Primary Epstein–Barr Virus Infection: Impact of Age at Acquisition, Coinfection, and Viral Load

Abstract

Primary Epstein–Barr virus (EBV) infection acquired at an early age or in concert with another pathogen can result in poor control of EBV replication and may be a risk factor for subsequent chronic illnesses including malignancy. Slyker and colleagues report in this issue of the Journal that primary EBV infection was more frequent and more severe in infants coinfected with human immunodeficiency virus type 1 (HIV-1) than in those who were HIV-negative [1]. Their clinical research study, which used repository samples and archival data from an investigation of Kenyan infants born to HIVinfected mothers [2, 3], makes several important observations. First, HIVinfected infants acquired primary EBV infection sooner than their HIVuninfected counterparts. Second, infants coinfected with EBV and HIV had higher EBV plasma loads that were slow to clear. Finally, primary EBV infection caused more pneumonia, hepatosplenomegaly, and hospitalization in coinfected infants than in HIV-negative infants. Moorman et al previously reported another example of coinfection damaging the host’s ability to contain EBV [4]. Kenyan children aged 1–4 years from a district of intense perennial malaria transmission (Kisumu) had a higher percentage of parasitemia and higher EBV blood viral loads than children of the same age from a low malaria transmission district (Nandi). In this case, the coinfecting pathogen was Plasmodium falciparum instead of HIV. Piriou and colleagues [5] recently extended these results by showing that infants in Kisumu, the holoendemic malaria district, acquired primary EBV sooner and had higher viral loads throughout the first 2 years of life than infants in Nandi, the low malaria transmission district. Both parasitemia and EBV loads were higher among children living in the Kisumu district and among those infected with EBV at a younger age. What are the implications of these