Viral load monitoring has become a more definitive method of monitoring disease progression than CD4 counts, according to Hoffman La-Roche (www.Roche-HIV.com or www.hivatis.org/)

Viral load should be measured upon initial diagnosis of HIV infection and at 3 - 4 month intervals thereafter. Viral load should not be measured during an infection or after vaccination, since these events can cause significant but transient increases in viral load. Initial viral load measurement is used to determine the baseline viral load, assess the risk for rapid progression to AIDS and guide the decision of whether to initiate antiretroviral therapy. In asymptomatic patients with viral load >20,000 copies/mL, antiretroviral treatment should be offered. In patients receiving treatment, the viral load should be measured 2 - 8 weeks and 3 - 4 months following commencement of therapy to permit an initial assessment of drug efficacy and determine the maximum effect of the regimen respectively. The goal of antiretroviral therapy is maximal and durable suppression of viral load.

Protease inhibitors with their closer tailoring to the viral target have been in the vanguard of new approaches to the treatment of HIV. As protease inhibitors are almost exclusively used with partner drugs the safety profile of the partner drug can contribute or dominate. Drug-specific effects include pigmentation and gastrointestinal intolerance with zidovudine, diarrhea with dianosine and nelfinavir, hypersensitivity with abacavir, central nervous system symptoms with efavirnez and renal stones with indinavir. Finally a characteristic proximal renal tubular dysfunction is associated with adefovir dipivoxil - the first analogue reverse transcriptase inhibitor currently to be approved for the treatment of HIV.

The genetic variability of HIV means that sooner or later drug resistance will emerge, which will be typically reflected in a rebound of viral load. Use of a different combination therapy directed against the same or different viral mechanisms will then provide some degree of restoration of viral control.

Patients with poor prognostic signs may require aggressive therapy using four or more agents. While the CD4+ response provides a general index of disease status, this is a far from complete picture, particularly in terms of immune function restoration following antiviral therapy. A good CD4+ response is a welcome sign but should not supplant the more relevant guidance provided by plasma viral load, which must continue to be monitored.

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