As with tuberculosis, earlier identification and treatment is the way to tackle HIVBMJ 2012; 344 doi: http://dx.doi.org/10.1136/bmj.e2874 (Published 27 April 2012) Cite this as: BMJ 2012;344:e2874
- Philip Mortimer, retired virologist, Oxford
After 30 years and thousands of scientific papers published on AIDS and its virus, can we see the wood for the trees? Would earlier diagnosis and treatment, by interrupting HIV transmission and limiting its rising incidence, better control its spread and ultimately reduce costs?
Analogies sometimes help. Even before HIV had been discovered AIDS was being compared with chronic hepatitis B. The groups at risk and the routes of transmission were similar, and in both infections a carrier state eventually led to the exhaustion of the target tissue. HIV has, however, proved itself unlike hepatitis B virus—it has continued to resist attempts to develop a vaccine against it, but is much more susceptible to antiviral treatment.
With the drug treatment of HIV now offering such promise, a better analogy lies in the conquest of tuberculosis by combined drug treatment in the 1950s. The stigma that attached to tuberculosis might have allowed case finding and contact tracing to be deemed too difficult, but it was generally accepted that intensified measures to find cases of active tuberculosis were justified to get the full benefit from streptomycin based treatments. On evidence or suspicion of an exposure, and even without, mobile mass x ray units were dispatched to factories and schools. At recruitment centres and in nurses’ homes young people were skin tested. If reactive they were referred for a chest radiograph. Self referral was also made possible.
The possibility of exposure to tuberculosis was less easily recognised than for HIV, so case finding was not cheap. In 1950 it cost as much as £632 (at least £17 000 (€20 800; $27 300) in 2011 terms) to identify an active case of tuberculosis by mass radiography.1 But once a case was found treatment was started and steps were taken to ensure compliance and as far as possible detect and deal with relapses. Counts of acid fast bacilli and culture of sputum smears were used to estimate infectivity and check for drug resistance. To delay treatment until a case deteriorated or became open was not an option.
With the introduction of combined drug treatment, notifications of respiratory tuberculosis in England and Wales fell, from 42 435 in 1950 to 20 799 in 1960, and to a low of 3942 in 1990.2 Dispensaries and sanatoriums, immobilisations and sunlight exposures, surgical pneumothoraces and pneumonectomies: these treatments were all abandoned. Effective case detection and combined drug therapy made tuberculosis an uncommon disease.
The prevalence of HIV infection in the UK may by now have exceeded that of active tuberculosis in the era immediately before antibiotics, and this prompts the question: might earlier diagnosis and antiviral treatment do for epidemic HIV what the introduction of streptomycin did for tuberculosis? Antiviral drug combinations are already restoring normal life to those whose immune function is faltering, but they could offer all those found to be infected the suppression of HIV replication, the possibility of longer preservation of immune function,3 and the likely elimination of infectivity other than in the special circumstances of blood, tissue, or organ donation.4 The extent to which transmissions during the early hyperinfectious phase would continue would depend on the level of antiretroviral coverage.
Before antituberculous drugs were available, chest physicians who were concerned with the threat to families and workmates from open but recoverable cases consigned many patients to sanatoriums. To minimise HIV infectivity simply by prompt drug treatment seems, by comparison, an opportunity not to be missed, though the concomitant problems of adherence, resistance, and cumulative toxicity will, as with tuberculosis therapy, have to be borne in mind.
A recent House of Lords report has identified some weaknesses in present clinical practice.5 It suggests that reluctance to test for HIV in general practice means that some symptomatic infections are not being diagnosed, and it calls for people at highest risk to be empowered to monitor their own HIV status. Self testing—freely available for pregnancy diagnosis, for example—is feasible for HIV, but is illegal. The report recommends that this regulation be scrapped. A person who becomes HIV infected is now better off knowing as soon as possible, and self testing would facilitate this. It would encourage behavioural change even in the absence of treatment, and the decision to treat might be taken earlier based on viral load rather than depleted CD4 count; that is, on cause not effect.
Strategically, early treatment should be seen as the first step in controlling incident HIV, and not just as leading to further drug expenditure (though for the medium term it will inevitably do this). The analogy with tuberculosis cannot be stretched as far as to claim that it will conquer HIV in a generation, but within that time span real clinical and public health benefits would have accrued. Delays in diagnosis and drug treatment are currently contributing to the rising HIV incidence in the UK.
Cite this as: BMJ 2012;344:e2874
Competing interests: The author has completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declares no support from any organisation for the submitted work; no financial relationships with any organisations that might have an interest in the submitted work in the previous three years; and no other relationships or activities that could appear to have influenced the submitted work.
Provenance and peer review: Not commissioned; externally peer reviewed.