4th International Workshop on HIV Drug Resistance & Treatment Strategies

12-16 June 2000, Sitges, Spain


Session 1: New antiretrovirals
Abstracts 1 thru 13, Pages 3 to 10
1 HEPATITIS B VIRUS DRUG RESISTANCE: LESSONS FOR HIV TREATMENT FAILURE
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):3
S Locarnini and A Bartholomeusz
In addition to this mutation, changes at L426V/I, T474N (P120T in HBsAg) and W/R499Q (G145R in HBsAg) have been selected in the presence of lamivudine alone, lamivudine+HBIG and famciclovir+HBIG, respectively, which have a higher replication capacity than wild-type virus, and tend to be associated with more aggressive liver disease. The implications for these mutations and other mutations in the A and B domains, as well as the A-B interdomain detected in the clinical setting, will be developed against the present modelling status of nucleoside analogue resistance in HIV.
2 FAVOURABLE ANTIVIRAL RESISTANCE PROPERTIES OF SP1093V, AN INHIBITOR OF THE RIBONUCLEASE H ACTIVITY OF HIV-1 REVERSE TRANSCRIPTASE
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):3
MA Parniak, D Arion and N Sluis-Cremer
All amino acid substitutions tested, other than Y501F, eliminated the ability of BBNH to inhibit RT RNase H activity. However, these same substitutions also resulted in significant decreases in the RNase H and/or DNA polymerase activity of RT. Our results suggest that the development of HIV-1 resistance to SP1093V may be significantly prolonged compared to that of the current clinically-used therapeutics, since mutation of a residue crucial for BBNH binding to the RNase H domain would likely result in significant attenuation of viral reverse transcription.
3 POTENT ALKYLGLYCEROL FOSCARNET PRODRUGS INHIBIT NUCLEOSIDE ANALOGUE-RESISTANT HIV-1 AND SELECT FOR MUTATIONS IN RT THAT REVERSE ZIDOVUDINE RESISTANCE
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):4
J Hammond1, D Koontz1, H Bazmi1, J Beadle2, S Hostetler2, G Kini2, K Aldern2, D Richman2, K Hostetler2 and J Mellors1
When introduced into a zidovudine-resistant background (67N, 70R, 215F, 219Q), the W88G, S117T and M164I mutations reversed zidovudine resistance. This reversal of zidovudine resistance is consistent with the effects of other foscarnet resistance mutations that reduce ATP-dependent removal of zidovudine monophosphate from terminated template primers. The favourable activity and resistance profiles of these PFA prodrugs warrant their further evaluation as clinical candidates.
4 ANTI-HIV ACTIVITY PROFILE OF TENOFOVIR (PMPA) AGAINST A PANEL OF NUCLEOSIDE-RESISTANT CLINICAL SAMPLES
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):4
MD Miller1, NA Margot1, K Hertogs2, B Larder3 and V Miller4
The presence of the M184V mutation increases tenofovir susceptibility in multiple HIV genotypes, resulting in wild-type susceptibility for HIV expressing the K65R RT mutation. Furthermore, tenofovir is uniquely active against multinucleosideresistant HIV expressing the Q151M complex, but shows some cross-resistance to the currently rare T69S insertions. These in vitro analyses also demonstrate the broad susceptibility and limited cross-resistance to tenofovir of HIV with common forms of zidovudine and lamivudine resistance and corroborate Phase II clinical trial results demonstrating the anti-HIV activity of tenofovir disoproxyl fumarate in heavily antiretroviral-experienced patients.
5 DAPD: A NOVEL INHIBITOR OF HIV AND HBV REPLICATION IS ACTIVE AGAINST DRUG-RESISTANT VIRUSES
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):5
PA Furman1, R Chin2, K Borroto-Esoda1, J Mewshaw1, B Dent2, A Barthalomews2 and S Locarnini2
Using a transient transfection assay, a panel of drug-resistant mutants of HBV (V519L, L526M, M550I, V553I, L526M/M550V, V519L/ L526M, and V519L/L526M/M550V) has been tested in LMH cells for the effect of DAPD on the levels of replicative intermediates from intracellular cores and/or excreted virus. None of these mutants showed any substantial cross-resistance to DAPD. Therefore, DAPD shows promise as a treatment for wild-type and drug-resistant HIV-1 and HBV.
6 PRELIMINARY PROFILE OF THE ANTIVIRAL ACTIVITY, METABOLIC EFFECTS AND SAFETY OF DMP-450, A NOVEL CYCLIC UREA PROTEASE INHIBITOR
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):6
J Sierra1, S Niño1, P Volkow2, D Sereni3, P Yeni4, S Staszewski5, J Gatell6, L Wang7, N McMillan7, F Rousseau7 and GD Miralles7
To date, DMP-450 appears to have good antiviral activity and tolerability at all doses tested.
