Anti-interleukin-6 antibodies inhibit herpes simplex virus reactivation.
Herpes simplex viruses (HSVs) infect epithelial cells, become localized in neurons, and can reactivate in response to a variety of stimuli, including ultraviolet light and hyperthermia. The sequence of gene activation during viral replication is known, but the molecular linkage between exogenous stimuli and HSV reactivation has not been determined. It was hypothesized that interleukin (IL)-6 acts as a signal between exogenous stimuli and neurons, stimulating HSV reactivation from latency. Mouse corneas were infected with HSV-1, and ocular reactivation was induced 5-7 weeks later by thermal stress or corneal exposure to ultraviolet light. Anti-IL-6 monoclonal antibodies were administered to the latently infected mice 8-12 h before the reactivation stimulus. Treatment with anti-IL-6 antibodies resulted in significantly lower frequencies of ocular reactivation compared with those in mice treated with a control immunoglobulin. These results support the hypothesis that IL-6 plays a role in HSV reactivation from latency.
Kriesel
J D
JD
Department of Medicine, University of Utah School of Medicine, Salt Lake City 84132, USA.
Gebhardt
B M
BM
Hill
J M
JM
Maulden
S A
SA
Hwang
I P
IP
Clinch
T E
TE
Cao
X
X
Spruance
S L
SL
Araneo
B A
BA
D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology*; D005260:Female; D015850:Interleukin-6 / Q000502:physiology*; D051379:Mice; D008807:Mice, Inbred BALB C; D018139:Simplexvirus / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology; D014775:Virus Activation
D000911:Antibodies, Monoclonal; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha