**1. Introduction**

62 Bacterial Artificial Chromosomes

[55] Balciunas D, Davidson AE, Sivasubbu S, Hermanson SB, Welle Z, Ekker SC. (2004).

[56] Kawakami, K., Takeda, H., Kawakami, N., Kobayashi, M., Matsuda, N., and Mishina,

[57] Kawakami, K. (2005) Transposon tools and methods in zebrafish. *Developmental* 

[58] Ellingsen S, Laplante MA, Konig M, Kikuta H, Furmanek T, Hoivik EA, Becker TS

[59] Nagayoshi, S., Hayashi, E., Abe, G., Osato,N., Asakawa, K., Urasaki, A., Horikawa, K.,

developmental genes: tcf7 and synembryn-like. *Development* 135(1), 159-169 [60] Woolfe A, Goodson M, Goode DK, Snell P, McEwen GK, Vavouri T, Smith SF, North P,

[61] Kleinjan DA, Bancewicz RM, Gautier P, Dahm R, Schonthaler HB, Damante G,

regulated genes in zebrafish. *Developmental Cell* 7, 133-144

*Genomics.* 5: 62.

3799-3811.

*Dynamics* 234, 244-254

development. *PLoS Biol.* (2005) Jan; 3: e7.

divergence. *PLoS Genet.* 4: e29

Enhancer trapping in zebrafish using the Sleeping Beauty transposon. *BMC* 

M. (2004) A transposon-mediated gene trap approach identifies developmentally

(2005) Large-scale enhancer detection in the zebrafish genome *Development.* 132:

Ikeo, K., Takeda, H., and Kawakami, K. (2008) Insertional mutagenesis by the Tol2 transposon-mediated enhancer trap approach generated mutations in two

Callaway H, Kelly K, Walter K, Abnizova I, Gilks W, Edwards YJ, Cooke JE, Elgar G. (2005) Highly conserved non-coding sequences are associated with vertebrate

Seawright (2008). A, Hever AM, Yeyati PL, van Heyningen V, Coutinho P. Subfunctionalization of duplicated zebrafish pax6 genes by cis-regulatory The varicella-zoster virus (VZV or Human Herpesvirus-3) is a member of the human herpesvirus family. Identified as the causative agent of chickenpox and shingles, VZV is a significant pathogen in the United States, infecting over 90% of the US population (Abendroth & Arvin, 1999). Primary VZV infections generally occur during childhood and result in a relatively benign illness termed varicella (chickenpox). However, like all herpesviruses, VZV will establish latency in the host's sensory neurons. This occurs specifically in the trigeminal ganglia and dorsal root ganglia (Arvin, 1996; Gilden et al., 2000), where the virus can hide from the immune system for years and often a lifetime.

Reactivation of this virus with increasing age or immunosuppression results in herpes zoster (shingles). Herpes zoster is a more painful, neurocutaneous infection associated with acute or chronic neuropathic pain and a significant incidence of post-herpetic neuralgia, a complication causing many patients to continue suffering excruciating pain, lasting anywhere from months to years after infection due to the resulting nerve damage (Cohen et al, 2007). This not only greatly increases the cost of medical care, but also significantly compromises the quality of life in the elderly (Pickering & Leplege, 2010; Opstelten et al., 2010; Burgoon et al, 1957).
