Immunologic benefits of enfuvirtide in patients enrolled in a drug assistance program.
ABSTRACT Randomized clinical trials have demonstrated that enfuvirtide plus an optimized background regimen can cause a significant increase in CD4+ cell counts and a reduction in HIV RNA levels.
To describe and analyze CD4+ cell count and HIV RNA changes in HIV-infected patients receiving enfuvirtide and a prescribed background regimen (PBR) in a primarily clinical setting.
A retrospective review from September 1998 through August 2005 of CD4+ cell counts and HIV RNA changes from baseline was conducted in patients receiving enfuvirtide. Data were stratified and analyzed according to baseline CD4+ cell count and HIV RNA.
A mean CD4+ cell count increase of approximately 102 cells/mm(3)was observed, regardless of baseline CD4+ cell count, in 187 patients receiving enfuvirtide during a mean of 19.4 months of follow-up. During 3 years of follow-up, patients initiating enfuvirtide at CD4+ cell counts less than 100 cells/mm(3)never achieved absolute CD4+ cell counts comparable to the counts in patients starting enfuvirtide at CD4+ cell counts of 100 cells/mm(3)or more. In 38.3% of patients achieving an undetectable HIV RNA level, a mean CD4+ cell count increase of 185 cells/mm(3)was observed. An unexpected finding was that a mean CD4+ cell count increase of 76 cells/mm(3)occurred in 61.7% of patients not achieving complete viral suppression.
Immunologic benefits were observed in subjects continuing enfuvirtide plus a PBR irrespective of baseline CD4+ cell count, complete viral suppression, or antiretroviral susceptibility data. Data suggest that initiation of enfuvirtide at CD4+ cell counts greater than 100 cells/mm(3)may be immunologically advantageous and independent of complete virologic response.
- SourceAvailable from: Robert Blumenthal[Show abstract] [Hide abstract]
ABSTRACT: In previous studies on mechanisms of HIV-1-mediated pathogenesis we showed that bystander apoptosis mediated by cell surface-expressed HIV-1 Env correlated with the fusogenic properties of the gp41 subunit of Env. A crucial step in HIV gp41-mediated fusion is the refolding of the protein into a six-helix bundle along the N- and C-terminal coiled-coil domains. These domains have been targeted by peptide inhibitors that inhibit gp41-mediated fusion. One of these inhibitors, enfuvirtide, is the first such drug approved for therapy. More recently, clinical data suggest that the beneficial effects of enfuvirtide extend beyond virus suppression and are associated with certain resistance mutations in gp41. In this study we characterized the bystander apoptosis-inducing potential of mutants associated with increased CD4 counts that arise during enfuvirtide therapy. Whereas all mutant clones were reduced in both cell-to-cell fusion activity and apoptosis induction there was limited effect on virus infection or replication. The viruses were found to have apoptosis-inducing activity in the order WT > V38M > V38A > G36D > V38E, which correlated with cell-to-cell fusion but not infection. Interestingly, the level of resistance as determined by the IC(50) of enfuvirtide also correlated inversely with both cell fusion and apoptosis in that the most resistant Envs were the least fusogenic and pathogenic. This suggests the beneficial effects of enfuvirtide therapy beyond virus suppression may be mediated by selecting less pathogenic HIV isolates over time.AIDS research and human retroviruses 08/2009; 25(8):811-7. · 2.18 Impact Factor
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ABSTRACT: Although both tipranavir and darunavir are important options for the management of patients with multidrug resistant HIV, there are at present no studies comparing the effectiveness and safety of these 2 antiretroviral drugs in this population of patients. Objective: To compare the effectiveness and safety of ritonavir (TPV/r)- and darunavir/ritonavir (DRV/ r)-based therapies in treatment-experienced patients (n = 38 and 47, respectively). Multicenter, retrospective cohort study. The median baseline viral load and CD4 count were 4.7 copies/mL (interquartile range [IQR] 4.3, 5.2) and 168 cells/mm( 3) (IQR 80, 252) for TPV/r patients and 4.7 copies/mL (IQR 3.7, 5.1) and 171 cells/mm(3) (IQR 92, 290) for DRV/r patients. The median number of years on antiretroviral therapy (ART) prior to starting DRV/r or TPV/r were 12.7 (10.2-15.5) and 10.5 (8.4-12.6), respectively (P < .01). Current raltegravir (RAL) use (odds ratio [OR] 5.53, 95% CI 1.08-28.34) was significantly associated with virologic suppression at week 24 in multivariable logistic regression models, whereas the use of TPV/r was not significantly associated with virologic suppression compared to DRV/r (OR 0.93, 95% CI 0.27-3.18, P = .91). No significant difference was observed between DRV/r and TPV/r in terms of virologic suppression.Journal of the International Association of Physicians in AIDS Care (JIAPAC) 01/2010; 9(6):382-9.
2003 as the first of a class of antiretroviral
(ARV) medications called fusion in-
hibitors. Enfuvirtide works extracellularly
by binding to glycoprotein 41 in the enve-
lope region of HIV type 1 and blocking
the fusion of the viral membrane to the
host’s CD4+ cell membrane.1
In 2 randomized open-label studies
entitled TORO 1 and 2 (T-20 vs Opti-
mized Regimen Only study 1 and 2),2,3
491 and 504 highly treatment-experi-
enced subjects, respectively, were ran-
domized to receive the study drug plus an
optimized background regimen (OBR)
versus an OBR alone. At 6 months, the
HIV RNA in the enfuvirtide groups in
TORO 1 and 2 decreased by 1.696 log10
copies/mL and 1.429 log10copies/mL, re-
spectively, compared with a decrease of
0.764 log10copies/mL and 0.648 log10
copies/mL in the control groups (p <
0.001), respectively. In the treatment ver-
sus control groups, CD4+ cell count in-
creased by 76 cells/mm3versus 32 cells/
mm3, respectively (p < 0.001), in TORO
1, and 65.5 cells/mm3versus 38 cells/
mm3(p < 0.02), in TORO 2.
Based on these studies and clinical
observations, it is apparent that enfuvir-
tide plus an OBR causes a significant increase in the CD4+
cell count,2,3which may be independent of enfuvirtide’s ef-
fect on viral load.4The objective of our study was to de-
nfuvirtide was approved by the Food
and Drug Administration (FDA) in
scribe and evaluate CD4+ cell counts and HIV RNA
changes in subjects enrolled in the California AIDS Drug
Assistance Programs (ADAP) who were receiving enfuvir-
tide and a prescribed background regimen (PBR) chosen
by their provider. This cohort consisted of patients who
were continuing enfuvirtide after clinical trials or expand-
The Annals of Pharmacotherapy I
2008 May, Volume 42 I
Immunologic Benefits of Enfuvirtide in Patients Enrolled in a
Drug Assistance Program
Parya Saberi, Nikolai H Caswell, Cristina I Gruta, Jason N Tokumoto, and Betty J Dong
Author information provided at the end of the text.
BACKGROUND: Randomized clinical trials have demonstrated that enfuvirtide plus
an optimized background regimen can cause a significant increase in CD4+ cell
counts and a reduction in HIV RNA levels.
OBJECTIVE: To describe and analyze CD4+ cell count and HIV RNA changes in
HIV-infected patients receiving enfuvirtide and a prescribed background regimen
(PBR) in a primarily clinical setting.
METHODS: A retrospective review from September 1998 through August 2005 of
CD4+ cell counts and HIV RNA changes from baseline was conducted in
patients receiving enfuvirtide. Data were stratified and analyzed according to
baseline CD4+ cell count and HIV RNA.
