Related Experiment Video
Updated: Sep 29, 2026

Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors
Published on: April 9, 2014
Immunologic and virologic consequences of temporary antiretroviral treatment interruption in clinical practice
Ray Y Chen1, Andrew O Westfall, James L Raper
1Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
To determine the long-term immunologic and virologic effects of antiretroviral treatment interruptions, a retrospective analysis of an ongoing observational database was performed at a university HIV clinic. All patients who began highly active antiretroviral therapy (HAART) after January 1, 1996 and (1) were HAART experienced for >/=90 days, (2) had a treatment interruption (TI) for >/=30 days, (3) resumed HAART for >/=30 days, and (4) had CD4(+) cell counts performed pre- and post-TI were included. Main outcome measures included the following: Immunologic success was defined as a post-TI CD4(+) cell count >90% of the pre-TI CD4(+) cell count (post-TI/pre-TI, >90%). Virologic success was defined as a post-TI viral load (VL) less or equal to twice the pre-TI VL (post-TI/pre-TI, =2) or a post-TI VL of <1000 copies/ml. The pre-TI (baseline) value was the value at the start of the TI (range, -20 to +7 days); the post-TI value was the highest CD4(+) cell count and lowest VL copy achieved during the follow-up window (270 days). One thousand and eight patients were included in the analysis and 75 met the inclusion criteria. Forty-four of 75 patients (58.6%) achieved a successful immunologic outcome and 52 of 68 patients (76.5%; 7 patients did not have a VL determined within the specified periods) achieved a successful virologic outcome. No factors predicting success were identified. The median CD4(+) cell counts pre- and post-TI were 233 and 231 cells/microl, respectively; the median VLs pre- and post-TI were 11,456 and 404 copies/ml, respectively. We conclude that the majority of our patients in virologic failure who underwent a temporary TI recovered 90% of their baseline CD4(+) cell counts and returned to within 2-fold of their baseline VL when HAART was resumed.
To determine the long-term immunologic and virologic effects of antiretroviral treatment interruptions, a retrospective analysis of an ongoing observational database was performed at a university HIV clinic. All patients who began highly active antiretroviral therapy (HAART) after January 1, 1996 and (1) were HAART experienced for >/=90 days, (2) had a treatment interruption (TI) for >/=30 days, (3) resumed HAART for >/=30 days, and (4) had CD4(+) cell counts performed pre- and post-TI were included. Main outcome measures included the following: Immunologic success was defined as a post-TI CD4(+) cell count >90% of the pre-TI CD4(+) cell count (post-TI/pre-TI, >90%). Virologic success was defined as a post-TI viral load (VL) less or equal to twice the pre-TI VL (post-TI/pre-TI, =2) or a post-TI VL of <1000 copies/ml. The pre-TI (baseline) value was the value at the start of the TI (range, -20 to +7 days); the post-TI value was the highest CD4(+) cell count and lowest VL copy achieved during the follow-up window (270 days). One thousand and eight patients were included in the analysis and 75 met the inclusion criteria. Forty-four of 75 patients (58.6%) achieved a successful immunologic outcome and 52 of 68 patients (76.5%; 7 patients did not have a VL determined within the specified periods) achieved a successful virologic outcome. No factors predicting success were identified. The median CD4(+) cell counts pre- and post-TI were 233 and 231 cells/microl, respectively; the median VLs pre- and post-TI were 11,456 and 404 copies/ml, respectively. We conclude that the majority of our patients in virologic failure who underwent a temporary TI recovered 90% of their baseline CD4(+) cell counts and returned to within 2-fold of their baseline VL when HAART was resumed.
Related Concept Videos
Inhibitors of Viral Protein Synthesis
Retrovirus Life Cycles
Antiviral Nucleoside Inhibitors
Immunodeficiency Diseases
There are three main causes of immunodeficiency disorders...
Therapeutic Drug Monitoring: Affecting Factors
Pulmonary Tuberculosis I
Causative Organism
The primary infectious agent causing tuberculosis is Mycobacterium tuberculosis, a slow-growing, acid-fast, aerobic rod that exhibits sensitivity to heat and ultraviolet light. Instances of Mycobacterium bovis and Mycobacterium avium contributing to the development of TB infection are rare.
Mode of...

