Common infections may increase cardiovascular risk in HIV patients

L-R: Dr James McMahon, Dr Janine Trevillyan, Prof Jenny Hoy
and Dr Norm Roth (GP at Prahran Market Clinic) conferring. Jenny
and Janine are co-authors together with Victoria Berquist, a former
CCS BMedSc(Hons) student, on the paper on CV risk in HIV patients

by Anne Crawford

When human immunodeficiency virus (HIV) erupted more than 30 years ago, the lifespan of people with fully-blown AIDS was short. Management of the disease often meant palliative care.

Now, with effective drugs, the longevity of a person living with AIDS in Australia is approaching that of the general population. But there’s still a gap of some eight to 10 years lost over a lifetime, mostly due to heart attack and cancers. Monash University researchers at the Alfred Hospital are investigating the factors behind increased cardiovascular risk in HIV-positive individuals and what can be done to about them. 

Anti-AIDS drug can affect platelet activation

By Dr Jodie Abramovitch

Abacavir is an anti-retroviral medication that is commonly used to treat HIV infection to prevent or control the development of AIDS. Abacavir use has been associated with an increased risk for cardiovascular disease (CVD). However, it is unknown how abacavir leads to this increased risk of CVD.

Dr Janine Trevillyan - HIV researcher and
lead author of this study

Monash researchers from the Department of Infectious Diseases and the Australian Centre for Blood Diseases (ACBD) theorised that abacavir could be affecting platelet activation thus leading to the development of CVD. Therefore the aim of their study was to determine if platelet reactivity was altered with abacavir administration.

Patients with well controlled HIV infection on non-abacavir treatments were recruited from the Infectious Diseases clinic at the Alfred Hospital. Twenty selected patients were given abacavir alongside their non-abacavir treatments for 15 days and had blood samples taken at day 0, 15 (treatment ceased) and 28. Platelet reactivity (as measured by VASP-index) was significantly decreased during abacavir treatment (at day 15 compared to day 0). A measurable decrease in soluble glycoprotein VI levels (sGPVI) was also indicative of lower platelet reactivity. Platelet surface protein integrin-β3 was also observed to be lower which may suggest a change in platelet structure. At day 28 following clearance of abacavir from the body, measurements were similar to those taken at day 0.

The findings in this study show that abacavir does have an effect on platelet reactivity, though this is reversible following cessation of treatment. The link between platelets and CVD needs to be explored further and the clinical implications of these results requires more research in a larger group of patients. This study has identified possible markers of disease in sGPVI and integrin- β3.

Reference: Trevillyan JM, Arthur JF, Jing J, Andrews RK, Gardiner EE, Hoy JF. Effects of abacavir administration on structural and functional markers of platelet activation. AIDS. 2015 Nov: 29;2309-13. 

doi: 10.1097/QAD.0000000000000848

CCS successes in 2015 NHMRC funding