RESULTS: A mean CD4+ cell count increase of approximately 102 cells/mm3was
observed, regardless of baseline CD4+ cell count, in 187 patients receiving
enfuvirtide during a mean of 19.4 months of follow-up. During 3 years of follow-
up, patients initiating enfuvirtide at CD4+ cell counts less than 100 cells/mm3
never achieved absolute CD4+ cell counts comparable to the counts in patients
starting enfuvirtide at CD4+ cell counts of 100 cells/mm3or more. In 38.3% of
patients achieving an undetectable HIV RNA level, a mean CD4+ cell count
increase of 185 cells/mm3was observed. An unexpected finding was that a mean
CD4+ cell count increase of 76 cells/mm3occurred in 61.7% of patients not
achieving complete viral suppression.
CONCLUSIONS: Immunologic benefits were observed in subjects continuing
enfuvirtide plus a PBR irrespective of baseline CD4+ cell count, complete viral
suppression, or antiretroviral susceptibility data. Data suggest that initiation of
enfuvirtide at CD4+ cell counts greater than 100 cells/mm3may be immuno-
logically advantageous and independent of complete virologic response.
KEY WORDS: CD4+ cell count, enfuvirtide, viremia.
Ann Pharmacother 2008;42:621-6.
Published Online, 15 Apr 2008, www.theannals.com, DOI 10.1345/aph.1K572
A For Our Patients summary of this article is available at www.ForOurPatients.info
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ed access programs prior to the FDA approval of enfuvir-
tide, as well as patients initiating enfuvirtide after its ap-
Study approval was received from the Committee on
Human Research at the University of California, San Fran-
cisco. A retrospective review of the CD4+ cell count and
HIV RNA of patients receiving enfuvirtide through the
California ADAP from September 1998 through August
2005 was conducted.
Patients were stratified according to baseline CD4+ cell
count (defined as a CD4+ cell count value obtained within
6 months of starting enfuvirtide and PBR) into 2 cate-
gories: less than 100 cells/mm3and 100 cells/mm3or
greater. Overall and incremental changes in CD4+ cell
count during enfuvirtide treatment periods were analyzed.
To determine the overall CD4+ cell count change from
baseline, a time-weighted CD4+ cell count change from
baseline was calculated. This value was estimated by taking
the difference between the time-weighted mean of all post-
baseline CD4+ cell count observations for a patient and that
patient’s baseline CD4+ cell count. The time-weighting fac-
tor for each CD4+ cell count observation was the number of
days between that count and the previous count.
Additionally, we stratified the cohort based on the tim-
ing of enfuvirtide initiation into subjects who had initiated
enfuvirtide prior to FDA approval (March 13, 2003) and
subjects initiating enfuvirtide after FDA approval. Incre-
mental changes in CD4+ cell count during the respective
treatment periods were analyzed.
ARV susceptibility data were available in a subset of
subjects. Based on the California ADAP approval criteria,
this group was divided into 2 categories. Category A in-
cluded patients who were either naïve to one class of ARV
(other than enfuvirtide) or susceptible to 2 or more ARV
agents and had a CD4+ cell count cut-off of less than 200
cells/mm3. Category B consisted of patients who had sus-
ceptibility to one or no ARV agent and had a CD4+ cell
count cut-off of less than 100 cells/mm3. Data regarding
the actual number of active drugs in the patients’ PBR
were not known. Changes in CD4+ cell count were ana-
lyzed in this subset of subjects.
In addition, patients were sorted based on detectability
of the last available HIV RNA value within a 6-month
(4–8 months) period as well as the last available HIV
RNA level for the entire length of follow-up into 2 groups
of less than 75 copies/mL and 75 copies/mL or more. Be-
cause the baseline CD4+ cell count was the major criterion
for California ADAP coverage of enfuvirtide, a few sub-
jects did not have any HIV RNA values and some had
only a baseline HIV RNA reported. Therefore, not all pa-
tients were included in the HIV RNA analysis.
Statistical analysis included linear regression and ANOVA
models for the calculation of p values. A p value less than
0.05 indicated a statistically significant difference. A 95%
confidence interval was employed to determine the extent
of the variation in data.
From the initial patient population (N = 310), 122 pa-
tients were excluded due to incomplete CD4+ cell count
follow-up data, and 1 was excluded due to malignancy.
