Immune Mechanisms in Murine Gammaherpesvirus-68 Infection
The murine gamma-herpesvirus-68 (MHV-68) is a relative of the Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV) that infects mice. All these gamma-herpesviruses are subject to immune control, but limit the impact of this control through immune evasion. Molecular evasio...
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Published in | Viral immunology Vol. 18; no. 3; pp. 445 - 456 |
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Format | Journal Article |
Language | English |
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01.09.2005
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Abstract | The murine gamma-herpesvirus-68 (MHV-68) is a relative of the Kaposi's sarcoma-associated herpesvirus
(KSHV) and Epstein-Barr virus (EBV) that infects mice. All these gamma-herpesviruses
are subject to immune control, but limit the impact of this control through immune evasion. Molecular
evasion mechanisms have been described in abundance. However, we can only speculate what
EBV and KSHV immune evasion contributes to the viral lifecycle. With MHV-68, we can analyze
in vivo
the contribution of immunological and virological gene expression to pathogenesis. While the
physiology of infection seems quite well conserved between these viruses, the pathologies associated
with immune suppression are obviously very different. MHV-68 is therefore more suited to uncovering
the basic biology of gamma-herpesvirus infection than to testing disease interventions. Nevertheless,
it may make some useful predictions about effective strategies of vaccination and infection
control. This review aims to outline our current state of knowledge and to highlight some
limitations of the MHV-68 model as it stands, in the hope of stimulating constructive progress. |
---|---|
AbstractList | The murine gamma-herpesvirus-68 (MHV-68) is a relative of the Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV) that infects mice. All these gamma-herpesviruses are subject to immune control, but limit the impact of this control through immune evasion. Molecular evasion mechanisms have been described in abundance. However, we can only speculate what EBV and KSHV immune evasion contributes to the viral lifecycle. With MHV-68, we can analyze in vivo the contribution of immunological and virological gene expression to pathogenesis. While the physiology of infection seems quite well conserved between these viruses, the pathologies associated with immune suppression are obviously very different. MHV-68 is therefore more suited to uncovering the basic biology of gamma-herpesvirus infection than to testing disease interventions. Nevertheless, it may make some useful predictions about effective strategies of vaccination and infection control. This review aims to outline our current state of knowledge and to highlight some limitations of the MHV-68 model as it stands, in the hope of stimulating constructive progress. The murine gamma-herpesvirus-68 (MHV-68) is a relative of the Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV) that infects mice. All these gamma-herpesviruses are subject to immune control, but limit the impact of this control through immune evasion. Molecular evasion mechanisms have been described in abundance. However, we can only speculate what EBV and KSHV immune evasion contributes to the viral lifecycle. With MHV-68, we can analyze in vivo the contribution of immunological and virological gene expression to pathogenesis. While the physiology of infection seems quite well conserved between these viruses, the pathologies associated with immune suppression are obviously very different. MHV-68 is therefore more suited to uncovering the basic biology of gamma-herpesvirus infection than to testing disease interventions. Nevertheless, it may make some useful predictions about effective strategies of vaccination and infection control. This review aims to outline our current state of knowledge and to highlight some limitations of the MHV-68 model as it stands, in the hope of stimulating constructive progress.The murine gamma-herpesvirus-68 (MHV-68) is a relative of the Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV) that infects mice. All these gamma-herpesviruses are subject to immune control, but limit the impact of this control through immune evasion. Molecular evasion mechanisms have been described in abundance. However, we can only speculate what EBV and KSHV immune evasion contributes to the viral lifecycle. With MHV-68, we can analyze in vivo the contribution of immunological and virological gene expression to pathogenesis. While the physiology of infection seems quite well conserved between these viruses, the pathologies associated with immune suppression are obviously very different. MHV-68 is therefore more suited to uncovering the basic biology of gamma-herpesvirus infection than to testing disease interventions. Nevertheless, it may make some useful predictions about effective strategies of vaccination and infection control. This review aims to outline our current state of knowledge and to highlight some limitations of the MHV-68 model as it stands, in the hope of stimulating constructive progress. The murine gamma-herpesvirus-68 (MHV-68) is a relative of the Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV) that infects mice. All these gamma-herpesviruses are subject to immune control, but limit the impact of this control through immune evasion. Molecular evasion mechanisms have been described in abundance. However, we can only speculate what EBV and KSHV immune evasion contributes to the viral lifecycle. With MHV-68, we can analyze in vivo the contribution of immunological and virological gene expression to pathogenesis. While the physiology of infection seems quite well conserved between these viruses, the pathologies associated with immune suppression are obviously very different. MHV-68 is therefore more suited to uncovering the basic biology of gamma-herpesvirus infection than to testing disease interventions. Nevertheless, it may make some useful predictions about effective strategies of vaccination and infection control. This review aims to outline our current state of knowledge and to highlight some limitations of the MHV-68 model as it stands, in the hope of stimulating constructive progress. |
Author | Stevenson, Philip G. Efstathiou, Stacey |
Author_xml | – sequence: 1 givenname: Philip G. surname: Stevenson fullname: Stevenson, Philip G. – sequence: 2 givenname: Stacey surname: Efstathiou fullname: Efstathiou, Stacey |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16212523$$D View this record in MEDLINE/PubMed |
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Snippet | The murine gamma-herpesvirus-68 (MHV-68) is a relative of the Kaposi's sarcoma-associated herpesvirus
(KSHV) and Epstein-Barr virus (EBV) that infects mice.... The murine gamma-herpesvirus-68 (MHV-68) is a relative of the Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV) that infects mice.... |
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SubjectTerms | Animals Antibodies, Viral Epstein-Barr Virus Infections - immunology Epstein-Barr Virus Infections - virology Gammaherpesvirinae - genetics Gammaherpesvirinae - immunology Gammaherpesvirinae - pathogenicity Genes, Viral Herpesviridae Infections - immunology Herpesviridae Infections - virology Herpesvirus 8, Human - immunology Herpesvirus 8, Human - pathogenicity Humans Mice Models, Biological Special Focus Section on Herpesvirus T-Lymphocytes - immunology Vaccination |
Title | Immune Mechanisms in Murine Gammaherpesvirus-68 Infection |
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