Publication: Evaluating immunologic response and clinical deterioration in treatment-naive patients initiating first-line therapies infected with HIV-1 CRF01-AE and subtype B
Issued Date
2013-03-01
Resource Type
ISSN
10779450
15254135
15254135
Other identifier(s)
2-s2.0-84876374290
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Mahidol University
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SCOPUS
Bibliographic Citation
Journal of Acquired Immune Deficiency Syndromes. Vol.62, No.3 (2013), 293-300
Suggested Citation
Rebecca A. Oyomopito, Patrick C.K. Li, Somnuek Sungkanuparph, Praphan Phanuphak, Kok Keng Tee, Thira Sirisanthana, Pacharee Kantipong, Shinichi Oka, Chris K.C. Lee, Adeeba Kamarulzaman, Jun Yong Choi, Annette H. Sohn, Matthew Law, Yi Ming A. Chen Evaluating immunologic response and clinical deterioration in treatment-naive patients initiating first-line therapies infected with HIV-1 CRF01-AE and subtype B. Journal of Acquired Immune Deficiency Syndromes. Vol.62, No.3 (2013), 293-300. doi:10.1097/QAI.0b013e31827a2e8f Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/32474
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Title
Evaluating immunologic response and clinical deterioration in treatment-naive patients initiating first-line therapies infected with HIV-1 CRF01-AE and subtype B
Other Contributor(s)
University of New South Wales (UNSW) Australia
Queen Elizabeth Hospital Hong Kong
Mahidol University
The HIV Netherlands Australia Thailand Research Collaboration
University of Malaya
Chiang Mai University
Chiang Rai Regional Hospital
National Center for Global Health and Medicine
Hospital Sungai Buloh
Yonsei University
amfAR - The Foundation for AIDS Research
National Yang-Ming University Taiwan
Queen Elizabeth Hospital Hong Kong
Mahidol University
The HIV Netherlands Australia Thailand Research Collaboration
University of Malaya
Chiang Mai University
Chiang Rai Regional Hospital
National Center for Global Health and Medicine
Hospital Sungai Buloh
Yonsei University
amfAR - The Foundation for AIDS Research
National Yang-Ming University Taiwan
Abstract
Background: HIV-1 group M viruses diverge 25%-35% in envelope, important for viral attachment during infection, and 10%-15% in the pol region, under selection pressure from common antiretrovirals. In Asia, subtypes B and CRF01-AE are common genotypes. Our objectives were to determine whether clinical, immunological, or virological treatment responses differed by genotype in treatmentnaive patients initiating first-line therapy. Methods: Prospectively collected longitudinal data from patients in Thailand, Hong Kong, Malaysia, Japan, Taiwan, and South Korea were provided for analysis. Covariates included demographics, hepatitis B and C coinfections, baseline CD4 T lymphocyte count, and plasma HIV-1 RNA levels. Clinical deterioration (a new diagnosis of Centers for Disease Control and Prevention category B/AIDS-defining illness or death) was assessed by proportional hazards models. Surrogate endpoints were 12-month change in CD4 cell count and virologic suppression post therapy, evaluated by linear and logistic regression, respectively. Results: Of 1105 patients, 1036 (93.8%) infected with CRF01-AE or subtype B were eligible for inclusion in clinical deterioration analyses and contributed 1546.7 person-years of follow-up (median: 413 days, interquartile range: 169-672 days). Patients > 40 years demonstrated smaller immunological increases (P = 0.002) and higher risk of clinical deterioration (hazard ratio = 2.17; P = 0.008). Patients with baseline CD4 cell counts > 200 cells per microliter had lower risk of clinical deterioration (hazard ratio = 0.373; P = 0.003). A total of 532 patients (48.1% of eligible) had CD4 counts available at baseline and 12 months post therapy for inclusion in immunolgic analyses. Patients infected with subtype B had larger increases in CD4 counts at 12 months (P = 0.024). A total of 530 patients (48.0% of eligible) were included in virological analyses with no differences in response found between genotypes. Conclusions: Results suggest that patients infected with CRF01-AE have reduced immunologic response to therapy at 12 months, compared with subtype B-infected counterparts. Clinical deterioration was associated with low baseline CD4 counts and older age. The lack of differences in virologic outcomes suggests that all patients have opportunities for virological suppression. Copyright © 2012 by Lippincott Williams and Wilkins.