Data from the remaining 187 patients, including 581
CD4+ cell counts and 547 HIV RNA observations over a
mean of 19.4 months (range 1.4–87.3; median 13.8), were
reviewed. Mean baseline CD4+ cell counts and HIV RNA
levels are shown in Table 1. Overall, a significant mean
CD4+ cell count increase of approximately 102 cells/mm3
(95% CI 88 to 117; p < 0.01) was observed, regardless of
baseline CD4+ cell count (p = 0.9; Figure 1). As shown in
Figure 2, the sharpest increase in CD4+ cell count oc-
curred during the first 6 months of therapy (mean slope
13.3 CD4+ cells/mo; 95% CI 11.1 to 16.2), after which the
rate of incline decreased during the 3-year follow-up peri-
od (mean slope 2.4 CD4+ cells/mo; 95% CI 1.5 to 4.7). At
3 years, despite similar net changes in CD4+ cell count of
102 cells/mm3, subjects initiating enfuvirtide at CD4+ cell
counts less than 100 never achieved values comparable to
those in patients starting enfuvirtide at CD4+ cell counts of
100 cells/mm3or more (Figure 2).
As shown in Table 1, it is apparent that patients start-
ing enfuvirtide pre- and post-FDA approval had similar
baseline CD4+ cell count and HIV RNA levels. Figure 2
demonstrates that these 2 groups of patients had similar
increases in CD4+ cell count over the periods of follow-
The Annals of Pharmacotherapy I
2008 May, Volume 42
P Saberi et al.
Table 1. Summary of Mean Baseline CD4+
Cell Counts and HIV RNA Levels
CD4+ Cell Count
CD4+ <100 (n = 149)
CD4+ ≥100 (n = 38)
Category A,a(n = 38)
Category B,a(n = 26)
Preapproval group (n = 58)b
Postapproval group (n = 129)b
aCategory A: patients either naïve to one class of antiretroviral (other
than enfuvirtide) or susceptible to ≥2 antiretroviral agents and who
had a CD4+ cell count cut-off of <200 cells/mm3. Category B: patients
susceptible to one or no antiretroviral agents and with a CD4+ cell
count cut-off of <100 cells/mm3.
bEnfuvirtide received Food and Drug Administration approval on March
At 2 years, the net change in CD4+ cell count was not
significantly different between category A patients (ie, sus-
ceptible to ≥2 ARVs; mean increase 97 cells/mm3) and cat-
egory B patients (ie, susceptible to ≤1 ARV; mean increase
72 cells/mm3; p = 0.1).
At a mean of 6 months (range 4–8), 60 patients with
available viral load data achieved a mean 1.77 log10reduc-
tion in HIV RNA and a 101 cell/mm3increase in CD4+
cell count. As shown in Table 2, in 38.3% of subjects who
had an undetectable viral load (HIV RNA <75 copies/mL), a
mean CD4+ cell count increase of 113 cells/mm3was
achieved. Conversely, in 61.7% of subjects, whose viral load
remained detectable, a mean CD4+ cell count increase of 92
cells/mm3was observed. Comparable results were noted
across all subjects at a mean of 17 months of follow-up
(Table 2). Stratification of patients by baseline CD4+ cell
count did not appear to influence viral detectability. In 38.8%
(40/103) of patients initiating enfuvirtide at CD4+ cell counts
less than 100 cells/mm3and in 36% (9/25) of patients starting
enfuvirtide at CD4+ cell counts 100 cells/mm3or more, an
undetectable viral load was observed.
This study demonstrates our patients’ clinical response
to enfuvirtide during a 3-year follow-up period, primarily
outside of a controlled clinical trial setting. At 6 months,
patients with a detectable viral load achieved HIV RNA
reductions and CD4+ cell count increases comparable to
those in the enfuvirtide plus OBR arm of the TORO tri-
als.2,3Despite the obvious differences in study design, sim-
ilar outcomes were observed in both studies. In addition,
subjects who achieved complete viral suppression in our
study had a CD4+ cell count increase of approximately
113 cells/mm3at 6 months of follow-up.
