ASHM Report Back

Clinical posts from members and guests of the Australasian Society for HIV, Viral Hepatitis and Sexual Health Medicine (ASHM) from various international medical and scientific conferences on HIV, AIDS, viral hepatitis, and sexual health.

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The inaugural Hepatitis Session was held on the morning of the opening day of the meeting. This was held in the main hall and was almost full, reflecting the increased interest by the Infectious Diseases community in the rapidly advancing direct acting antivirals for the treatment of both HIV/HCV co-infection and HCV mono-infection. 

In the afternoon, a symposium on HCV was held, with international experts discussing areas of unmet need

Press release from CROI 

1. 12 wks of ABT-450r nonnucl inhibitor and ribavirin achieved SVR24 in >90% treatment-naïve HCV GT1 patients and 47% prior nonresponders. Lawtiz E, et al. A38

This presentation included final results from both the PILOT and CO-PILOT  Phase II studies, where all patients with HCV mono-infection received 12 weeks combination therapy with the ritonivir-boosted protease inhibitor, ABT-450, ribavirin and one of two non-nucleoside NS5B polymerase inhibitors (ABT-072 and later ABT-333 In Cohorts 1, 2 and 3, 44/44 treatment naïve patients achieved end-of-trearment response, of whom 2 relapsed within the first 12 weeks post-treatment, 3 more relapsed between 12 and 24 weeks post and 1 between 24 and 48 weeks post. Late relapses (more than 12 weeks post-treatment) is not seen following conventional treatment with PEG/RBV or PI/PEG/RBV and this observation emphasizes the need for longer post-treatment follow-up. This regimen was less effective in treatment-experienced patients. In Cohort 4, only 8/17 patients achieved SVR. In view of these suboptimal results, Abbott has added a third DAA, the NS5A inhibitor ABT-267, to the combination of ABT-450/r and ABT-333, in order to prevent post-treatment relapse. Current Phase III studies of this regimen are underway.

2. STARTVerso 4: High Rates of Early Virologic Response in Hepatitis C Virus Genotype 1/HIV Co-infected Patients Treated with Faldaprevir + Pegylated Interferon and Ribavirin. Dieterich D, et al. LB40

Faldaprevir is an oral second generation protease inhibitor, which is administered once daily with no food effect and no need for ritonivir boosting.  Interim study results from STARTversoTM 4 presented today at CROI+ show that 84 percent of hepatitis C (HCV) patients also infected with HIV had undetectable levels of HCV at week 12 of treatment with faldaprevir (BI 201335) combined with pegylated interferon and ribavirin (PegIFN/RBV), regardless of whether they were treatment-naïve or relapsed after prior treatment for HCV. Patients who achieved early treatment success may be eligible for 24 weeks rather than the standard 48 weeks of treatment with PegIFN/RBV. The most frequent adverse events were nausea (37%), fatigue (33%), diarrhoea (27%), headache (23%), and weakness (22%), similar safety results to those observed in HCV mono-infected treatment-naïve patients in prior faldaprevir clinical studies.

3. Telaprevir for Acute Hepatitis C Virus in HIV+ Men both Shortens Treatment and Improves Outcome. Fierer D. LB156

Pre-existing HIV infection reduced the rate of spontaneous clearance of HCV following acute HCV infection and also reduces the rate of successful eradication following interferon-based treatment. In this open-labeled study, 18 HIV+ patients with acute HCV infection received 12 weeks triple therapy with telaprevir- based triple therapy and 15 (83%) achieved SVR (compared to around 60% in historical controls treated with 48 weeks PEG/RBV). Although a small study, the higher SVR rate and shorter duration would support the future use of triple therapy for all cases of acute HCV superinfection in HIV+ patients.   However, caution is needed with direct drug interactions with anti-HIV medications

4. ANRS-HC27 BocepreVIH Interim Analysis: High Early Virologic Response with Boceprevir + Pegylated Interferon + Ribivirin in Hepatitis C Virus/HIV Co-infected Patients with Previous Failure to Pegylated Interferon + Ribavirin. Poizot-Martin E, et al. A37

Preliminary on-treatment results were presented from this Phase II study of boceprevir-based triple therapy in HIV/HCV coinfected patients, who have failed to respond to prior PEG/RBV. Of 64 patients who commenced treatment, 12 stopped within 12 weeks (1 discontinued for personal reasons, 4 for adverse events and 7 for treatment failure). The remaining 52 patients all had undetectable HCV RNA at week 12 and week 16.

