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Human herpesvirus 6.

D A Clark1

  • 1Department of Virology, Royal Free and University College Medical School, London, UK.

Reviews in Medical Virology
|May 18, 2000
PubMed
Summary
This summary is machine-generated.

Human herpesvirus 6 (HHV-6) causes common childhood illness and persists lifelong. Two variants, HHV-6A and HHV-6B, show distinct epidemiological and pathological differences, requiring further research into their roles in diseases like multiple sclerosis.

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Area of Science:

  • Virology
  • Immunology
  • Neurology

Background:

  • Human herpesvirus 6 (HHV-6) is a widespread beta-herpesvirus, typically infecting infants and causing febrile illnesses.
  • HHV-6 infects T lymphocytes and other cells, utilizing CD46 as a receptor, and establishes persistent infections.
  • The virus is implicated in post-transplant complications, HIV progression, and controversially, in multiple sclerosis (MS).

Purpose of the Study:

  • To compare the two variants of HHV-6 (A and B).
  • To elucidate the biological, genetic, epidemiological, and pathological differences between HHV-6A and HHV-6B.
  • To highlight the need for further understanding of HHV-6 neurotropism in diseases like MS.

Main Methods:

  • Comparative analysis of complete nucleotide sequences of HHV-6 variants.

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  • Review of existing epidemiological and pathological data.
  • Discussion of cellular tropism and receptor identification.

    • Main Results:

    • HHV-6A and HHV-6B genomes are collinear with high homology but show significant variation in specific regions.
    • HHV-6B is predominantly associated with childhood febrile illness and is more common in healthy individuals.
    • HHV-6A is less prevalent, and its epidemiology requires further definition.

    Conclusions:

    • The two HHV-6 variants are biologically, genetically, epidemiologically, and pathologically divergent.
    • Further research is needed to clarify the role of HHV-6, particularly its neurotropism, in diseases such as multiple sclerosis.
    • Understanding variant-specific differences is crucial for comprehending HHV-6 pathogenesis.