Similar net gain in CD4+ cell counts across all cate-
gories suggests that initiation of enfuvirtide at a CD4+
greater than 100 cells/mm3may be immunologically ad-
vantageous. Immunologic benefits were observed with the
continued use of enfuvirtide plus a PBR regardless of
baseline CD4+ cell count, complete viral suppression, or
ARV susceptibility data.
This immunologic benefit of enfuvirtide has been de-
scribed in a study by Poveda et al.,5where 4 treatment-ex-
perienced patients had either a significant gain or a sus-
tained CD4+ cell count despite virologic failure at 80
weeks of follow-up. They concluded that CD4+ cell count
increase or maintenance may occur due to a reduction in
overall immune activation.
One trial demonstrated that the V38A/E mutations in-
curred by the continued use of enfuvirtide in the presence
of viremia were associated with immunologic benefits.4
These mutations produced a 4.5-fold and a sixfold increase
in the CD4+ cell count at 24 and 36 weeks, respectively,
compared with baseline. In contrast, other mutations, such
as Q40H and L45M, were associated with the loss of
CD4+ cell counts. Although enfuvirtide genotypic tests
were not performed in our study, we speculate that patients
who had a gain in CD4+ cell count despite virologic
breakthrough may have harbored the V38A/E mutations.
In a poster presented at the 12th Conference on Retro-
viruses and Opportunistic Infections, the investigators not-
ed that virologic failure to an enfuvirtide-based regimen
occurred with a rapid increase in HIV RNA back to pre-
treatment levels.6However, in patients with virologic fail-
ure, CD4+ cell counts increased and remained elevated
through 6 months of follow-up. In another abstract at this
conference, a modest increase in HIV RNA level and a
rapid reduction in enfuvirtide-resistant strains were noted
after the discontinuation of enfuvirtide.7The authors con-
cluded that enfuvirtide mutations may be asso-
ciated with a reduction in the “fitness” of the
virus and therefore a decrease in the viral repli-
In an abstract presented at the 15th Confer-
ence on Retroviruses and Opportunistic Infec-
tions, the investigators reported longitudinal
immunological analyses of T-cells in patients
treated with enfuvirtide for 12 months.8They
noted that virologic response to enfuvirtide
was associated with the expansion of naïve
and central memory T-cells and sustained de-
creases in T-cell activation. Additionally, en-
fuvirtide treatment reduced the expression of
R5 and X4 coreceptors on T-cells. At this con-
ference, another poster presented results show-
ing that interleukin-2 failed to increase CD4+
cell count; however, treatment with enfuvirtide
was highly associated with immunological
Immunologic Benefits of Enfuvirtide
The Annals of Pharmacotherapy I
2008 May, Volume 42 I
Figure 1. Changes in absolute CD4+ cell count from baseline. Broken line indicates
mean change across all observations = 102 cells/mm3.
success at week 52, even in poorly optimized background
In a cost-effectiveness study, the projected quality-ad-
justed life expectancy for subjects with an average base-
line CD4+ cell count of 133 cells/mm3was 45.4 months
for patients on an OBR alone versus 54.9 months when
enfuvirtide was added to an OBR.10This difference of 9.5
months corresponded to a 21% increase in quality-adjust-
ed life expectancy. The projected survival benefit
achieved with the use of enfuvirtide plus an OBR was
also shown to increase with longer follow-up. The incre-
mental cost-effectiveness difference of enfuvirtide plus an
OBR compared with an OBR alone was $69,500 per
quality-adjusted life-year. Similar but more modest results
were reported in another cost-effectiveness study.11
The decision to continue enfuvirtide in patients with
incomplete viral suppression has to be determined on an
individual basis. Factors to consider when evaluating
the risks versus benefits of continuing enfuvirtide in-
clude cost, twice-daily subcutaneous route of delivery,
likelihood of adverse effects, possibility of cross-resis-
tance to second-generation fusion inhibitors, potential
for achieving undetectability with newer antiretroviral
agents (eg, CCR5 inhibitors or integrase inhibitors), and
net CD4+ cell count changes compared with the start of
therapy. In some highly treatment-experienced patients,
where complete viral suppression may not be possible,
the CD4+ cell count gain from continued use of enfuvir-
tide may outweigh the risks associated with drug contin-
The Annals of Pharmacotherapy I
2008 May, Volume 42
P Saberi et al.
