kB , there are essential viral genes which also appear to regulate 
the transition from latent to active infection. An important 
viral regulatory protein in this process is Rev, an 18 kd nuclear 
protein which controls export of viral RNA from the nucleus to 
the cytoplasm of infected cells. In contrast to NF-/cB, the Rev 
protein is unique to the virus and unlikely to regulate essential 
cellular functions. It therefore becomes a preferred target for 
anti-viral gene therapy. 
Viral replication is critically dependent on the interaction 
of viral gene products with host cell factors. Because viruses 
are intimately associated with their host cells, it has been 
difficult to selectively interfere with replication in vivo. 
Successful anti-viral approaches have selectively targeted viral 
gene products. For example, the treatment of herpes simplex 
virus (HSV) infection has taken advantage of the ability of a 
viral gene, thymidine kinase, to modify a drug which is toxic to 
the host cell. This approach led to the development of guanosine 
analogues, including acyclovir and ganciclovir (2-4) , which are 
converted to DNA chain terminators only in HSV infected cells. 
In HIV infection, traditional pharmaceutic targeting has 
thus far provided limited benefits. Although AZT has relative 
selectivity for viral reverse transcriptase, its toxic effect on 
host cell function and its low therapeutic index has provided 
limited protection against the progression of AIDS. 
Although drug discovery has led to the identification of 
additional anti-viral drugs, the high rates of virus mutation has 
lead to the generation of resistant viral mutants. More 
Recombinant DNA Research, Volume 18 
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