Loss of cytomegalovirus (CMV) viraemia following highly active antiretroviral therapy in the absence of specific anti-CMV therapy

Citation
J. Deayton et al., Loss of cytomegalovirus (CMV) viraemia following highly active antiretroviral therapy in the absence of specific anti-CMV therapy, AIDS, 13(10), 1999, pp. 1203-1206
Citations number
18
Categorie Soggetti
Immunology
Journal title
AIDS
ISSN journal
02699370 → ACNP
Volume
13
Issue
10
Year of publication
1999
Pages
1203 - 1206
Database
ISI
SICI code
0269-9370(19990709)13:10<1203:LOC(VF>2.0.ZU;2-1
Abstract
Objective: To determine the effect of highly active antiretroviral therapy (HAART) on cytomegalovirus (CMV) viraemia and retinitis in patients at high risk of disease. Design: Sixteen patients with CMV viraemia, but no evidence of end organ di sease at the time of first receipt of HAART including a protease inhibitor, were studied. No patient had ever received specific anti-CMV therapy. Methods: CMV load in blood was measured using quantitative competitive PCR at baseline and for a median follow-up of 21 months. Regular ophthalmologic al screening for retinitis was conducted throughout the study period. Results: All 16 patients became CMV negative by PCR following the commencem ent of HAART. CMV loads prior to treatment ranged From 2.0 x 10(3) to 4.1 x 10(6) copies/ml (median, 7.6 x 10(4) copies/ml). The median time to becomi ng PCR negative was 13.5 weeks (range, 5-40 weeks). Fourteen patients remai ned CMV negative throughout follow-up. CMV viraemia recurred in two patient s; these individuals were indistinguishable with respect to either baseline parameters or response to antiretroviral therapy. None of the 16 patients developed CMV retinitis. Conclusions: HAART including a protease inhibitor can result in the complet e suppression of CMV viraemia, an effect not previously observed in HIV-inf ected patients in the absence of specific anti-CMV therapy. This response c orrelated with protection against CMV retinitis in a group of patients at h igh risk of development of disease. These results help to explain why the n atural history of CMV disease has altered since the introduction of such th erapeutic regimens. (C) 1999 Lippincott Williams & Wilkins.