Table 2. Summary of CD4+ Cell Count Increases and HIV RNA Reductions Stratified by HIV RNA
CD4+ Cell Count (cells/mm3)
HIV RNA (log10 copies/mL)
(median, range)n p Valuep Value
6 mo (6, 4–8)60 38.3%a
61 (41 to 82)
54 (37 to 71)
72 (51 to 94)
65 (48 to 73)
113 (72 to 154)
92 (61 to 124)
185 (142 to 228)
76 (58 to 95)
4.67 (4.35 to 5)
4.92 (4.67 to 5.16)
4.61 (4.35 to 4.88)
4.89 (4.74 to 5.04)
2.84 (2.51 to 3.16)
1.1 (0.74 to 1.46)
2.78 (2.52 to 3.05)
1.11 (0.85 to 1.37)
17 mo (13, 1–87)
aPercentage of subjects who had an undetectable viral load (HIV RNA <75 copies/mL).
bPercentage of subjects who had a detectable viral load (HIV RNA ≥75 copies/mL).
0–6 months, nb,c
12–18, n18–24, n 24–30, n 30–36, n
FDA = Food and Drug Administration.
aNumber of CD4+ observations.
bOne month = 30 days.
cNumber of observations decreases postbaseline due to differences in CD4+ measurement frequency.
dCategories of subjects receiving enfuvirtide before and after approval.
Figure 2. Changes in mean CD4+ cell count over time by baseline CD4+ and FDA approval categories.
Due to the retrospective nature of this study, there are
inherent biases and limitations. Subject referral and subse-
quent reassessments were determined and initiated by the
patients’ physicians. Additional limitations include the lack
of knowledge about the patients’ PBR, rates of adherence,
loss to follow-up, and lack of a control group. Lastly, al-
though these data span an 8-year timeframe (1998– 2005),
during which HIV therapy has changed considerably, 76.5%
of our subjects initiated enfuvirtide after the date of enfuvir-
tide’s approval by the FDA. With the acknowledgment that
24.5% of our subjects were enrolled in the pre-FDA approval
clinical trials or expanded-access programs and may have
constituted a different patient population, we evaluated their
exclusion from the final data analysis to determine their ef-
fect on the final results. The exclusion of these subjects did
not result in a clinical or statistical difference in our final re-
sults. Therefore, these subjects were included to demonstrate
results in a larger sample size.
With the approval of new antiretroviral drug classes,
there are more options to achieve virologic suppression in
many treatment-experienced patients. The continuation of
enfuvirtide plus a PBR may be reasonable when complete
virologic suppression is not possible and an increase in
CD4+ cell count has been attained. Prospective studies are
needed to demonstrate causality.
The immunologic benefit shown in our study was ob-
served with the continued use of enfuvirtide plus a PBR re-
gardless of subjects’ baseline CD4+ cell count, degree of vi-
ral suppression, or ARV susceptibility data. In highly treat-
ment-experienced patients with limited treatment options for
achieving virologic suppression who have attained an in-
crease in CD4+ cell count with enfuvirtide, it may be reason-
able to continue enfuvirtide as part of a maintenance regimen
while awaiting the availability of active agents.
