Flashback: A Summary of HHV-6's Destructivenss
From an article by Abdel-Haq NahedM, Asmar BasimI
in The Indian Journal of Pediatrics (2004,Volume 71,
Issue 1, Page 89-96)
in The Indian Journal of Pediatrics (2004,Volume 71,
Issue 1, Page 89-96)
HHV-6 preferentially infects CD4+ T-lymphocytes;[17]
but can also infect other cell lines of epithelial,
fibroblastic and neuronal origins with different
efficiency.[18],[19],[20] The surface marker CD46 acts
as part of a co-receptor for infection by both HHV-6A
and HHV-6B.[21] Although CD46 is expressed by most
nucleated human cells and may explain the wide
cellular tropism of HHV-6, the virus does not infect
all CD46-positive cells. Following infection, HHV-6
persists and establishes latency in different cells
and organs including monocytes/macrophages, salivary
glands, the brain and the kidneys. Because the main
target cells for infection are the CD4-positive
lymphocytes and monocytes, HHV-6 infection has
important effects on the immune system. These include
enhancement of natural killer cells, inhibition of
T-cell proliferation, induction of cytokine release
such as tumor necrosis factor-alpha, and interleukin
1-beta as well as modifying the expression of key cell
receptors such as CD3, CD4 and CXCR4.[17],[22],[23]
but can also infect other cell lines of epithelial,
fibroblastic and neuronal origins with different
efficiency.[18],[19],[20] The surface marker CD46 acts
as part of a co-receptor for infection by both HHV-6A
and HHV-6B.[21] Although CD46 is expressed by most
nucleated human cells and may explain the wide
cellular tropism of HHV-6, the virus does not infect
all CD46-positive cells. Following infection, HHV-6
persists and establishes latency in different cells
and organs including monocytes/macrophages, salivary
glands, the brain and the kidneys. Because the main
target cells for infection are the CD4-positive
lymphocytes and monocytes, HHV-6 infection has
important effects on the immune system. These include
enhancement of natural killer cells, inhibition of
T-cell proliferation, induction of cytokine release
such as tumor necrosis factor-alpha, and interleukin
1-beta as well as modifying the expression of key cell
receptors such as CD3, CD4 and CXCR4.[17],[22],[23]
