12th Annual Conference of the British HIV Association

HIV Treat Bull - Vol. 7, No. 5, May 2006

HIV in the UK – summaries from BHIVA

Simon Collins, HIV i-Base

The UK has approximately 60,000 people living with HIV, one-third of whom are undiagnosed, and around half of those diagnosed are on ARV treatment. Although, this is a relatively small number of people compared to many countries (<0.1% prevalence), the numbers of new diagnoses has increased for each of the last 3 years and was around 8,000 for 2005.

The following information about the specific situation in the UK is provided in summary studies from the recent BHIVA conference.

One in five patients with CD4 <200 are not on treatment

Victoria Bryant from the Health Protection Agency (HPA) presented a breakdown of access to treatment by CD4 count, drawn from the annual Survey of Prevalent HIV Infections Diagnosed (SOPHID) database. [1]

Of 35,000 people registered HIV-positive in England, Wales and Northern Ireland, just under 5,000 (14%) currently have a CD4 count <200 cells/mm³ – the marker used to recommend starting ARV treatment in the UK.

One in five of these patients (950/4934) are not currently on treatment – a proportion that varied from 9% in Northern Ireland to 36% in the North East. There was little difference observed by ethnicity, exposure category or sex. Reports in previous years suggested that this figure was largely driven by late presenters, who are diagnosed when their CD4 counts are already below 200 cells/mm³. However, in this study, recent diagnoses accounted for only 16% (84/514) of individuals not on ART with CD4 <200 cells/mm³ in London.

Growing viral diversity with non-B subtype reported in gay men

Two studies presented at the conference, looked at incidence of non-B infections.

Ana Garcia from the Royal Free Hospital reported that 44% (88/ 200) new diagnoses at the Royal Free from April 2004 to November 2005 were non-B subtypes. [2]

The 112 subtype-B infections were predominantly white (81%) and MSM (89%) with median age 35 (19-57); 25% were diagnosed during primary HIV infection. Non-B subtypes comprised 36 C (41%), 14 A (16%), 10 CRF02 (11%), 7 D (8%), 5 G (6%), 4 CRF01 (5%), 4 CRF06 (5%), 1 CRF13 (1%), 1 CRF16 (1%), and five complex mosaic sequences (6%). The non-B population comprised 34 males (39%), 61 (69%) black Africans, 72 (82%) heterosexuals, 5 (5%) MSM, and 9 (10%) recent seroconverters.

Transmission of drug resistance was detected in 14/200 (7%) by IAS and 9/200 (4.5%) by Stanford database. This was almost exclusively in MSM with subtype-B (12/112; 11%), with 1/12 heterosexual with subtype-B and 1/12 heterosexual with complex mosaic sequence.

The authors concluded “genetic diversity of HIV-1 continues to increase in London and that although non-B subtypes are commonly associated with immigration from Africa or Asia, they are no longer restricted to non-indigenous populations”.

Julie Cox and colleagues from Imperial College, also reported that non-B subtypes were transmitted to white gay men, in London patients referred to their primary HIV infection cohort. [3]

5/140 patients, diagnosed in primary infection from 2000-2004, all had recombinant variants. One transmitting pair, confirmed by sexual history as well as phylogenetic analysis, were both infected with A/EPRO: DRT, one with CPRO:BRT, one DPRO:BRT, and one with CRFO2-AGPRO:KRT. All reported sexually acquired infection with partners in the UK.

Viral rebound – stability of treatment and viral blips

Several studies looked at durability of suppression and implications of viral blips.

Andrew Benzie from St Marys, London, presented an interesting analysis of the duration of viral suppression based on previous treatment experience in the UK Collaborative HIV Cohort (UK CHIC). [4]

10,243 patients who achieved viral suppression <50 copies/mL for the first time on ARV combinations were followed until viral rebound (two consecutive tests >400 copies/mL).

Previous treatment experience related closely to the risk of viral rebound in people who only maintained suppression for a short period. For example, in people suppressed for less than one year, rates of rebound ranged from 8.4 (per 100/patient years) in treatment naïve patients to 41.9 for people who had failed >5 previous regimens,

More optimistically, the larger difference in rebound rates relating to treatment experience, diminished with longer duration of suppression. After 2-3 years of suppression the rate of rebound was 4.1 in naïve and 5.5 in >5 regimen failure; and after > 4 years, rates were 3.0 and 8.1 in the naïve and most-experienced groups respectively.

Previous studies have highlighted that viral blips in patients on stable therapy are often lab inconsistencies – perhaps in as many as 50% of cases. Gaia Nebbia and colleagues form the Royal Free Hospital looked at trends in viral blips in 486 patients on stable PI or NNRTI-based therapy. Duplicate samples were taken at each timepoint, and the second sample tested in the case of any result >50 copies/mL. [5]

During the first year after an initial suppression to <50 copies/mL, 76% of patients maintained suppression and 24% experienced a rebound that was subsequently undetectable (blip). 30% of these blippers (35/119) blipped more than once (2-4 times).

For the majority of the 32 retested blips, the second sample was < 50 copies/mL; VL was >50 copies/mL in 11/32 (34%); detectable at <50 (10–42) copies/mL in 13/32 (41%); and undetectable in 8/32 (25%).

COMMENT

While confidence values and statistical significance were not presented between each group in the UK CHIC abstract, the trend of reduced risk of rebound once suppressed to <50 copies/mL is consistent with other data supporting the importance of early maximal suppression.

The small sample of retested ‘blip’ results is probably too small for the results to be statistically significant, but the general conclusion that over 50% of low level blips cannot be confirmed when the same sample is retested, is reassuring.

References

Unless otherwise stated, all references are the Abstracts of the 12th Annual conference of the British HIV Association, Brighton, UK. 29 March – 1 April 2006, published as a supplement to HIV Medicine (Volume 7, Supplement 1, March 2006. This supplement is available free online:

The British HIV Association.

1. Bryant V, Chadborn T, Patel B et al. Adults with low CD4 cell counts that were not receiving antiretroviral therapy in England, Wales and Northern Ireland in 2004. 12th BHIVA, 29 March – 1 April 2006, Brighton, 2006. Oral abstract O1.
2. Garcia A, Booth C, Nebbia G et al. The demographic, clinical and virological characteristics of patients newly diagnosed with non-B HIV-1 subtypes in London. 12th BHIVA, 2006. Oral abstract O2.
3. Fox J, Dustan S, Steve Kaye S et al. Incident non-B clade HIV-1 infection in white gay men infected in UK between 2000 and 2005. 12th BHIVA, 2006. Oral abstract O3.
4. Benzie AA, Bansi LK, Sabin C et al. Viral rebound in patients on antiretroviral therapy with viral suppression: association with extent of previous virological failure and time with viral suppression. 12th BHIVA, 2006. Oral abstract O9.
5. Nebbia G, Booth C, Smith C et al. The reproducibility and clinical significance of HIV viral-load blips in patients on stable first-line HAART. 12th BHIVA, 2006. Oral abstract O6.

2008-03-10
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