Background:
The improvements in HIV infection therapy and the large availability of antiretroviral drugs have led
to an increased survival among HIV infected people, and a simultaneously to a raised morbidity and mortality due to notAIDS-related events in this group compared to the general population. An increased systemic inflammation and a persistent
immune activation play a pivotal role in determining high rates of non-AIDS comorbidities. In the last years, many natural or
synthetic immunomodulatory molecules acting by different mechanisms have been conceived. Pidotimod is a synthetic
dipeptide molecule showing immunomodulatory properties. The aim of this pilot study was to evaluate the effects of
Pidotimod supplementation on residual inflammation in HIV infected population.
Methods:
Forty HIV positive individuals under cART were enrolled: 30 were treated with Pidotimod supplementation (study
group) and 10 served as control group (without Pidotimod supplementation). For all participants, Cystatin C, PCR, ESR,
microalbuminuria, TNF-α, INF-γ, IL-4, IL-10, IL1β, IL-18 and IL-2 were measured at enrolment (T0), 4 weeks after of
Pidotimod supplementation (T1), and 4 weeks after completing supplementation (T2).
Results:
In HIV positive participants treated with Pidotimod, the evaluation of cytokine levels showed that IL-10, IFN gamma,
and IL-4 were significantly higher at enrolment compared to the control group. The increase under Pidotimod treatment
persisted after supplementation suspension, while the pro-inflammatory cytokines levels were reduced. Salivary IgA also
increased during 4 weeks of supplementation and persisted at 4 weeks after completing supplementation. On the other hand ,
the Cystatin C and microalbuminuria levels decreased over the time, at greater extent the Cystatin C serum levels.
Conclusions:
The study findings showed that the HIV population receiving Pidotimod achieved a rebalancing of proinflammatory and anti-inflammatory cytokines as well as a significant reduction in cystatin C levels. The treatment further
allowed for an increase in salivary IgA levels at all the analyzed times, as secondary event to a remodulation of the
immunological status obtained with pidotimod. This approach could represent a new way to design new intervention strategies
aimed at improving the persistent immune activation status in the virologically suppressed HIV population.
