Maraviroc in Immunological Non-Responder (INR) HIV-1-infected Subjects
Status:
Completed
Trial end date:
2011-04-01
Target enrollment:
Participant gender:
Summary
Suboptimal improvement in cluster of differentiation 4 (CD4) cell count is not uncommon in
HIV-1-infected patients with suppressed plasma HIV-Ribonucleic acid (RNA) levels, and a
decrease in CD4 cell count in patients with suppressed or low level viremia has been
observed.
Although the efficacy of current antiretroviral medications is well established, some
antiviral combinations are very effective in suppressing HIV-1 load whereas do not exert any
effect on immune reconstitution.
Both T-cell immune activation and fibrosis of peripheral lymphoid tissue could create an
environment in which CD4 T cell count decrease in the setting of low or suppressed plasma
viremia is likely to occur.
Another fascinating hypothesis, which has still to be elucidated, is that reconstitution of
the depleted CD4 pool is blocked by an excess of glycoprotein 120 (gp120) HIV-1 protein. This
extra-production could be counteracted by an inhibitor of the chemokine (C-C motif) receptor
5 (CCR5) co-receptor that represents one of the major docking tools of HIV-1.
With this in mind, the investigators would like to propose and design a pilot exploratory
clinical trial involving a population of HIV-1-infected patients that rapidly reached a
virologic suppression without a reconstitution of their immune system.
Phase:
Phase 4
Details
Lead Sponsor:
ASST Fatebenefratelli Sacco Ospedale L. Sacco – Polo Universitario