The prior response to PEG/RBV determined on-treatment response to boceprevir-based triple therapy: HCV RNA was undetectable after 16 weeks in 90% prior responder-relapsers, 61% in partial responders and 38% in prior Null responders.

The early on-treatment virologic response rates observed in this study are similar to those achieved with boceprevir in HCV mono-infection but post-treatment responses are awaited.

5. High Early Virological Response with Telaprevir-Pegylated-Interferon-Ribavirin in Treatment-experienced Hepatitis C Virus Genotype 1/HIV Co-infected Patients: ANRS HC26 TelapreVIH Study. Cotte L, et al. A36

Preliminary on-treatment results were presented from this Phase II study of telaprevir-based triple therapy in HIV/HCV coinfected patients, who have failed to respond to prior PEG/RBV. Of 69 patients who commenced treatment, 8 stopped within 12 weeks (1 discontinued for treatment failure and 7 for adverse effects). The remaining 61 patients all had undetectable HCV RNA at week 12 and week 16.

68/69 patients had at least one adverse event, of which the most common was anaemia requiring intervention (41/69 patients).

The early on-treatment virologic response rates observed in this study are similar to those achieved with telaprevir in HCV mono-infection but post-treatment responses are awaited.

6. Suppression of Viral Load through 4 Weeks Post-Treatment Results of a Once-daily Regimen of Simeprevir + Sofosbuvir with or without Ribavirin in Hepatitis C Virus GT 1 Null Responders. Lawitz E, et al. LB155

These are the long awaited results from an exciting Phase II study combining two of the most potent direct acting antivirals currently in clinical development – the nucleotide polymerase inhibitor sofosbuvir (GS-7977) and the protease inhibitor simeprevir (TMC-435), in the most difficult-to-treat patient population – those with HCV GT-1 infection, who had Null response to prior treatment with PEG/RBV. The assumption was that the NUC would prevent the emergence of resistance to the protease inhibitors. 12 weeks combination sofosbuvir/simeprevir achieved SVR4 in 26/27 patients whilst 12 weeks combination sofosbuvir/simeprevir/ribavirin achieved SVR4 in 13/14 patients. Additional arms of 24 weeks combination sofosbuvir/simeprevir±ribavirin had similar SVR but higher rates of AEs and treatment discontinuation.

The authors concluded that the combination sofosbuvir/simeprevir for 12 weeks was highly effective and did not require the addition of ribavirin or extension to 24 weeks.

Tagged in: CROI2013

Long-acting PrEP; Fem and VOICE PrEP sing same sorrowful song; PrEP not associated with increased risk of future HIV seroconversion

The provision of HIV antiretroviral pre-exposure prophylaxis (PrEP) is one of the four key action items of the ‘Action on HIV- Melbourne Declaration 2012’.  PrEP was discussed in several different sessions at CROI 2013. Here are some of the highlights:

In Session 8, ‘HIV prevention: ARV, Counseling, Contraception and Condoms’, Chasity Andrews from David Ho’s group at the Aaron Diamond AIDS Research centre gave an excellent talk on GSK744 which is a new, potent integrase inhibitor (abstract 24LB).  GSK744 exists both in an oral and a long acting parenteral formulation. The oral formulation has been evaluated as monotherapy and affords a 2-2.5 log10 decrease in plasma HIV-1 viral load.  It’s half-life is approximately 3.71 weeks when given intramuscularly at 800mg.

In Ho’s study 8 Rhesus Macaques were injected with GSK744 twice, at week -1 and week 3+. All animals were intra-rectally challenged from week zero with SHIV 162P3 and received a total of 8 challenges, or until SHIV infection was confirmed.

None of the 8 Macaques receiving GSK744 became infected during the challenge, or during the 10-week follow-up phase whilst all Macaques receiving placebo GSK744 became infected.  In follow-up, there was no evidence of DNA in PBMCs nor an antibody response to SHIV in any of the actively treated Macaques.

Further work to be done with GSK744 includes (1) postmortem of the Macaques receiving active GSK744 to determine if there was contained local infection, (2) determining the minimum protective dose for rectal challenge, (3) determining its capacity to protect again HIV vaginal challenge in female macaques.

