| MicrobiologyBytes: Virology: HHV-6/7 | Updated: September 11, 2007 | Search |
(A.K.A. "HBLV"). Isolated in 1986 in lymphocytes of patients with lymphoreticular disorders - tropism for CD4+ lymphocytes. Complete genome sequence ~160kbp. HHV-6 is now recognised as being a nearly universal human infection:
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Discovery of the virus solved a longstanding mystery - primary infection in childhood causes "roseola infantum" a.k.a. "sixth disease", a common childhood rash whose cause was previously unknown. Ab titres are highest in children and decline with age. Consequences of childhood infection appear to be mild. Primary infections of adults are rare but have more severe consequences - mononucleosis/hepatitis. HHV-6 infection is a problem in immunocompromised patients, although the importance of HHV-6 infection in AIDS patients is not clear.
Santoro F, et al.(1999) CD46 is a cellular receptor for human herpesvirus 6. Cell 99: 817-827
HHV-6 shows a pattern of susceptibility to antiviral drugs similar to that of cytomegalovirus (HHV-5), since its replication is inhibited by ganciclovir, phosphonoformate (foscarnet, PFA), and phosphonoacetic acid (PAA), but is relatively resistant to acyclovir.
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First isolated from human CD4+ cells in 1990. Complete genome sequence ~145kbp, organization similar to but distinct from HHV-6. The complete genome sequence of HHV-7 has been determined and this shows a high degree of conservation of genetic content and encoded amino acid sequences to HHV-6. However, there is only limited antigenic cross-reactivity between the two viruses. At present, there is no clear evidence for the direct involvement of HHV-7 in any human disease, but HHV-7 might be a co-factor in HHV-6-related syndromes ???
Pityriasis rosea:
There is epidemiological evidence to suggest and involvement
of HHV-7 in pityriasis rosea, a common skin rash of young people. Although pityriasis
rosea may occur in more than one person in a household at a time, it is not
thought to be contagious.
HHV-6 and other viruses have also been implicated in this condition. HHV–7
DNA has been found in both the lesions and the plasma in patients with PR.
In addition, a separate study found HHV-7 DNA in
lymphocytes in 75% of patients with PR, compared with 9% of controls. PCR has
shown both HHV-7 and HHV-6 DNA in a variety of tissues and secretions from
patients with PR. In the same study, in situ hybridization of lesional lymphocytes
showed both HHV-7 and HHV-6 mRNA. However, the causative link has not been
definitively proved because HHV-7 is frequently found in healthy individuals.
HHV-7 has been reported to upregulate CD46 and CD59. CD46 functions as a complement-regulatory protein (CRP) and a receptor for some viruses, including measles virus and HHV-6. Complement is part of the innate immune defence system. Upregulation of CRPs may be a possible mechanism for HHV-7 to evade humoral immunity exerted via complement, and HHV-7-infected cells are more resistant to complement-dependent cytotoxicity (CDC) than mock-infected cells (Human herpesvirus 7 infection increases the expression levels of CD46 and CD59 in target cells. 2007 J Gen Virol 88: 1415-1422).
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