Mechanisms of HIV-1 to escape from the host immune surveillance

Since the beginning of the acquired immune deficiency syndrome (AIDS) pandemic in 1981, research on human immunodeficiency virus (HIV) has been focused on mechanisms by which the virus escapes from immune surveillance. Several human leucocyte antigen haplotypes have been shown to be associated with...

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Bibliographic Details
Published in:European journal of clinical investigation 2000-08, Vol.30 (8), p.740-746
Main Authors: Kamp, W, Berk, M B, Visser, C J, Nottet, H S
Format: Article
Language:English
Subjects:
Acquired Immunodeficiency Syndrome - genetics
Acquired Immunodeficiency Syndrome - immunology
Acquired Immunodeficiency Syndrome - metabolism
Gene Expression Regulation
Gene Products, nef - metabolism
Gene Products, tat - metabolism
Genes, MHC Class I - genetics
HIV
HIV Infections - genetics
HIV Infections - immunology
HIV Infections - metabolism
HIV-1 - genetics
HIV-1 - immunology
HIV-1 - metabolism
Human immunodeficiency virus 1
Human Immunodeficiency Virus Proteins
Humans
immune surveillance
Immunologic Surveillance
MHC-I
Nef
nef Gene Products, Human Immunodeficiency Virus
Tat
tat Gene Products, Human Immunodeficiency Virus
Viral Regulatory and Accessory Proteins - metabolism
Vpu
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Summary:Since the beginning of the acquired immune deficiency syndrome (AIDS) pandemic in 1981, research on human immunodeficiency virus (HIV) has been focused on mechanisms by which the virus escapes from immune surveillance. Several human leucocyte antigen haplotypes have been shown to be associated with rapid disease progression or resistance to disease progression. In addition, HIV is able to down‐regulate major histocompatibility complex type I (MHC‐I) on the surface of the host cell. For this down‐regulation HIV seems to use three different mechanisms mediated by three different viral proteins. The viral Tat protein represses transcription of the MHC‐I, Vpu retains nascent MHC‐I chains in the endoplasmic reticulum and Nef mediates selective internalization of MHC‐I molecules from the plasma membrane. The last mechanism also provides protection to natural killer cells that attack cells with little or no MHC‐I on the cell surface. Together these mechanisms provide a very efficient escape from the host immune system.
ISSN:0014-2972
1365-2362
DOI:10.1046/j.1365-2362.2000.00697.x