This drug has the potential to be given monthly or quarterly. 

Clinical trials, in addition to determining drug efficacy will need to carefully monitor for both short and longterm toxicity (including for a period of time after injections have ceased). If efficacious, this possible shift in the formulation of PrEP drugs could be remarkably beneficial for people at risk of HIV infection, but will still require appropriate ‘effectiveness’ studies to determine adherence, risk compensation and any informal use of PrEP as an injection.  Also in different countries, monthly or quarterly PrEP injections could potentially lead to infringement of human rights for some, including sex workers and people who inject drugs.

In the next talk of session 8, James Smith from the CDC provided further encouraging trial results that showed that a Tenofovir Disoproxil Fumarate (TDF) intravaginal polyurethane ring was able to completely protect 8 female macaques from SHIV vaginal challenge on 16 occasions over 4 months and using 4 ring changes during that time (abstract 25LB). There was no toxicity, no microflora change and Phase 1 Clinical trials will commence in Q3 2013. Very interesting presentation in terms of the machinations of developing the ring so that it effectively delivers the more potent form, TDF which is 500 times more potent than tenofovir and also has activity against HSV-2.

(Note-these two talks complement another session held later on that day “New approaches to HIV drug delivery”, Session 13).

In session 8 Jeanne Marazzo next presented the findings of the VOICE study (Abstract 26LB).

VOICE was a randomised, 5-arm, double-blind, placebo-control trial of PrEP that enrolled5,029 HIV negative women from Zimbabwe, South Africa and Uganda. Most participants were enrolled in South Africa (4,077).  Eligible participants had to have had sex in the previous 3 months, be willing to use oral contraception and not be pregnant, or breastfeeding. Participants were randomised to oral tenofovir, oral tenofovir- emtricitabine, oral placebo, 1% tenofovir gel or gel placebo. 

An interim DMSB in September 2011 ceased the oral TDF arm because it was safe but not effective.  In November 2011 the TFV vaginal gel arm was stopped because it was safe but not effective.  In August 2012 follow up of TDF-FTC arm was possible.

The mean age of the participants was 25.3 year. Most women were using injectable contraception. 17% reported anal sex at baseline. 85% reported use of a condom at last vaginal sex. Study retention was excellent with an overall 91% retention rate at study end

Adherence was assessed using monthly count of unused study products (pills or applicators) and quarterly audio-computer assisted self interview (A-CASI). Product return suggested 89% adherence and self-report by A-CASI found an adherence of 90% or above.

There were 334 HIV acquisition events for the intention-to-treat analysis. 22 women were HIV+ by PCR at enrolment. Hence there were 312 HIV acquisitions in the primary analysis, giving an overall HIV incidence of 5.7%. None of the three studied PrEP modalities afforded protection from HIV. The incidence of HIV was highest in women who were less than 25 years old and unmarried. The HIV incidence per 100 person-years in South African women < 25 years of age was 8.7 [7,6-10], > 25 years of age 4.7 [3.8, 5.8], married 0.9 [0.2-2.7] and unmarried 7.5 [6.6, 8,4].

Adherence appears to be the key factor in the observed failure of the study drug as at least 50% of women tested had no TFV found in sampling across the three study arms. These results are consistent with the Fem-PrEP study (Van Damme et al, NEJM 2012), which showed that oral TDF-FTC did not significantly reduce HIV infection compared to placebo and that adherence appeared to be very low in the study.

The disappointing conclusions that the VOICE study team drew were that we need to consider PrEP agents and delivery systems that are long acting and require minimal daily adherence and that a greater understanding of HIV risk perception and biomedical, social and cultural determinants of adherence in these high-risk populations is urgently needed.

In follow-up questions we learned that very few women in the VOICE study reported that they were CSWs and that the study team are doing a separate study, VOICE-D, to explore via in-depth qualitative interviews the issues around risk perception and PrEP adherence.

Finally, to end on a more positive note we learnt from Bob Grant of the iPrEx study team (abstract 27) that during a gap phase that occurred between the iPrEx study ending and an open-label extension of the iPrEx study beginning (where gap times ranged from 7-19 months across the study sites and during which no PrEP was available), that there was no excess incidence of HIV infection observed. Here the theoretical concern was that the use of PrEP during the iPrEx study had simply delayed HIV infection and that when PrEP was ceased during the gap phase that an excess in HIV seroconversions would be observed. This speaks to the notions of biological and behavioural prevention futility where an intervention like PrEP may fail ultimately if it does not alter the conditions that allow transmission.  An excellent talk to catch on the webcast.

