The July 1999 issue of Nature Medicine has the experts calling for an "urgent clinical evaluation of HIV entry inhibitors", which are now needed due to the limitations of the HAART therapies (Michael and Moore, 1999). The article further describes the major role of CCR5 (R5) tropic viruses in early infection. Drugs, which target entry via this receptor, could have high clinical impact.

Peptide T® is such a drug, and three independent laboratories have recently confirmed Peptide T'sŪ potent R-5 mediated anti viral effects. Recent clinical results show an antiviral effect in patients (Polianova et al., 2003 and new data from the NIMH). Of particular interest was the ability of Peptide T to suppress virus in monocyte and persistently infected PBMCs, the treatement resistant viral reservoir. HAART drugs do not effectively suppress infection of the monocytes and even some T cells remain productively infected. These cells reinfect the body and are a major impediment to a durable treatment or cure. Peptide T seems to provide unique benefits in targeting these cellular reservoirs.

Peptide T® which use the CCR5 receptor (Polianova, 2001; Polianova, 2005). These "R5-tropic" isolates typically initiate infection, populate the brain where they cause Neuro-AIDS, and predominate during the early and middle periods of infection. Peptide T blocks the CCR5 receptor and can be added to current therapies without added toxicities. No obvious viral resistance was detected in pateints receiving Peptide T for 6 months. Peptide T might be useful during treatment interuptions to provide antiviral benefit in the absence of HAART therapies. This possibility needs to be determined in controlled trials.preferentially blocks HIV strains.

Part of the excitement and the renewed hope for major clinical benefit has been generated by the Nature Medicine article. It points out that the urgently sought R5 HIV entry inhibitor will produce the greatest reductions in virus levels when added to standard therapies since it interferes with an as yet un-exploited part of the viral life cycle. Peptide T® has recently been shown to be an antagonist at R5 chemokine receptors and a potent inhibitor of HIV strands which use the CCR5 chemokine receptors to enter and infect cells. Peptide T suppressed virus in patients are in particularly effective when used together with correct HAART therapies (Polianova et al, Antiviral Res., 2005). Peptide T's® non-toxic profile would further enable it to be rationally added to any anti-viral regimen where the development of resistance has started to increase virus levels.