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1. An infant received antiretroviral therapy (ART) 30 hours post birth due to high-risk exposure to HIV-1. The standard diagnostic criterion for HIV-1 infection was met and the ART treatment was continued until 18 months of age, when treatment was discontinued.Â
2. At 30 months of age (12 months after treatment cessation), clinical assessment of the infant revealed undetectable levels of plasma HIV-1 RNA, proviral DNA, and HIV-antibodies.Â
Evidence Rating Level: 4 (Below Average) Â Â Â Â Â
Study Rundown: The study identified a 30-month-old infant that has previously met the clinical criteria for HIV-1 infection in utero and was started on ART from 30 hours to 18 months of age. ART therapy was discontinued at 18 months of age due to loss of follow-up. At 26 months, virologic assays performed on the infant revealed presence of HIV-1 proviral DNA but no presence of replication-competent HIV-1 in resting CD4+ T-cells. At 30 months of age, the child demonstrated no evidence of ongoing HIV-infection nor rebound viremia typically observed in infants who receive early treatment of ART and was subsequently discontinued on therapy. The presence of trace HIV-nucleic acids without replicate-competent HIV in the patient suggests early use of ART may affect the quality of persistent HIV reservoirs in infants.
Click to read the study in NEJM
Click to read an accompanying editorial in NEJM
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In-Depth [case report]: The infant met the HIV-1 DNA and HIV-1 RNA levels diagnostic of HIV-1 infection at 30 and 31 hours of age, respectively. ART was initiated at this time (zidovudine, lamivudine, and nevirapine). At 24, 26, and 28 months HIV-1 antibodies were not detected. Virologic tests revealed no viral RNA copies by 26 months of age. The presence of a large viral load at 30 hours of age as well as detectable viremia until 19 days of age strongly suggested an in utero infection. Furthermore, the patient showed a biphasic viremia decline following the initiation of ART which corresponds with the pattern of active infection inhibition. Both the mother and infant did not have HLA class I alleles and both are non-mutated for CCR5. However, no clinical samples were saved from the peripartum period that prevents additional confirmation of viral infection as well as linkage analysis to maternal viral variants.
By David Wang and Andrew Bishara
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