be linked to graft-vs-host disease. Virology Structure A mature virus particle measures about in diameter. The genome of HHV-7 is very similar to that of HHV-6, although it is about 10% smaller, with a DNA genome of about 145,000 base pairs. There are a number of key differences between the genome of HHV-7 and that of HHV-6, but the importance of them for viral DNA replication is not yet known. Additionally, the HHV-7 virion appears to share much structural similarity to the HHV-6 virion. Despite this, some morphological characteristics of the viruses differ. Cellular effects HHV-7 resides mostly in CD4+ T cells, albeit only in certain strains of them. To enter CD4+ T cells, HHV-7, unlike HHV-6, uses CD4 and possibly some cell-surface glycoproteins to enter CD4+ T cells. Despite this, HHV-7 may be able to enter cells that do not express the CD46 receptor. About a week after HHV-7 has infected a cell, it begins to downregulate CD4 transcription, which interferes with HIV-1 infection but may reactivate HHV-6 infection. It is however unclear exactly what effect HHV-7 has on HIV infection. There has been some inquiry into the relationship between HHV-7 and HIV-1 co-receptors CXCR4 and CCR5. During infection, HHV-7 causes a loss of CXCR4 in CD4+ T-cells in addition to lowering intracellular Ca2+ flux and chemotaxis in response to stroll cell-derived factor 1 (SDF-1). Additionally, a CXCR4 antagonist that was effective against HIV was shown to be ineffective at inhibiting HHV-7. This information indicates that CXCR4 and CCR5 are not essential receptor proteins for HHV-7 infection. The trademark indication of HHV-7 infection at the cellular level is the presence of aforementioned syncytia. It is thought that these cells form via polyploidization resulting from a dysregulation of cyclin dependent kinase cdc2 and cyclin B. Giant cells form when the cell cycle is disrupted and accumulate between the G2 and M phase. However, syncytia formation is more complex than initially thought. Some research has shown that syncytia formation in betaherpesviruses can vary based on the type of envelop protein expressed by the virion as well as the particular type of cell that the virus is infecting. HHV-7 also notably activates IL-15 upon infection. Activation of IL-15 leads to an increased natural killer (NK) cell response. This is thought to be one of the immune system's main methods of responding to HHV-7 infection. HHV-7 also has a number of other effects