Abstract Book Vol. 1 [International Conference on AIDS (16th: 2006: Toronto, Canada)]

Monday
14 August
Poster
Exhibition

type to mortality and examine associated factors in subjects presenting for HIV
care at VA clinics from 10/97 to 12/02.
Methods: Using centralized VA records, the blood count closest to first HIV
care episode was identified for 6825 HIV-infected men. Anemia was defined
as hemoglobin <13g/dl with anemia type based on mean corpuscular volume.
Cox proportional hazards models were used to examine relationship of anemia
type with mortality, adjusting for demographics and clinical factors. Multinomial
logistic regression was used to determine the factors associated with anemia
type.
Results: Anemia was present in 2375 (35%), with 11% microcytic, 74%
normocytic, and 15% macrocytic. At baseline, median CD4 and viral load were
265 cells/mm3 and 22,600 copies/ml, and 14% had received HAART in the prior
90 days. Median follow-up was 3.5 years. While microcytic anemia (Hazard
Ratio [HR] 1.5, 95%CI 1.2-2.0), and normocytic anemia (HR 1.6, 95%CI 1.4 -1.8) were significantly associated with mortality, macrocytic anemia (HR 2.5,
95%CI 2.0-3.1) had a larger impact. In decreasing order of magnitude, age,
CD4, hepatitis C, viral load, alcohol abuse and hepatitis B were associated with
mortality. In a separate model also including zidovudine, the impact of anemia
was unchanged. Baseline presence of macrocytic anemia was significantly
associated with (by decreasing strength of association) CD4, age, viral load,
zidovudine, black race, and hepatitis C. Only 40 (11%) of the 357 subjects with
macrocytic anemia received zidovudine. In subjects with anemia, 58% had
basic anemia work-up labs performed.
Conclusions: Macrocytic anemia was independently predictive of a 2.5-fold risk
of death, while microcytic and normocytic anemia were associated with 1.5-fold
increase. Clinical and demographic factors predicted macrocytic anemia.
MOPEOO56
Evaluating the prognostic value of the new WHO
pediatric clinical staging system in a cohort of
untreated HIV-infected children in Belo Horizonte,
Brazil
C.A.A. Cardoso, A.G. Dantas, A.C.M. Dias, Q.C. Lisboa, R.M. Linhares,
I.R. Carvalho, T.M.S. Candiani, J.A. Pinto. Federal University of Minas Gerais,
Maternal and Pediatric AIDS Group, Belo Horizonte, Brazil
Background: In November 2005, WHO published a provisional pediatric
clinical staging system intended to assist clinical care providers in determining
when to start, stop or substitute ARV therapy in HIV-infected children as well
as to serve as a HIV/AIDS surveillance tool in resource limited settings. This
study aimed to evaluate the prognostic value of WHO clinical staging system in
a cohort of untreated HIV-infected children in Belo Horizonte, Brazil.
Methods: Historic observational cohort of untreated children admitted at a
referral center from 1989 to 2003. WHO stages 1 to 4 were evaluated for the
risk to disease progression, defined as: HAART initiation or CDC/1994 category
C condition or death.
Results: 262 subjects were evaluable for this analysis, 51.1% males, median
age at admission 24.4 months. The median follow up period was 11.9 months.
At the end of observational period (December/2003), 220 (84%) subjects
remained in follow up, 13 (5%) died, 26 (9.9%) were lost to follow up and 3
(1.1%) were transferred to another clinic. In Kaplan Meier univariate analysis,
subjects presenting with stage 1 conditions were significantly less likely to
present disease progression (log rank: 12.01, p=0.0005) and subjects in
stages 3 and 4 were at significantly higher risk for progression (p=0.007 and
<0.00001, respectively). In multivariate analysis by Cox proportional hazards,
relative risks for disease progression were 0.52 (95% CI: 0.38-0.72), 1.46
(95% CI: 1.07-2.00) and 1.94 (95% CI: 1.20-3.16) for stages 1, 3 and 4,
respectively. Stage 2 was neutral in predicting the risk for progression (log
rank 2.45, p=0.12).
Conclusions: Stage 1 was protective for risk of disease progression and
stages 3 and 4 were good predictors of risk of progression in this cohort of
untreated Brazilian children. These findings support WHO proposition to start
ARV treatment for children in stages 3 and 4.
MOPEOO57
Long-term follow-up of HIV-1+ treatment naive
patients undergoing HAART
S. Magaev', M. Nikolova', A. Michova', D. Beshkov2, K. Kostov',
H. Taskov'. 'National Center of Infectious and Parasitic Diseases, Central
Laboratory of Immunology, Sofia, Bulgaria, 'National Center of Infectious
and Parasitic Diseases, National Reference Laboratory of HIV Virology, Sofia,
Bulgaria, 'Hospital of Infectious Diseases, Sofia, Bulgaria
Background: In a previous study we examined the recovery dynamics of COB
T cell subsets in HIV-I+ patients subjected to HAART for 24 months. Three
types of therapy response (immunological and virological) were established,
based on CD8 differentiation markers, CD4AC, VL and immune activation. Now
we extended our observations up to 48 months of HAART in order to check the
consistency of therapy response type in each patient group.
Methods: Fifty-two treatment-naive HIV-I+ patients receiving HAART (2 NRTI,