Parya Saberi PharmD, Clinical Pharmacist, Department of Family
and Community Medicine, University of California at San Francis-
co, San Francisco, CA
Nikolai H Caswell MA, Independent Analyst, San Francisco
Cristina I Gruta PharmD, Clinical Pharmacist, Department of Fami-
ly and Community Medicine, University of California at San Francisco
Jason N Tokumoto MD, Assistant Clinical Professor, Department
of Family and Community Medicine, University of California at San
Betty J Dong PharmD FCCP, Professor of Clinical Pharmacy, De-
partments of Clinical Pharmacy and Family and Community Medicine,
University of California at San Francisco
Reprints: Dr. Saberi, San Francisco General Hospital, UCSF Box
1365, San Francisco, CA 94143, fax 415/476-3454, Parya.saberi@
We thank Steven Deeks MD for his valuable comments and generosity with his time,
and the California AIDS Drug Assistance Program for its generosity with providing
the data for this study. The authorized release of ADAP client and/or utilization data
by the California Department of Health Services, Office of AIDS, should not be con-
strued as an endorsement of the methodology, analyses, interpretations, or con-
clusions reached by the authors.
1. Wild C, Greenwell T, Matthews T. A synthetic peptide from HIV-1 gp41
is a potent inhibitor of virus-mediated cell–cell fusion. AIDS Res Hum
2. Lalezari JP, Henry K, O’Hearn M, et al. Enfuvirtide, an HIV-1 fusion in-
hibitor, for drug-resistant HIV infection in North and South America. N
Engl J Med 2003;348:2175-85.
3. Lazzarin A, Clotel B, Cooper D, et al. Efficacy of enfuvirtide in patients
infected with drug-resistant HIV-1 in Europe and Australia. N Engl J
4. Aquaro S, D’Arrigo R, Svicher V, et al. Specific mutations in HIV-1 gp41
are associated with immunological success in HIV-1-infected patients re-
ceiving enfuvirtide treatment. J Antimicrob Chemother 2006;58:714-22.
5. Poveda E, Rodes B, Labernardiere JL, et al. Evolution of genotypic and
phenotypic resistance to enfuvirtide in HIV-infected patients experienc-
ing prolonged virologic failure. J Med Virol 2004;74:21-8.
6. Beatty G, Lu J, Hunt P, et al. Randomized pilot study of immediate enfu-
virtide-based therapy vs. a treatment interruption followed by enfuvir-
tide-based therapy in highly treatment-experienced patients (abstract
581). Presented at: 12th Conference on Retroviruses and Opportunistic
Infections, Boston, MA, February 22–25, 2005.
7. Deeks S, Lu J, Hoh R, et al. Interruption of enfuvirtide in patients with
enfuvirtide resistance (abstract 680). Presented at: 12th Conference on
Retroviruses and Opportunistic Infections, Boston, MA, February 22–
8. Dellamonica HC, Durant J, Ticchioni M, et al. Enfuvirtide therapy in-
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Los Beneficios Inmunológicos de Enfuvirtide en Pacientes que
Reciben Tratamiento en un Programa de Asistencia de
P Saberi, NH Caswell, CI Gruta, JN Tokumoto, y BJ Dong
Ann Pharmacother 2008;42:621-6.
TRASFONDO: Estudios clínicos aleatóreos han demostrado que enfuvirtide
(ENF) en combinación con un régimen antirretroviral óptimo (OBR)
puede resultar en un aumento significativo en el contaje de las células
CD4+ y en una reducción en los niveles plasmáticos del HVI-RNA.
OBJETIVOS: El objetivo de este estudio fue describir y analizar los cambios
en contaje de células CD4+ y los niveles en plasma de HIV-RNA, en
pacientes infectados con HIV que recibieron enfuvirtide en combinación
con un régimen antirretroviral prescrito principalmente en un scenario
MÉTODOS: Se llevó a cabo un estudio restrospectivo durante el período
comprendido entre septiembre 1998–agosto 2005, en el que se estudió
el cambio en el contaje de células CD4+ y HIV-RNA en plasma en
comparación con los valores pre-tratamiento en pacientes que fueron
Immunologic Benefits of Enfuvirtide
The Annals of Pharmacotherapy I
2008 May, Volume 42 I