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Excerpt
Infants typically have very high HIV-1 levels compared with adults [1–3]. In our previous study, we found that African infants undergoing perinatal infection had high HIV-1 levels that continued as a plateau during the first year of life [3]. However, that study obtained samples only after one month of age and could have missed a perinatal infection HIV-1 spike if it occurred in the first month. Other investigators have suggested that a viral spike can occur soon after primary infection in infants [4,5]. Although these studies followed infants longitudinally, they presented the results grouped by age rather than for individual subjects. Furthermore, in those studies, the first month visits were non-scheduled, which could have introduced bias into the patterns observed if the reasons for visiting affected viral levels. Changes in HIV levels during primary infection have not been described in individual infants.
To evaluate the profile of primary viraemia in infants, we studied HIV-exposed infants, scheduled weekly during their first month of life. After obtaining maternal consent, cord blood samples from newborns in Blantyre, Malawi were tested for HIV-1 antibody (HIV-1 enzyme immunoassay; Genetics Systems, Seattle, WA, USA). Reactive HIV-1 antibody results reflected the presence of passively acquired antibody from an HIV-infected mother. Mothers of vaginally delivered infants whose cord blood samples were HIV-1 antibody positive were asked to bring their infants to our clinic at 1, 2, 3, 4, 6 and 12 weeks of age. At each visit, filter paper samples were obtained by heel stick. Additional samples obtained on days 1 or 2 of life were available from some babies who remained at the hospital after delivery because they or their mothers required an extended stay. The last available sample from each infant was tested for HIV by polymerase chain reaction (PCR). Filter paper samples from PCR-positive infants were then tested for viral levels by a second-generation quantitative isothermal nucleic acid silica-bound amplification assay (NucliSens HIV-1 RNA Q-T kit; Organon Teknika, Durham, NC, USA) previously found to be reliable in filter paper samples [3,6]. To exclude in-utero infections, cord blood samples were also PCR tested and, if positive, these infants were excluded from the study. Viral testing was performed by a laboratory in Canada that also participated in the Virology Quality Assurance Program of the AIDS Clinical Trial Group. All infants were breast-fed and therefore could have become infected by early breast-feeding. No infants were treated with antiretroviral agents.
Of 89 infants born to 87 HIV-1-infected women (two sets of twins), 50 had samples obtained at 28 days of life or older and were tested by PCR for HIV-1. One infant was cord blood PCR-positive (in-utero infection), and two infants first tested positive at 90 and 366 days, respectively, indicating transmission that probably occurred via breast milk. Seven subjects were PCR-negative in cord blood samples but positive in the first 28 days of life (1, 7, 14, 14, 14, 24 and 28 days), suggesting infection at or near the time of delivery. Evidence of a spike in viral replication was clearly apparent, with the highest level being 107.6 copies/ml (39 million copies) one week after viraemia was first detected (Fig. 1).
