An improvement in virologic response to highly active antiretroviral therapy in clinical practice from 1996 through

Richard D Moore1, Jeanne C Keruly, Kelly A Gebo

  • 1Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. rdmoore@jhmi.edu

Early studies of highly active antiretroviral therapy (HAART) use in clinical practice suggested suboptimal rates of viral suppression. HAART regimens and expertise in the use of HAART have since evolved, and we sought to determine how virologic response to HAART has changed in clinical practice. We compared all patients who started a first HAART regimen from 1996 through 2002 in a longitudinal cohort of HIV-infected patients in care in Baltimore. There were significant improvements in suppressing HIV RNA to < 400 copies/mL, ranging from 43.8% (1996) to 72.4% (2001-2002) by 6 months and from 60.1% (1996) to 79.9% (2001-2002) by 12 months (both P < 0.01 for trend). There were also significant improvements in CD4 cell response. Over time, there was a significant increase in the use of a nonnucleoside reverse transcriptase inhibitor (NNRTI) or boosted protease inhibitor (PI) regimen compared with a single PI as well as an increase in the number of patients who were antiretroviral (ARV) naive. There was also a significant temporal trend from 1996 through 2002 in achieving a suppressed HIV RNA level, adjusting for being ARV naive, specific HAART regimen, CD4 cell count, HIV-1 RNA level, and demographic factors. This suggests that improved virologic response may also be attributable to other factors such as a greater focus on medication adherence, improved ARV tolerability, and ease of dosing.

Related Concept Videos

Retrovirus Life Cycles01:10

Retrovirus Life Cycles

Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the retrovirus to...
Antiviral Nucleoside Inhibitors01:22

Antiviral Nucleoside Inhibitors

Antiviral Nucleoside InhibitorsAntiviral nucleoside inhibitors are structural analogs of natural nucleosides that interfere with viral DNA or RNA synthesis. These compounds selectively target viral polymerases due to their resemblance to host nucleosides, thereby disrupting viral genome replication.Mechanism of Acyclovir ActionAcyclovir is a guanosine analog with a three-carbon acyclic side chain. It selectively targets herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2),...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...