Abstract
Herpes simplex causes latent infections that periodically reactivate. Specific immunization attempts are failing to control herpes, prompting a fresh look at which host responses predominate. We report a NK complex-linked genetic locus, Rhs1, whose alleles influence the magnitude of experimental herpes simplex. Rhs1 provided rapid control of primary infection but caused a reciprocal increase in the number of latently infected neurons. Thus, in principle, establishment of latency is a consequence of efficient front line defense against herpesvirus infection. Based on conservation between human and mouse NK complexes, the data predict the presence of a human Rhs1 orthologue on chromosome 12p12-13.
Publication types
-
Comparative Study
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Acute Disease
-
Animals
-
Antigens / physiology
-
Antigens, Surface
-
Chromosome Mapping
-
Female
-
Ganglia, Sensory / immunology
-
Ganglia, Sensory / virology
-
Genetic Markers / immunology
-
Herpes Simplex / genetics
-
Herpes Simplex / immunology*
-
Herpes Simplex / mortality
-
Herpes Simplex / virology
-
Immunity, Innate / genetics
-
Killer Cells, Natural / immunology*
-
Killer Cells, Natural / virology*
-
Lectins, C-Type
-
Lethal Dose 50
-
Mice
-
Mice, Congenic
-
Mice, Inbred BALB C
-
Mice, Inbred C57BL
-
NK Cell Lectin-Like Receptor Subfamily B
-
Neurons / immunology*
-
Neurons / virology*
-
Peripheral Nerves / immunology
-
Peripheral Nerves / virology
-
Phenotype
-
Proteins / physiology
-
Skin / immunology
-
Skin / pathology
-
Skin / virology
-
Species Specificity
-
Viral Load
-
Virus Latency / genetics
-
Virus Latency / immunology*
Substances
-
Antigens
-
Antigens, Surface
-
Genetic Markers
-
KLRB1 protein, human
-
Lectins, C-Type
-
NK Cell Lectin-Like Receptor Subfamily B
-
Proteins