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Previous Volume 341:77-84 July 8, 1999 Number 2 Next

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ABSTRACT

Background and Methods Cytomegalovirus (CMV) has been implicated as a cofactor in the progression of human immunodeficiency virus type 1 (HIV-1) disease. We assessed 440 infants (75 of whom were HIV-1–infected and 365 of whom were not) whose CMV status was known, who were born to HIV-1–infected women, and who were followed prospectively. HIV-1 disease progression was defined as the presence of class C symptoms (according to the criteria of the Centers for Disease Control and Prevention [CDC]) or CD4 counts of less than 750 cells per cubic millimeter by 1 year of age and less than 500 cells per cubic millimeter by 18 months of age.

Results At birth the frequency of CMV infection was similar in the HIV-1–infected and HIV-1–uninfected infants (4.3 percent and 4.5 percent, respectively), but the HIV-1–infected infants had a higher rate of CMV infection at six months of age (39.9 percent vs. 15.3 percent, P=0.001) and continued to have a higher rate of CMV infection through four years of age (P=0.04). By 18 months of age, the infants with both infections had higher rates of HIV-1 disease progression (70.0 percent vs. 30.4 percent, P=0.001), CDC class C symptoms or death (52.5 percent vs. 21.7 percent, P=0.008), and impaired brain growth or progressive motor deficits (35.6 percent vs. 8.7 percent, P=0.005) than infants infected only with HIV-1. In a Cox regression analysis, CMV infection was associated with an increased risk of HIV-1 disease progression (relative risk, 2.59; 95 percent confidence interval, 1.13 to 5.95). Among children infected with HIV-1 alone, but not among those infected with both viruses, children with rapid progression of HIV-1 disease had higher mean levels of HIV-1 RNA than those with slower or no progression of disease.

Conclusions HIV-1–infected infants who acquire CMV infection in the first 18 months of life have a significantly higher rate of disease progression and central nervous system disease than those infected with HIV-1 alone.

Source Information

From the Maternal–Child HIV Management and Research Center, Los Angeles County and University of Southern California Medical Center, and the Division of Pediatric Infectious Diseases, University of Southern California School of Medicine — both in Los Angeles (A.K.); the Department of Biostatistics and Epidemiology (M.S., K.E.) and the Division of Pediatric and Adolescent Medicine (J.G.), Cleveland Clinic Foundation, Cleveland; the Section of Infectious Diseases, Department of Pediatrics (G.D.), and the Department of Allergy and Immunology (W.S.), Baylor College of Medicine, Houston; the Department of Pediatrics, Columbia–Presbyterian Medical Center, New York (P.L., J.P.); the Department of Pediatrics, Boston Medical Center, Boston (E.C.); the Division of Pediatric Infectious Diseases, Department of Pediatrics (D.H.), and the Pediatric Pulmonary and Critical Care Division (M.K.), Mount Sinai School of Medicine, New York; and the Division of Infectious Disease, Children's Hospital, Boston (K.M.). Presented in part at the Third National Conference on Human Retroviruses and Opportunistic Infections, Washington, D.C., January 28–February 1, 1996, and the 11th International Conference on AIDS, Vancouver, B.C., Canada, July 7–12, 1996.

Address reprint requests to Dr. Kovacs at the Health Research Associates Bldg., 1640 Marengo St., 3rd Fl., Los Angeles, CA 90033, or at akovacs{at}hsc.usc.edu.

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Infants with CMV and HIV-1
Rohrer T. R., Engelcke G., Rudin C., Kovacs A., Demmler G., McIntosh K.
Extract | Full Text  
N Engl J Med 1999; 341:1476-1477, Nov 4, 1999. Correspondence

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