1 PI) were followed for 48 months (at baseline and every 3 months thereafter).
At 24 months the study subjects were retrospectively divided in three groups: A
(good immunological and virological response: n=28, log VL_2.7, ACD4AC_150
cells/ii); B (transient response, n=9, log VL>2.7, ACD4AC<_150 cells/pi) and C
(discordant response, n=15, VL>2.7 log RNA copies/ml, ACD4AC_150 cells/ l).
CD4AC and percentage, and the quantitative expression of CD38 on CD8 T cells
were determined by multicolor flow cytometry, HIV-1 RNA plasma levels - by
RT-PCR. Significant differences between groups were determined by KruskalWallis ANOVA.

Results: In the majority of patients the therapy response pattern, defined at
the end of the second year, was preserved during the 24 months of follow-up.
Good responders marked a significant increase of CD4AC (p<0.01), while the
levels of CD38 and VL were similar to those at 24th month. In the transient
responders group all parameters of the immunological response remained
steady, while VL significantly increased (p<0.01). Importantly, in the end of
follow-up the discordant responders were characterized by a significantly lower
CD4AC as compared to good responders (p<0.05), in contrast to the 24th
month when both groups had similar CD4AC.
Conclusions: A discordant immunological and virological response may not be
beneficial in the long-term, underlining the importance of the early and precise
definition of the therapy response in HIV+ patients subjected to HAART.
MOPEO058
Declining CD4+ cell counts during suppressed or
low level viremia
A.M.L. Anderson', AS. Kosinski2, J.A. Bartlett'. 'Duke University, Department
of Medicine, Durham, United States, 2Duke University, Department of
Biostatistics and Bioinformatics, Durham, United States
Background: Observations on declining CD4+ cell counts in HIV-infected
patients with suppressed or low level viremia have been described previously.
Our aim was to identify the prevalence and predictors of this phenomenon in
a clinic cohort.
Methods: We queried the Duke University Adult Infectious Diseases Clinic
database (N= 3949). Criteria for declining CD4+ cell counts ("case") included:
1)Decline in absolute CD4+ count of _10% relative to the previous value on >_2
consecutive timepoints OR 2)Absolute decline in CD4+ percent of _3% relative
to the previous value on _2 consecutive timepoints. Two controls were matched
for each case by age, sex, year, and absolute CD4+ cell count. All subjects had
plasma HIV RNA levels of <1000 copies/ml.
Results: 41 cases were identified, representing a prevalence of 1.04% in our
population. Few cases (7/41 or 17.1%) or controls (9/82 or 11%) had plasma
HIV RNA levels >500 copies/ml at any timepoint during the decline. Univariable
regression showed that hepatitis C antibody status, race (Caucasian compared
with African-American), and plasma HIV RNA >500 copies/ml on _1 timepoint
were not independently associated with decline. By univariable regression, we
were not able to detect an association between decline and these medications:
didanosine, (odds ratio [OR] 0.667, 95%CI 0.135-3.303); zidovudine, (OR 1.5,
