HHV-6 and Natural Killer Cells




P.P. Banerjee on IFN-gamma-Dependent Demyelinating Activity by Natural Killer Cells is Regulated by HLA-G Upregulation on Oligodendrocytes During HHV-6 Infection.

HHV-6 Modulates Natural Killer Cells Via IL-15 Production

HHV-7 and Natural Killer Cells
The Human Herpesvirus-7 (HHV-7) U21 Immunoevasin Subverts NK-Mediated Cytoxicity through Modulation of MICA and MICB
Christine L. Schneider and Amy W. Hudson
Abstract
Herpesviruses have evolved numerous immune evasion strategies to facilitate establishment of lifelong persistent infections. Many herpesviruses encode gene products devoted to preventing viral antigen presentation as a means of escaping detection by cytotoxic T lymphocytes. The human herpesvirus-7 (HHV-7) U21 gene product, for example, is an immunoevasin that binds to class I major histocompatibility complex molecules and redirects them to the lysosomal compartment. Virus infection can also induce the upregulation of surface ligands that activate NK cells. Accordingly, the herpesviruses have evolved a diverse array of mechanisms to prevent NK cell engagement of NK-activating ligands on virus-infected cells. Here we demonstrate that the HHV-7 U21 gene product interferes with NK recognition. U21 can bind to the NK activating ligand ULBP1 and reroute it to the lysosomal compartment. In addition, U21 downregulates the surface expression of the NK activating ligands MICA and MICB, resulting in a reduction in NK-mediated cytotoxicity. These results suggest that this single viral protein may interfere both with CTL-mediated recognition through the downregulation of class I MHC molecules as well as NK-mediated recognition through downregulation of NK activating ligands.

The Human Herpesvirus-7 (HHV-7) U21 Immunoevasin Subverts NK-Mediated Cytoxicity through Modulation of MICA and MICB
Christine L. Schneider, Amy W. Hudson
Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America
Abstract
Herpesviruses have evolved numerous immune evasion strategies to facilitate establishment of lifelong persistent infections. Many herpesviruses encode gene products devoted to preventing viral antigen presentation as a means of escaping detection by cytotoxic T lymphocytes. The human herpesvirus-7 (HHV-7) U21 gene product, for example, is an immunoevasin that binds to class I major histocompatibility complex molecules and redirects them to the lysosomal compartment. Virus infection can also induce the upregulation of surface ligands that activate NK cells. Accordingly, the herpesviruses have evolved a diverse array of mechanisms to prevent NK cell engagement of NK-activating ligands on virus-infected cells. Here we demonstrate that the HHV-7 U21 gene product interferes with NK recognition. U21 can bind to the NK activating ligand ULBP1 and reroute it to the lysosomal compartment. In addition, U21 downregulates the surface expression of the NK activating ligands MICA and MICB, resulting in a reduction in NK-mediated cytotoxicity. These results suggest that this single viral protein may interfere both with CTL-mediated recognition through the downregulation of class I MHC molecules as well as NK-mediated recognition through downregulation of NK activating ligands.

Popular Posts in the Last 7 Days

Dr. Bhupesh Prusty and Professor Thomas Rudel discuss their HHV-6 research

Will Fauci screw up Zika as much as he has screwed up HHV-6, AIDS and Chronic Fatigue Syndrome?

The Chronic Fatigue Syndrome and HHV-6 Scientist of the Year

If you want to know the whole truth about Chronic Fatigue Syndrome, you need to go Beyond Unrest

Why is the Chronic Fatigue Syndrome community ignoring the biggest breakthrough?

Is the CDC giving out a drug that will kill gay people and African Americans?

Popular Post in the Last 30 Days

Dr. Bhupesh Prusty and Professor Thomas Rudel discuss their HHV-6 research

If you want to know the whole truth about Chronic Fatigue Syndrome, you need to go Beyond Unrest

More evidence HHV-6 is the cause of Chronic Fatigue Syndrome.

Will Fauci screw up Zika as much as he has screwed up HHV-6, AIDS and Chronic Fatigue Syndrome?

Popular Posts from the Last Year

Dr. Bhupesh Prusty and Professor Thomas Rudel discuss their HHV-6 research

Oral Kaposi's Sarcoma looks like the Crimson Crescents in Chronic Fatigue Syndrome patients.

If you want to know the whole truth about Chronic Fatigue Syndrome, you need to go Beyond Unrest

More evidence HHV-6 is the cause of Chronic Fatigue Syndrome.

All Time Most Popular Posts

Dr. Bhupesh Prusty and Professor Thomas Rudel discuss their HHV-6 research

Anthony Fauci was part of the gang that silenced and destroyed Judy Mikovits.

Is Chronic Fatigue Syndrome the other AIDS epidemic in the gay community?

Was Judy Mikovits destroyed because her XMRV work would have ultimately shown HIV is a total fraud?