The Role of Immune Mechanisms in Control of Herpes Simplex Virus Infection of the Peripheral Nervous System
Underlying the recurrent cutaneous lesions caused by herpes simplex virus (HSV) is a sophisticated virus-host relationship involving primary sensory neurons. These cells may become productively infected, but sometimes virus replication is interrupted for long periods, producing a reservoir of latent herpes in the nervous system from which infection can periodically reactivate. How the balance is tipped in favor of either productive or latent infection and how productive infection of neurons is rapidly controlled (which, in general, it is) are prominent contemporary questions for herpes virologists. In this chapter, we critically review the clinical and experimental evidence suggesting that the host’s adaptive immune response makes a vital contribution to the control of established HSV replication in the nervous system, and we dwell on the controversial issue of the fate of productively infected neurons.
KeywordsDorsal Root Ganglion Herpes Simplex Virus Herpes Simplex Virus Type Primary Sensory Neuron Herpes Simplex Virus Infection
Unable to display preview. Download preview PDF.
- Cunningham AL (1991) Strategies for control of recurrent herpes simplex. Todays Life Sci 3: 32–40Google Scholar
- DeMaeyer-Guignard J, Dandoy F, Bailey DW, DeMaeyer E (1986) Interferon structural genes do not participate in quantitative regulation of interferon production by If loci as shown by C57BL/6 mice that are congenic with BALB/c mice at the alpha interferon gene cluster. J Virol 58: 743–747Google Scholar
- Field HJ, Bell SE, Elion GB, Nash AA, Wildy P (1979) Effect of acycloguanosine treatment on acute and latent herpes simplex infections in mice. Antimicrob Ag Chemother 15: 554–561Google Scholar
- Simmons A, Tscharke DC (1992) Anti-CD8 impairs clearence of HSV from the nervous system: implications for the fate of virally infected neurons. J Exp Med (in press)Google Scholar
- Steiner I, Spivack JG, Deshmane SL, Ace CI, Preston CM, Fräser NW (1990) A HSV 1 mutant containing a nontransinducing Vmw65 protein establishes latent infection in vivo in the absence of viral replication and reactivates efficiently from explanted trigeminal ganglia. J Virol 64:1630–1638PubMedGoogle Scholar
- Teague O, Goodpasture EW (1923) Experimental herpes zoster. J Med Res 24:185–200Google Scholar
- Wildy P, Field HJ, Nash AA (1982) Classical herpes latency revisited. Symposium 33, Society for General Microbiology. Cambridge University Press, CambridgeGoogle Scholar
- Yasukawa M, Zarling JM (1984) Human cytotoxic T-cell clones directed against herpes simplex virus-infected cells. II. Bifunctional clones with cytotoxic and virus-induced proliferative activities exhibit herpes simplex virus types 1 and 2 specific or type common reactivities. J Immunol 133: 2737–2742Google Scholar