95%CI 0.701-3.209); or stavudine, (OR 1.842, 95%CI 0.832-4.078). None of
our cases and three controls were taking the didanosine/tenofovir combination,
which has been associated with decline.
Conclusions: Declining CD4+ cell count in the setting of low plasma HIV
RNA levels is relatively rare in our population. The vast majority of cases had
plasma HIV RNA levels consistently <500 copies/ml and none were taking the
didanosine/tenofovir combination, suggesting the involvement of other factors.
We examined several independent variables, including hepatitis C antibody
status and antiretroviral medications, but none were detected to be associated
with decline.
MOPEOO59
Absence of sustained benefit of HAART followed by
structured treatment interruptions (STI) in primary
HIV-1 infection (PHI): prolonged follow-up of
patients enrolled in the PRIMSTOP (ANRS 100) trial
B. Hoen', C. Deveau2, I. Fournier', C. Lacabaratz4, M. Burgard', S. Izard3,
L. Meyer2, F. Raffi6, Primstop study group & Primo Cohort. 'CHU de Besangon -
Universite de Franche-Comte, Maladies Infectieuses et Tropicales & EA 3186,
Besangon, France, 2INSERM, Unite 569, Le Kremlin Bicetre, France, 3INSERM,
SC 10, Villejuif, France, 4INSERM, E 109, Le Kremlin Bicetre, France, sCHU
Necker-Enfants Malades, Laboratoire de Virologie & EA-MRT 3620, Paris,
France, 6CHU de Nantes, Maladies Infectieuses et Tropicales, Nantes, France
Background: The Primstop trial enrolled 29 patients with early symptomatic
PHI who were given HAART continuously for 34 weeks (W) and then entered
the STI phase that consisted of 3 consecutive periods of 2, 4, and 8 W off
HAART, each separated by 12 W on HAART. HAART was stopped at W84. Of
the 26 patients who completed the trial, no patient had restarted HAART 6
months after HAART discontinuation. Only one patient (3.8%) had plasma viral
load (PVL) < 50 copies/ml, while 6 (23.1%) had PVL < 1000 copies/ml (JAIDS
2005; 40:307-16).
Methods: The post-trial long-term follow-up (F-U) of the 22 patients who
accepted such F-U assessed the changes in CD4 count and plasma viral load
and the time to HAART re-initiation. Analysis was performed in December
2005, after a median duration of F-U of 36 months (range 20-43) after HAART
discontinuation.
Results: Six patients (27%/) restarted HAART after a median of 12 months
(range 7-25), at a median CD4 count of 245/mm3 (range 197-266) and a
median PVL of 4.75 log10 copies/mi (range 3.86-5.44). One of these was the

single patient whose PVL was < 50 copies/ml throughout the 6 months after
HAART discontinuation. Among the 16 patients who did not restart HAART,
30 months after HAART discontinuation, the median absolute CD4 count was
456/mm3 (range 333-639); the median loss of CD4 cells was 240 cells/mm3;
the median PVL increase was 3.1 log10 copies/ml; and 11 (68%) patients had
a PVL > 4 log10 copies/ml. One patient experienced clinical progression (oral
candidiasis) and one developed non-Hodgkin lymphoma.
Conclusions: These data show that virtually no PHI patient can maintain

XVI INTERNATIONAL AIDS CONFERENCE * 13-18 AUGUST 2006 * TORONTO CANADA * ABSTRACT BOOK VOLUME 1