HAART therapy

Lipodystrophy, well recognized with stavudine, has also been reported in nine of 56 patients taking combined HAART therapy including nevirapine, although there must be some doubt as to which drug or combination was responsible (838). 

Highly Active Antiretroviral Therapy (HAART) HAART slows or inhibits reverse transcriptase and protease enzymes by using several antiretroviral agents. HAART decreases the viral load. The viral load measures the amount of virus in the body. A decreased viral load causes an increase in CD4+ T cells and results in the immune system being able to identify, neutralize, and destroy non-self-cells. HAART therapy must be adhered to because the virus can become resistant to the antiretroviral agents. The patient must also adhere to nutritional therapy and avoid infections. 

Treatment for CMV retinitis and systemic CMV infection has markedly improved over the last decade (57). There are two treatment principles for CMV infection. The first principle is to reverse or improve the underlying cause of immunosuppression. This may be possible in some cases by decreasing immunosuppressive medications, for example, after organ transplantation. This is now possible in AIDS by commencing or altering HAART therapy to improve the immune status (4,24). 

Use of the ganciclovir implant and eventual discontinuation of systemic therapy may be possible in selected patients with improved immunity due to HAART and this approach may result in better long-term visual outcomes (100,106,107). In patients who have not yet received HAART when the CMV retinitis is treated with an implant, systemic therapy for CMV is indicated until the CD4+ count has stabilized appropriately at an elevated level. In patients who develop their initial episode of CMV retinitis while undergoing HAART therapy, this is a sign of progressive immune dysfunction and reassessment of the antiretroviral therapy is indicated. Use of the implant may be especially useful in these patients who are undergoing readjustment of HAART or who have failed HAART as longer term CMV control can be provided by the implant. 

It is unclear as to whether the latently infected resting reservoir is important in the strong viral load re-emergence that follows the cessation of HAART therapy. However, it is clear that the lifetime of these infected resting cells may prevent the eradication of the HIV-1 from the patient [127]. At the same time, the efficacy of prolonged HAART therapy is compromised by the side effects of the drugs, and by the emergence of resistant viruses. 

As cellular activation induces viral expression, and causes the former latent viruses to become exposed to HAART therapy, several efforts have been made to activate in vivo the silent proviruses by activating the resting CD4 T cells. However, the adverse effects and poor clinical benefit found indicate that this approach is not of value [147, 148]. Prostratine and DPP are not tumor-promoting phorbol esters, but are under examination because they can activate the provirus without complete activation of the cell [149, 150]. However, the elimination of cells infected with latent proviruses is not yet sufficiently efficient, and much needs to be done to address the... 

The patient must adhere to HAART therapy as the virus becomes resistant and the antiretroviral agents lose their therapeutic effect. In addition, patients must avoid opportunistic infections and aggressive prophylaxis and treatment of opportunistic infections that do occur is recommended. Nutritional therapy, complementary therapy, and supportive care are also necessary. 

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