Dear readers, if you have not already done so please sign the Melbourne Declaration at as Australia, Asia and the Pacific Region gear up to host World AIDS 2014 next year in Melbourne. Act now and be part of this endeavour!



Tagged in: CROI2013

HIV Testing and Monitoring the Epidemic: New Tools for Patients and Populations. Session 51 Symposium

This was one of the conference’s last sessions and was very well attended.

HIV self-testing: Opportunities and Challenges. Abstract 162

Dr Julie Myers, New York City Department of Health

This was an important talk given that increased access to HIV point-of-care testing is one of the key aims of the Melbourne Declaration. It is worth watching on the CROI webcast.

Last year the FDA approved the Alere Determine HIV Combo home self-testing kit, also known as Orasure.

Dr Myers provided the results from a recent 5,000+ patient trial of the Orasure rapid HIV home testing kit, which was conducted across 20 sites in the USA.

These data were given to the FDA Advisory Committee last year by the product sponsor but have not yet been published.

In this study they found that 82% of people using the test were from high HIV prevalence areas.

5,055 patients were evaluable for test results. The overall prevalence was 2.12%. See slide below from Dr Myer’s talk for further results of this study.

Note that the sensitivity is only 91.67%. Of note when trained professionals use this test its sensitivity is over 98%. 

As we know this product went on to become licensed in the USA. Of note, people who use the kit have 24-hour phone access for support and for referral to sites for confirmatory testing.


There are few post marketing data available but there have been some published data to indicate that users of the test find it is ‘easy to use’.

How homebased self-testing tests are being used

Dr Myer then discussed the way that the tests are being used including by those who are at risk and by potential sexual partners. Dr Myers reviewed some recent publications that showed that rapid tests are being used to test prospective sexual partners and acquaintances and that no sex occurred with partners who tested positive. The numbers in these studies were fairly small however.

Concerns noted by Dr Myers

1. Propensity for self-harm and violence

Similarly although there are no data to support ongoing concerns that HIV home self-testing kits will lead to an increased risk for self-harm and suicide and inter-partner violence Dr Myers noted that more work and study needs to be undertaken in this area.

2. Lost opportunities

In addition Dr Myers noted that home self-testing kits mean there is an increased chance for patients to lose the opportunity to have additional STI testing and to be referred for other appropriate services.

3. False reassurance

A major concern is that some people will be falsely reassured that they are HIV negative when they have false-negative results.


Cost is a real concern because the kit costs US$40 and those most at risk of HIV are those who are most financially disadvantaged. Only 17-18% of people in the US and Europe would be willing to pay this amount for a kit in studies cited by Dr Myers.

5. Risk compensation

There are not yet any data on whether home HIV self-testing kits are associated with risk compensation- meaning an increase in risk-taking.

Dr Myers noted an important study presented at CROI 2013 Abstract#1064 by Katz et al where modeling done around MSM in Seattle suggested that switching from clinic to home-based testing using Orasure would lead to an increase in HIV transmission.

6. Linkage to care

There are not data to show whether use of these tests will lead those people who test HIV positive to seek appropriate medical care. Although 88% of people in the self-test clinical trial presented to the FDA last year said that they would ‘definitely get follow-up’ this remains an important area to monitor and study.

7. Resource constrained settings

Limits of supply chain and also quality assurance.

 During question time Dr Myers got hammered by two audience members who were particularly concerned about how little data there are available about whether home-testing would improve linkage to care in the USA. However, as another audience member noted, the US linkage to care using clinic based testing is pretty poor! This is also an issue that Australia must address.


Point of care assays for immunological and virological monitoring of HIV disease. Abstract 163.

Dr Ilesh Jani, Mozambique

Dr Jani gave a fantastic talk and overview about point of care testing for HIV diagnosis and monitoring regarding POCT for CD4 cell counts and HIV viral load including for children.

