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Journal ArticleDOI

Viral mutations, tcr antagonism and escape from the immune response

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TLDR
This data indicates that TCR contact sites within individual viral epitopes in certain persistent human viruses can abrogate or antagonize the recognition of the corresponding wild-type epitope, and it has been suggested that such mutations may contribute to viral persistence.
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This article is published in Current Opinion in Immunology.The article was published on 1995-08-01. It has received 54 citations till now. The article focuses on the topics: Epitope & T-cell receptor.

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Citations
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Journal ArticleDOI

Pathogenesis of chronic hepatitis C: immunological features of hepatic injury and viral persistence.

TL;DR: The dominant cause of viral persistence during HCV infection may be the development of a weak antiviral immune response to the viral antigens, with corresponding inability to eradicate infected cells.
Book

Immunology and Evolution of Infectious Disease

TL;DR: In this age of modern era, the use of internet must be maximized to get the on-line immunology and evolution of infectious disease book, as the world window, as many people suggest.
Journal ArticleDOI

Immunological significance of cytotoxic T lymphocyte epitope variants in patients chronically infected by the hepatitis C virus.

TL;DR: Interestingly, follow up analysis over a period of up to 46 mo revealed that, in contrast to the relatively high frequency of escape variants initially observed, the subsequent emergence rate of CTL escape variants was very low.
Journal ArticleDOI

Hepatitis C Virus Infection Involves CD34+Hematopoietic Progenitor Cells in Hepatitis C Virus Chronic Carriers

TL;DR: It is suggested that HCV replication can occur in the early differentiation stages of hematopoietic progenitor cells, and that they may be an important source of virus production.
References
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Journal ArticleDOI

TH1 and TH2 cells: different patterns of lymphokine secretion lead to different functional properties.

TL;DR: Two types of cloned helper T cells are described, defined primarily by differences in the pattern of lymphokines ynthesized, and the different functions of the two types of cells and their lymphokine synthesis are discussed.
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Rapid turnover of plasma virions and CD4 lymphocytes in HIV-1 infection

TL;DR: Treatment of infected patients with ABT-538 causes plasma HIV-1 levels to decrease exponentially and CD4 lymphocyte counts to rise substantially, indicating that replication of HIV- 1 in vivo is continuous and highly productive, driving the rapid turnover ofCD4 lymphocytes.
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A cell culture model for T lymphocyte clonal anergy

TL;DR: The T cell enters an unresponsive state known as clonal anergy in which the T cell is incapable of producing its own growth hormone, interleukin-2, on restimulation.
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Cytotoxicity mediated by T cells and natural killer cells is greatly impaired in perforin-deficient mice

TL;DR: Perforin-deficient mice have been generated by homologous recombination to determine whether the effects of CDS+ cytolytic T cells and natural killer cells are mediated by pore formation involving perform, and perforin is therefore a key effector molecule for T-cell- and natural Killer- cell-mediated cy tolysis.
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Hepatitis B virus immunopathogenesis

TL;DR: Elucidation of the immunological and virological basis for HBV persistence may yield immunotherapeutic and antiviral strategies to terminate chronic HBV infection and reduce the risk of its life-threatening sequellae.
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