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Aim of anti-HIV drugs is to keep viremia levels or viral load as low as possible.
Viral load measures how many copies of the HIV virus there are in a unit of the
individual’s blood. Viral load changes are often described as “log” changes. The
viral load test is one of several important tools for physicians to assess the effi ciency
and health of a person’s immune system. Current HAART anti-HIV therapies aim
to destroy the viruses in circulation and reduce viremia levels. Various studies have
shown that viremia levels correlate with length of survival. However, AIDS is a
dynamic condition, in which the rate of creation of new virus particles is balanced
by the rate of their destruction, primarily by the body’s innate defenses. Viral load
rises sharply if mutations occur in HIV. Secondary infection can precipitate progres-
sion to the AIDS stage, which is characterized by rapidly rising HIV viral loads
(viremia), and concomitantly rapidly declining CD4+ T cells (an important compo-
nent of human immune system). Eventually, the patient dies of complications
related to the debilitation of immune response, often by a variety of secondary
infections or even various cancers.
HAART has transformed AIDS from an inevitably fatal condition to a chronic,
manageable disease in some settings. The median survival of asymptomatic HIV-
infected individuals with viremia under control is ~10 years. During the asymptom-
atic stage, it is known that the level of the steady state viremia correlates with the
future progression of the disease and the life span of the patient. In most patients,
HAART therapy is usually initiated only after the CD4+ T cell count falls <350 per
ul. The two important reasons for delaying the initiation of HAART are (i) patient’s
economic conditions, and (ii) the fear that when resistance against HAART due to
mutations, there is no recourse, although changes in the drug combinations may
provide “temporary” control.
A 48-week course of antiretroviral therapy in patients with primary HIV infec-
tion delayed disease progression, although not signifi cantly longer than the duration
of the treatment (SPARTAC Trial Investigators 2013 ). The fi nding that this approach
altered the course of the two main markers of HIV disease progression, CD4+ count
and the HIV RNA level, beyond the treatment period is an intriguing observation
that requires further evaluation.
Survival varies a lot and depends on the stage HIV infection is detected and the
treatment. Patients who have already developed AIDS at presentation have a high
risk of mortality within 1 year, and a much worse life expectancy. Patients with
newly diagnosed asymptomatic HIV infection in the HAART era may survive for
20 years after diagnosis according to current projections. These results are limited
by uncertainty regarding some factors. For example, the effi cacy of HAART may
gradually decrease over time due to accumulation of resistance mutations. Although
this may be balanced by the introduction of a more potent salvage therapy, the
impaired immune functions and the adverse effects of some HAART regimens on
metabolic profi les may also take their toll in the late course of the illness, and may
interact synergistically rather than additively with underlying diabetes mellitus or
coronary artery disease.
11 Personalized Management of Infectious Diseases