Amongst other things he discussed implementation issues and noted:

1. POCT is not error proof. It IS error prone in all phases of testing

2. Implementation of point of care tests is not always done efficiently.

In Mozambique his team's data showed that despite having POCT CD4 instrument on site, they lost 24% of people BEFORE people got tested with the POCT CD4 test. They only managed to test 50% of people on the same day as their HIV diagnosis. Median time to get a CD4 count was 3 days (Jani et al 2011

One key point that I took home from him was that whole blood viral load testing is likely to become common in the future. In patients whose plasma HIV viral is undetectable they may still have a detectable HIV viral load in their whole blood test. He explained that we don’t really know what this means clinically and we don’t know the correlation between plasma and whole blood HIV viral load testing


Accurate cross-sectional incidence testing. Abstract 164

Dr Laeyendecker, NIAID and Johns Hopkins

Dr Laeyendecker gave a masterful talk on this subject, which was valuable for a naïf such as myself. It’s a must watch talk for those who wish to understand how to optimize testing algorithms to assess HIV incidence in populations

Key points include (1) that there is a difference between how HIV clade D versus clades A and C perform in these testing algorithms wherein the tests overcall the prevalence of clade D infections and (2) that multi-assay algorithms perform best for HIV incidence testing in stable, expanding and waning HIV epidemics.


Viral load measures: patients, populations and interpretations. Abstract 165

Dr Irene Hall, CDC

This talk was good. The main point I learnt was that community viral load refers to the viral load of those people who have been diagnosed with HIV. Population viral load refers to all people in a population who are HIV infected including those who are unaware of their diagnosis. This is an important distinction because community viral load does not accurately reflect HIV transmission potential in the community.

Dr Hall noted an excellent oral presentation given at CROI 2013 Abstract 96 which reported on the first study in Swaziland of their HIV population viral load. This household-based counseling and testing study evaluated 18,169 individuals. 5802 individuals were identified as being HIV+ and, of these, only 67% knew that they were HIV+ and, of these, only 50% reported current ART use. A high viral load, defined as >50,000 copies/ml was found in 35% of the total population, (cue heartsink feeling here).

Overall an excellent session.



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Opportunities and Threats to ART success (session 36) and related CROI abstracts

Greetings from Atlanta, home to CDC, CNN and Coca Cola of which I have ingested output from all three during this visit.

For those interested in the obstacles to ART implementation and its therapeutic success including new antiretroviral drugs and formulations, there was a terrific symposium held yesterday that addressed these issues.

Jennifer Kates from Kaiser Family Foundation outlined issues arising from Obama’s Affordable Care Act (ACA) as they pertain to HIV care and treatment access. Like Australia, the US Federal- State divisions and discords can be disconcerting. In the US states have the choice of accepting the expansion of the public health fund Medicaid or not. For those states that accept it, people living with HIV will have greater access and financial support for their HIV care. Currently 68% of people living with HIV in the USA live in states that will support Medicaid’s expansion but this leaves the potential for disparate levels of care for people living in the remaining states who decline Medicaid expansion. A good talk for those who seek to better understand the ACA.

Sharon Lewin from Alfred/Burnet/Monash gave an outstanding talk on the impact of the residual inflammation experienced by virologically suppressed HIV positive people on ART.  Sharon addressed the impact of residual inflammation upon risk for mortality and non-AIDS diseases. She addressed the drivers of this inflammation and the current (largely theoretical) therapeutic approaches we could take to decrease inflammation. A must-watch talk on CROI’s webcast.

Raph Hamers from Academic Med Ctr of the University of Amsterdam gave a very good talk on ARV drug resistance. He discussed in detail transmitted drug resistance, which is a key issue for populations living in eastern and southern Africa where transmitted NNRTI resistance predominates. Also he addressed the recently published observation that K65R resistance appears to occur more rapidly in clade C infected patients whose first-line therapy included tenofovir. K65R is also selected in patients who have been treated previously with stavudine (d4t). He highlighted the importance of switch studies from first to second line therapy.

Of note ASHM President-elect Mark Boyd and his colleagues’ SECOND-LINE study’s 48-week results were presented as a late breaker poster (180LB).  The study results support switching to a boosted lopinavir + raltegravir, NRTI-sparing regimen for individuals failing their first-line NNRTI with 2N(t)RTIs regimens. This approach was non-inferior to switching to boosted lopinavir +2-3N(t)RTI regimens and was associated with a significantly higher CD4 cell recovery.

