunology*; D015497:HIV-1 / Q000276:immunology*; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007630:Kenya / Q000453:epidemiology; D008297:Male; D011379:Prognosis; D012307:Risk Factors; D019562:Viral Load; D014779:Virus Replication / Q000502:physiology
chemical_list: D004279:DNA, Viral