Recently a set of mathematical models have been developed by A.S. 
Perelson and
 others that have enhanced our understanding of the dynamics of HIV-1 
infection  
 in vivo.  Applying these models to data obtained from patients 
undergoing drug
 therapy has shown that they predict certain quantitative features of the
 interaction between HIV-1, the virus that causes AIDS, and the host 
defense
 system.  The most dramatic finding was that even though AIDS is a 
disease that
 occurs on a time scale of about 10 years, certain very rapid dynamical
 processes that underlie the disease process occur on time scales of hours
 to days. In addition, there are slower processes that occur on time 
scales of   
 weeks to months.  Because of the rapid dynamics it is important to 
analyze the  
 delays associated with the cellular dynamics and drug activation.  I 
have       
 extended previous models by including delays in the time course of 
infection.   
 Analysis of this model shows that cellular delay is negligible and hence 
allows 
 us to focus on the delay associated with the processing of AZT.  I then  
       
 developed a second model incorporating a delay in the processing of AZT, 
which  
 also includes an equation for a drug with variable efficacy.  This is 
the first
 time a model has looked at the variability of drug effectiveness and how 
it
 affects the dynamics of HIV-1 in infected patients.  I will discuss the 
current
 results of this model as well as future plans for adjusting the model to
 include further aspects of the biology.