Joe Eron from the University of North Carolina gave Trip Gulick’s talk on new ARVs, which was, thankfully optimistic. There are a number of new ARV formulations in the pipeline including atazanavir/cobicistat, darunavir/cobicistat which precludes use of ritonavir as a boosting agent. Rilpivirine is also being studied in a nanoparticle form and as a long-acting intramuscular injection. Efavirenz and atazanavir are also being considered for nanoparticle formulation. Antiretroviral agents can be formulated as solid or liquid suspension nanoparticles. Theoretically nanoparticles could afford better bioavailability and higher tissue concentrations as they are taken up and then released into tissues by mononuclear phagocytes. Abstract 513 reported on successful in vitro studies of Efavirenz formulated as solid drug nanoparticles.   

The talk provided an excellent table of all the up and coming drugs- check out this talk via the CROI webcast site to view the table.

Importantly Joe Eron mentioned the new tenofovir pro-drug tenofovir alafenamide (TAF). TAF is notable because its plasma levels are 90% lower than those of tenofovir but it has a 5-fold increase in intracellular TFV diphosphate compared to tenofovir, which affords it the potential for lower toxicity. Indeed significantly lower bone and renal toxicity was observed in the TAF arm of a phase 2 randomised, double blind trial presented as a late breaker oral presentation (abstract 99LB). Here elvitegravir/ cobicistat/ emtricitabine/tenofovir was compared to elvitegravir/cobicistat/emtricitabine/ tenofovir alafenamide. The two regimens had comparable efficacy at week 24 and the findings support scaling up to a phase 3 study. All points bulletin to bones and kidneys: watch this space!



Tagged in: CROI2013

Posted by on in Public Health and Prevention

CROI Tues am (session 21 - Abs #71) plenary speaker Prof Chris Beyrer from Johns Hopkins gave a clear, evidence-based, passionate and excellent summary of HIV in MSM (Men who have Sex with Men) (see also Lancet special issue 2012)

This presentation is well recommended to view from CROI website.

Key points:

1. Globally in first, middle income and third world countries, Global burden of HIV is stabilising or declining in most populations - MSM in all these regions is the exception.

2. MSM are disproportionately affected - eg USA 2010 - MSM 1-1.5% of population - 60% of diagnoses

3. WHY? - even in this era of ART?
Higher prevalence drives risk of acquisition, untreated STIs, unprotected receptive anal intercourse 18x greater risk than vaginal sex
Also clustering of population, "bursts" of transmission in primary infection
Structural issues - stigma & discrimination affects access to treatment and care, leads to depression and substance use
(Ironically MSM contributed so greatly to development of HIV treatments and are in many cases denied treatment and care in too many countries)

4. Achieving the end of HIV for everyone has to include MSM in all countries

5. Take home messages - applicable for our care in Australia - we need to combine all these:
 - Treat all MSM with HIV (treatment as prevention)
 - Test for HIV and test frequently
 - Condom protection for anal sex
 - PrEP for some, PEP
 - Test, diagnose and treat STIs
 - Access to care that's culturally sensitive
 - Address homophobic stigma, discrimination (legal and social) - the responsibility of all of us as health care workers, at work and at home


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Excellent session at CROI Monday 4-6pm "Cardiovascular disease and other non-AIDS events: Epidemiology and Pathogenesis".

This session (which will be webcast) very successfully pulled together different presentations to give an update on the heart and vascular disease as well as other SNAEs (serious non AIDS events) in HIV.

The key messages were

1. Adjusted risk of myocardial infarct for HIV+ was 80% higher than HIV- controls (VACS - Veterans Aging Cohort Study of 68,000 HIV- and 31,000 HIV+) with similar mean age of incidence

2. Plaque formation in coronary arteries measured on CT was 80% higher in HIV+ (vs HIV- at risk) MACS cohort

3. HIV+ patients more likely to have plaque but also more likely to have "vulnerable plaque" - i.e. plaque which is soft, lipid rich, monocyte rich, subject to remodelling and less calcified (spotty calcification) - these plaques less stable, more likely to rupture and cause myocardial infarct or sudden cardiac death

4. Vulnerable plaque associated with inflammation and in HIV+ this is monocyte-mediated as measured by soluble CD163 (and CD16)

5. So, in HIV+, there is the traditional risk factor (smoking, lipids, hypertension) coronary artery disease as in the general population. Additionally there is an inflammatory monocyte driven process which could partially account for higher CVD in HIV.



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