Maternal antibodies have been found to be detectable in infants of KSHV-positive mothers up to 6 months of age [45]. increases the risk for KSHV seroconversion early in existence. Keywords:Kaposi sarcoma-associated herpesvirus, HHV-8, KSHV, sub-Saharan Africa, malaria In Kenyan children followed to 24 months of age, children having a prior malaria illness became KSHV seropositive at a faster rate than children without malaria. Our findings will direct long term work on KSHV illness prevention in sub-Saharan Africa. Kaposi sarcoma-associated herpesvirus (KSHV), also known as human being herpesvirus 8 (HHV-8), is definitely a gammaherpesvirus which varies in seroprevalence across the globe: in certain areas of sub-Saharan Africa, up to 95% of adults are seropositive [1]. Factors associated with higher KSHV seroprevalence in sub-Saharan Africa are not completely understood but the geographic variations in KSHV distribution suggest environmental factors are involved. Sub-Saharan Africa, in addition to having high KSHV seroprevalence, is also an area of high endemicity for malaria, primarily caused by thePlasmodium falciparumspecies [2], pointing to an association between malaria and KSHV. Early ecological studies in Italy suggested malaria may be associated with KSHV illness and/or Kaposi sarcoma (KS) [36]. In Uganda, KSHV seropositive ladies and children were more likely to have malaria parasitemia [79] and higher antimalaria antibody levels [10]. Higher levels of anti-KSHV antibodies [11] and increasing KSHV DNA levels were associated with malaria [12] and in Cameroon mosquito bed online use was protecting for KS [13]. However, these studies were either cross-sectional or case-control designs and thus were unable to establish PF-04447943 a temporal association between malaria and KSHV infections. The only known longitudinal study of malaria and KSHV to day measured malaria exposure by self-report [14] but more specific measurements of malaria HDM2 are required to determine whether an association truly exists. In addition, after primary illness with KSHV, anti-KSHV antibodies have been shown to decrease to levels below detection, making serodiagnosis at a single time point demanding [1517]. To properly evaluate KSHV antibody fluctuations, a study design that steps antibodies at multiple timepoints is needed. KSHV seroepidemiology studies to date have also been constrained by the tools available to measure KSHV seropositivity as they have primarily used enzyme-linked immunosorbent assays (ELISAs) or immunofluorescence assays to detect antibodies to K8.1 and the ORF73 latency-associated nuclear antigen (LANA). K8.1 and LANA are well-established markers of KSHV-associated disease but the KSHV genome comprises over 85 open reading frames (ORFs), all of which are potentially antigenic at different viral phases [18]. Restricting the definition of seropositivity to detection of antibodies to just 2 antigens may underestimate KSHV seroprevalence in asymptomatic populations. More recently, we developed a bead-based multiplex assay to detect antibodies to a wider panel of KSHV antigens with a greater dynamic range than ELISA assay [19]. The ability to measure a range of anti-KSHV antibodies in small sample volumes is PF-04447943 definitely a potent tool to address the variability of anti-KSHV antibody reactions. The Prospective Infant PF-04447943 Cohort (PIC) Study enrolled a cohort of babies from 2 Kenyan areas with different malaria transmission intensities [20]. We required advantage of the studys longitudinal design and use of the multiplex assay to determine whether young children withP. falciparuminfection were more susceptible to early KSHV seroconversion. == METHODS == == Study Populace == Between April and May 2006, 224 children born.

Maternal antibodies have been found to be detectable in infants of KSHV-positive mothers up to 6 months of age [45]