7 THE EFFECT OF DRUG RESISTANCE MUTATIONS ON KINETICS OF HIV PROTEASE INACTIVATION BY IRREVERSIBLE INHIBITORS
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):6
S Gulnik, M Pototschnik, T Guerassina, M Smrcina, TN Bhat, M Eissenstat and JW Erickson
While kinact did not change significantly, mutant-dependent increases of Ki up to 100-fold were detected, which led to corresponding increase of half-life of enzyme inactivation. Our data suggests that this type of irreversible inhibitor may have an advantage over reversible compounds in treating drug-resistant viruses only if HIV protease is required to be active over a period of at least several minutes during viral maturation.
8 BMS-232632 SENSITIVITY OF A PANEL OF HIV-1 CLINICAL ISOLATES RESISTANT TO ONE OR MORE APPROVED PROTEASE INHIBITORS
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):7
RJ Colonno1, K Hertogs2, BA Larder2, K Limoli3, G Heilek-Snyder3 and N Parkin3
BMS-232632 appears to have a favourable resistance profile, which did not parallel any of the individual protease inhibitors currently in use. Loss of sensitivity to BMS-232632 was correlated with high-level cross-resistance to three or more inhibitors. Reciprocal studies examining cross-resistance of BMS-232632 resistant isolates will need to await analysis of treatment failures from ongoing trials.
9 SHORT-TERM MONOTHERAPY OF DAPD IN HIV-INFECTED PATIENTS
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):7
S Deeks1, H Kessler2, J Eron3, M Thompson4, F Raffi5 J Jacobson6, N Sista7, J Bigley7 and F Rousseau7
These results suggest a dose-dependent clinical antiviral activity of DAPD against HIV, a good short-term tolerability profile, and the absence of resistance mutations in a 15-day monotherapy study. These data warrant further clinical development of this novel molecule.
10 4′-DEAMINATED TSAO-T: PROTOTYPE OF A SECOND GENERATION OF TSAO NON-NUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITOR DERIVATIVES WITH A DIFFERENT RESISTANCE PROFILE
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):8
S Velázquez1, E Lobatón1, MJ Pérez-Pérez1, E De Clercq2, J Balzarini2 and MJ Camarasa1
We have synthesized the first TSAO molecule that lacks the amino group at the 3′-spiro moiety. This deaminated TSAO molecule showed an aberrant resistance spectrum. It kept its HIV-1 specificity (NNRTI-characteristic) but did not select for any of the classical NNRTI-specific mutations in the NNRTI binding pocket. The mutations are not yet unambiguously determined. Also, the resistant viruses that emerged with the deaminated TSAO were only resistant to this drug and not to other NNRTIs, including any other TSAOs that contain the amino group on the spiro moiety. This opens interesting perspectives for the development of novel types of TSAO molecules that may be of use in combination therapies.
11 A PILOT STUDY OF THE USE OF MYCOPHENOLATE MOFETIL AS A COMPONENT OF THERAPY FOR MULTIDRUG-RESISTANT HIV-1
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):9
JJ Coull1, M Betts1, D Turner2, T Melby3, ER Lanier3 and DM Margolis1,2
The use of low dose MMF appears to be well tolerated in late stage HIV disease. MMF may have contributed to the transient antiviral effect or the modest immunological benefit observed in this cohort with advanced disease and resistant HIV. Further studies of MMF in antiretroviral therapy are indicated.
12 ACTIVITY OF SJ-3366, A NOVEL NON-NUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITOR OF HIV-1, IN COMBINATION WITH OTHER ANTI-HIV AGENTS AGAINST WILD-TYPE AND SJ-3366-RESISTANT VIRAL ISOLATES
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):9
S Palmer1, JD Russell1, RW Buckheit Jr1, J-W Lee2, S-H Lee2, J-W Oh2, H-S Kwon2, S-G Chung2 and E-H Cho2
Consistent synergy and/or additivity exhibited in these combinations, and the absence of antagonistic interactions, suggests that SJ-3366 may hold considerable promise in the treatment of HIV, and might be favourably considered for clinical evaluation.
13 ACTIVITY OF HYDROXYUREA ON MULTIDRUG-RESISTANT HIV-1 VARIANTS
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):10
S Paulous, E Race and F Clavel
HU significantly and selectively reduces infectivity of some multidrug-resistant HIV-1 variants. This finding could constitute the basis for a rational and targeted use of this compound in antiretroviral salvage therapy.
