After acute infection, HHV-6 can latently persist in the host quiescently, with no production of infectious virions or with low levels of viral replication. Latency is believed to endure in several cell types, including monocytes and bone marrow progenitor cells [52, 53] , and may undergo chromosomal integration that can be vertically transmitted [54] . The confounding effects of chromosomal integration make differentiating between active and latent HHV-6 infections difficult when detecting HHV-6 sequence in Sequencing Viruses in Tropical Dengue-like Illness www.plosntds.org serum DNA [55, 56] . A previous study detected integrated HHV-6 genomic sequence in ,1% of healthy blood samples [57] . Since detection of HHV-6 nucleic acid in serum alone does not prove active viral infection, we cannot definitively confirm that the HHV-6 sequences in these samples were not derived from the vertical transmission of chromosomally integrated virus. However, the clinical, epidemiological, and virus sequence data suggest HHV-6 may be the etiologic agent in these febrile illness cases.