The advent of highly active antiretroviral therapy (HAART) at the end of the 20th century dramatically improved treatment for people with HIV-1 infection. Before HAART, cytomegalovirus (CMV) was a major cause of opportunistic infection in HIV-infected patients and was associated with accelerated progression to AIDS and death.
Paul Griffiths from the Royal Free and University College Medical School, London, UK, and colleagues investigated whether CMV remains a significant risk factor for progression of HIV disease and death in the era of HAART. 374 people with HIV-1 infection were studied; their CMV status was assessed by polymerase chain reaction (PCR) and rates of new CMV disease, new AIDS-defining disorders, and death were calculated over a 3-year period. CMV-positive status was significantly associated with more than a doubling in progression time to a new AIDS-defining disorder, and with a fourfold shorter time to death.
Professor Griffiths comments: "The detection of cytomegalovirus in blood by PCR continues to identify patients with a poor prognosis, even in the era of HAART. Randomised controlled clinical trials of drugs active against cytomegalovirus are needed to investigate whether this virus is a marker or a determinant of HIV disease progression."
In an accompanying Commentary (p 2101), Richard Whitley from the University of Alabama at Birmingham, USA, concludes: "The availability of this simple tool (PCR for assessment of blood specimens) could provide a useful addition to the management of HIV patients. Specifically, patients failing current HIV treatments could be probed for persistent detection of CMV DNA. Clearly such a strategy is not without expense.
However, the potential benefits to individuals with HIV disease must be considered, particularly with existing orally bioavailable drugs such as valganciclovir or new antivirals, that approach clinical development, including maribavir…With verification of these data, a randomised trial must be done in individuals known to be persistently PCR-positive for CMV DNA to assess the clinical benefit".
Contact: Professor Paul D. Griffiths, Department of Virology, Royal Free and University College Medical School, Rowland Hill Street, London NW3 2PF, UK; T): 44-0-20-7830-2997; F): 44-0-20-7830-2854; E): p.griffiths@rfc.ucl.ac.uk.
Dr. Richard J Whitley, University of Alabama at Birmingham, Departments of Pediatrics, Microbiology, Medicine, and Neurosurgery, Birmingham, AL 35233, USA; T) E): rwhitley@peds.uab.edu.
Journal
The Lancet