Group I Primary HIV infection
Primary HIV infection (PHI) is also called the seroconversion
illness or acute HIV infection. It represents the stage of
infection after the acquisition of the virus when antibodies are
developing as shown in Figure 4.1. Between 25% and 65% of
people have been found to present with symptoms at the time of
seroconversion. These can range from a mild, glandular feverlike
illness to an encephalopathy. Common symptoms and signs
are shown in Box 4.2. The severe symptoms are rare. The
differential diagnosis of the mild seroconversion illness is
protean and, without a high index of suspicion and a history
indicating relevant risk behaviours or factors, the diagnosis may
be missed.
The appropriate diagnostic tests for PHI, which should be
carried out on serial blood samples, include tests for HIV
antibodies and antigen. If these are negative and PHI is
suspected, the definitive test is an HIV RNA PCR, which is the
most sensitive test for the detection and quantification of the
virus. Some of these assays are not routine and the
interpretation of investigation results during PHI is difficult,
therefore close consultation with colleagues in virology is
strongly advised.
At the time of PHI there is sometimes a high rate of viral
replication, leading to a transient rise in HIV viral load and
concomitant immunosuppression due to a short-lived fall in the
CD4 count. This may result in manifestations of HIV disease which are normally seen later in the infection, for example oral
candida. Diagnostic confusion as to the stage of HIV infection
may arise, which can only be resolved by following up the
patient for long enough to see the symptoms and signs resolve,
HIV antibodies appear, the viral load fall and the CD4 count
rise.
Treatment should be directed at alleviating any symptoms,
and there is considerable interest in the possible use of
antiretroviral agents at this time because the virus may be more
susceptible due to the relatively low numbers of virus particles
which can replicate, the reduced ability of the predominantly
non-syncytium-inducing strains of virus to infect a wide variety
of cell types and the enhanced immune response seen in PHI.
Such treatment may decrease long-term damage to the
immune system and delay or even prevent the development of
AIDS.
However, if not started within 12–18 months of PHI the
theoretical advantage may be lost and, in any case, has to be
balanced against the uncertain outcome, drug toxicity,
adherence difficulties and the possibility of developing resistant
virus, limiting future treatment options.
