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defined as below 50 copies per ml) in blood. In one class, the nucleoside ana-
logues resemble the natural substances that become building blocks of HIV-
DNA; and when reverse transcriptase tries to add the drugs to a developing
strand of HIV-DNA, the drugs prevent completion of the strand. The other
agent in this class, non-nucleoside reverse transcriptase inhibitors, composed
of other kinds of substances, constitute the second class of anti-retrovirals.
Theotherclass,theproteaseinhibitors,blockstheactive,catalyticsiteofthe
HIV protease, thereby preventing it from cleaving newly made HIV proteins.
-
HIV therapy is classified into three classes: mono-therapy, combined therapy
and triple therapy. Mono-therapy (such as based on reverse transcriptase
inhibitor) or combined drug therapy (reverse transcriptase and protease in-
hibitors) are considered to suppress the viral multiplication. Because of in-
completely blocking the replication pathway and occasionally creation of a
resistant virus strain, the CD4 T counts will come back to the pre-treatment
baseline within many weeks (Fig. 2). The problem of drug resistance in the
treatment has become an increasing significant barrier in the effectiveness of
AIDS immune-therapy.
-
Currently, there is no single class of drug that can completely prevent HIV
from replicating. Treatment with drug combinations is in only 50% of the
cases successful in inhibiting viral replication to undetectable levels. In the
remaining 50% of cases viruses can be detected with a reduced sensitivity
to one or more drugs from the patients regimen. Theory and clinical trials
indicate that the best way to achieve maximum viral suppression is through
highly active anti-retroviral therapy (HAART), which consists of triple ther-
apy including two nucleoside analogues and a protease inhibitor.
CD4+T
CD4+T
70
20
60
50
weeks
10
20
30
40
50
60
40
30
-20
20
-40
10
weeks
10
20
30
40
50
60
70
-60
(a)
(b)
Fig. 2.
Clinical data for mono-therapy (CD4 + T count is compared with baseline):
(a) This study administered patients either with a placebo control (hash line) or AZT
(solid line) for 62 weeks. The treatment started when CD4 T counts were between 200
and 500/ml [1]. (b) The results indicated that the effects of mono-therapy AZT on
non-progressors can not be sustained above base line for more than 70 weeks [9].
