The news that a ‘second person’ (see later) has been cleared of HIV infection is a reminder that HIV infection is far from the death sentence it once was. It might also jog our industry’s collective conscience that many HIV-infected individuals are insurable risks and that protection cover might be found for more of them.
The first person to become HIV-negative after having been infected was Timothy Brown, the so-called ‘Berlin patient’. Brown, an American citizen, was diagnosed with HIV in 1995 while studying in Berlin and began antiretroviral therapy. In 2006 he was diagnosed with acute myeloid leukaemia for which he received a stem cell transplant a year later. The donor had a genetic mutation of a surface cell receptor, effectively blocking the ability of HIV to enter a human cell. After a relapse of the leukaemia Brown received a repeat stem cell transplant which has been successful and, as a result, he has remained free of leukaemia and HIV since.
(Actually there appears to have been a previous ‘Berlin patient’, a German man in his mid-twenties who remains anonymous. He was diagnosed with acute HIV infection in 1995 and was prescribed an experimental cocktail of drugs (which included antiretrovirals) subsequent to which HIV became almost undetectable. The patient has remained off antiretroviral therapy since. There has been some debate about the why the vast improvement should have taken place, one theory being that the patient’s genetic background played the role and not the therapy.)
The most recent patient to see elimination of HIV (dubbed the ‘London patient’) is Adam Castellejo, a 40 year-old diagnosed with HIV in 2003. He too developed a malignancy – in his case lymphoma – and he too had a stem cell transplant involving the same mutation on the CCR5 surface receptor. Castillejo has been free of active viral infection for 30 months, although he still has ’remnants’ of HIV DNA in some cells; according to his doctors these traces can be regarded as ’fossils’ because they are unlikely to allow the virus to replicate. Such remnants were also found in Timothy Brown’s case.
Fascinating though such cases are, both have an element of serendipity to them and the experts have warned that this approach to a ‘cure’ is far from being feasible or even desirable for the great majority of HIV-infected individuals. Indeed, stem cell transplantation is not without its hazards.
Nevertheless, management of HIV infection has come a long, long way since the 1980s. Combined antiretroviral therapy (cART) has been hugely successful in controlling viral replication, and some groups of patients have a very good outlook. Some studies report mortality being more or less the same as that of the general population.
So, should insurers be accepting more of these risks? Probably yes but the matter is not as straightforward as it may sound.
It is the case that cART is highly effective; CD4 cell counts can be restored to normal or near-normal levels with a consequent near elimination of opportunistic infections and the hitherto rare tumours that originally characterised AIDS. After successful treatment the mortality and morbidity risk factors are those typically found in the wider population.
But there appears to be a two- to three-fold increased risk of developing certain non-AIDS-related malignancies compared with the general population, and with earlier onset and a worse prognosis. And despite ART, HIV-positive subjects continue to suffer from a degree of disordered immunity and chronic inflammation, both of which increase susceptibility to illnesses such as cardiovascular disease, diabetes and neurological disorders. Interestingly, general ‘ageing’ seems to occur earlier.
Previous lifestyle is also a factor. The HIV group appears to have a higher proportion of ex-smokers compared with the general population, giving rise to an increased incidence of respiratory cancers. And notably, intravenous drug users do poorly as a group, their prognosis often worsened by the presence of hepatitis B and/or C.
Although selected HIV-positive groups might indeed be insurable, it is quite likely they are not standard risks. Insured populations, having undergone an underwriting – or ‘selection’ – process, have significantly lower rates of mortality and morbidity than the general population. Given the risk factors cited above, underwriters would tend to regard the great majority of such applicants as abnormal risks, even if the essential measures of viral activity – CD4 count and HIV RNA level – are satisfactory and stable.
While there are plenty of data regarding mortality in HIV infection, disability statistics are much harder to come by – and naturally the way that disability is defined in the studies does not match that traditionally used by insurers. So putting a price on income protection cover is a tough job indeed for the actuary.
The question of HIV and insurability reminds one of the steps taken many years ago to begin insuring applicants with diabetes, high blood pressure and coronary heart disease, conditions that usually meant an instant declinature. Led by a reinsurer, a number of life insurers clubbed together to form a pool to share such risks; via this experiment, cover was made available but with limited liability for each participating firm. In time the pools showed a profit and, having demonstrated that these risks were insurable (and having given underwriters generally the courage to take them on), they were eventually wound up.
Arguably HIV infection deserves the same sort of bold initiative, but in today’s world of ultra-thin margins, more new risks and unprecedented volatility (in everything) there is little appetite for experimentation. Which is a pity because, historically, the underwriting world has been good at improving its understanding of risks old and new and indeed at extending the frontiers of insurability for those in need.