HIV update - 1st April 2015

New treatment options

Clinicians trying to develop an HIV treatment involving fewer drugs – and which could perhaps be taken as a monthly or quarterly injection – have reported encouraging results.

Usually HIV treatment involves three or more different drugs. Two drugs are from the nucleoside class – for example the Truvada and Kivexa pills each combine two nucleoside drugs. And the third drug is from another drug class, such as the non-nucleosides, protease inhibitors or integrase inhibitors.

The approach tested by the researchers didn’t require people to take the nucleoside drugs in the long term.

People who had never taken HIV treatment before took a relatively conventional treatment for the first six months – two nucleosides and a new drug, cabotegravir, which is an integrase inhibitor. As long as they had achieved an undetectable viral load, they switched to a two-drug regimen after six months – cabotegravir and the non-nucleoside rilpivirine, both taken as daily pills. They continued this treatment for almost two years.

Their results were compared with a control group who took two nucleosides and efavirenz. The two groups had similar results in terms of keeping viral load down and in strengthening the immune system, but with fewer side-effects in those taking fewer pills.

This confirms that the two-drug regimen can work well for people who have already achieved an undetectable viral load using a three-drug regimen.

The researchers now want to try to develop both cabotegravir and rilpivirine as long-acting injections. Both of these drugs remain so long in the body that there may be potential for them to be provided as monthly or quarterly injections rather than daily pills.

For more information on current HIV treatment regimens, you can read our booklets ‘Anti-HIV drugs’ and ‘Taking your HIV treatment’ on our website at www.aidsmap.com/booklets

Statins may reduce the risk of heart disease

There is growing evidence that treatment with statins is beneficial for people living with HIV, reducing their risk of heart attack, stroke or other cardiovascular disease.

Rates of heart attack and coronary heart disease in people living with HIV are up to double those of HIV-negative people. While some of this is due to higher rates of risky behaviours such as smoking, researchers also think that HIV infection and the persistent immune activation and inflammation that it causes contributes to the higher rates.

For example, inflammation on the surface of the arteries encourages the development of fatty deposits in the arteries. These deposits cause the arteries to harden and narrow, raising the risk of a heart attack or stroke.

It’s well known that statins lower levels of LDL ‘bad’ cholesterol. But they can also help reduce inflammation.

Two randomised studies each offered a statin (in a pill to be taken daily) to people living with HIV. Both studies showed that the statin improved measures of plaque deposits in the arteries or of thickening in the arteries.

But the studies so far have not been large enough or of a long enough duration in order to measure the events of real concern – heart attacks, strokes and deaths due to cardiovascular disease. While use of statins does reduce these events in the general population, the somewhat different causes of cardiovascular disease in people living with HIV could mean that the benefit of statins is different. A large study is getting underway.

More people taking treatment as prevention

An increasing number of people living with HIV in the UK are choosing to take HIV treatment in order to reduce their risk of onward transmission.

While British treatment guidelines generally recommend that HIV treatment is begun with a CD4 count of around 350 cells/mm³, they also advise doctors to discuss the evidence for the effectiveness of antiretroviral treatment as prevention with all their patients. Regardless of CD4 cell count, any individual who wishes to take treatment in order to protect their partners from the risk of HIV infection should be able to do so.

Whereas 24% of those starting therapy had a CD4 cell count over 350 cells/mm³ in 2008, this had increased to 49% in 2013.

Moreover, the proportions with a CD4 cell count over 500 cells/mm³ rose from 8% to 27%.

Some groups were more likely to start treatment early than others – people aged 25-34, white people, gay men, people who had been diagnosed within a few months of their own infection and patients at larger HIV clinics. Awareness of treatment as prevention may be lower in other groups.

Find out more about the British HIV Association (BHIVA) treatment guidelines in our summary factsheets: www.aidsmap.com/uk-treatment-guidelines

Research towards a cure

Scientists remain enthusiastic about their work to find a cure for HIV but they have warned that progress is likely to be slow. "It will wind out over years or decades before we have functional cure applicable to many people with HIV," Dr John Mellors of the University of Pittsburgh told a recent scientific conference.

A number of researchers presented data from very early studies on a number of experimental agents that may play a role in achieving a 'functional cure' for HIV – in other words a prolonged period without ill-health or disease progression without the need for daily HIV treatment. The experimental agents include drugs that reactivate the latent HIV reservoir, interfere with expression of viral DNA and help the immune system target HIV-infected cells.

But the studies tend to show a similar pattern – encouraging results in some but not all people, for example in people with already low viral loads, but also sometimes in particular patients for no apparent reason. This suggests that no single approach is likely to work on its own and that researchers will need to combine several elements to achieve a cure.

Researchers also presented data on infants and adults who began to take antiretroviral therapy within a few weeks of their own infection. This does not eliminate the ‘reservoir’ of HIV’s latent genetic material (proviral DNA), but it does appears to limit the size of the reservoir and early treatment may delay the rebound in viral load after stopping treatment.