Session 2: Mechanism of HIV drug resistance
Abstract 14 thru 61, Pages 13 to 45
14 EFFECTS OF FOSCARNET RESISTANCE MUTATIONS IN HIV-1 REVERSE TRANSCRIPTASE: SUPPRESSION OF ZIDOVUDINE RESISTANCE THROUGH REDUCED REMOVAL OF ZIDOVUDINE-MP FROM BLOCKED PRIMER/TEMPLATES
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):13
PR Meyer1, R Chopra1, E Pendarvis1, S Matsuura1, H Bazmi2, AG So1, JW Mellors2 and WA Scott1
The decrease in ATP-dependent removal of zidovudine-MP from blocked primer/ templates conferred by foscarnet resistance mutations provides a likely explanation for the resensitization of zidovudine-resistant HIV-1 to zidovudine. The association between foscarnet resistance and decreased ATP-dependent and PPi-dependent primer rescue suggests that foscarnet, ATP and PPi may share a common binding site on the enzyme.
15 EFFECTS OF M41L AND T215Y MUTATIONS IN HIV-1 REVERSE TRANSCRIPTASE ON REMOVAL OF CHAIN-TERMINATORS FROM BLOCKED PRIMER/TEMPLATES
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):14
PR Meyer1, I Pfeifer1, S Matsuura1, H Bazmi2, AG So1, JW Mellors2 and WA Scott1
The M41L mutation had little effect on ATP-dependent removal of chain-terminators by itself, but enhanced the increased removal conferred by the T215Y mutation. The M41L/T215Y mutations conferred an increase in ATP-dependent removal of zidovudine-MP to almost the same extent as the D67N/K70R/T215F/K219Q mutations. These results agree well with the relative effects that these mutations confer on HIV-1 phenotypic zidovudine resistance. Our data also suggests that the T215Y mutation, in the context of the D67N, K70R and K219Q mutations, confers a higher increase in ATP-dependent removal of zidovudine-MP than the T215F mutation. Taken together, our results indicate that increased ATP- dependent removal of zidovudine-MP from blocked DNA chains is an important mechanism of zidovudine resistance.
16 BIOCHEMICAL MECHANISM OF HIV-1 REVERSE TRANSCIPTASE RESISTANCE TO STAVUDINE
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):14
J Lennerstrand1, K Hertogs2, DK Stammers3 and B Larder1
These results indicate that the 69 insertion mutations we studied could be involved in the same ATP-dependent mechanism analogous to pyrophosphorolysis as we previously reported for resistance to zidovudine-TP at the enzyme level. In contrast, the V75T mutant RT seems to be involved in decreased binding to stavudine-TP independently of added ATP.
17 UNIFYING MOLECULAR MECHANISMS OF RT-MEDIATED DRUG RESISTANCE: SPECIFIC TARGETTING OF DRUG-RESISTANT RT IN VITRO
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):15
B Selmi1, P Meyer3, B Schneider2, S Sarfati2, D Deville-Bonne2, C Guerreiro2, J Boretto1, J Janin3, M Véron2 and B Canard1
Our results call for an increasing effort to design pyrophosphorolysis inhibitors, as well as to vectorize nucleotide analogues into a bioavailable form. In that context, our novel analogues are excellent candidates to overcome the three limitations mentioned above, and might have a generic value in fighting viral drug resistance.
18 SENSITIVITY OF DETECTION OF MINORITY SPECIES IN A SINGLE CYCLE REPLICATION ASSAY IS INFLUENCED BY THE BIOCHEMICAL MECHANISM OF RESISTANCE: INSIGHT INTO THE MECHANISM OF NRTI-RESISTANCE AND CROSS-RESISTANCE IN PATIENT SAMPLES
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):16
MM Sartoris, W Huang, C Petropoulos and JM Whitcomb
We will present data supporting a model that explains mixing patterns based on proposed mechanisms of NRTI resistance (in other words phosphorolysis versus dNTP discrimination). The model also addresses the contribution of factors that are thought to influence viral replication capacity, or fitness (for example RT processivity). The model further provides a testable hypothesis to explain NRTI cross-resistance as a measure of the ability of different clusters of mutations to remove different chain terminators, via phosphorolysis.
19 COMPARISON OF EVOLUTIONARY DISTANCES BETWEEN DNA POLYMERASE AND RNASE H DOMAINS OF HIV-1 REVERSE TRANSCRIPTASE IN PATIENTS TREATED WITH ZIDOVUDINE AND LAMIVUDINE
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):16
TC Stoeckli, CY Duan, D Shugarts and DR Kuritzkes
Significantly higher non-synonymous evolutionary distances of the DNA polymerase domain of RT suggest higher selection pressure by treatment with nucleoside RT inhibitors on the DNA polymerase domain than on the RNase H domain of HIV-1 RT. This difference was still significant after excluding positions from the alignment at which resistance mutations occur, suggesting the selection of additional, possibly compensatory mutations in the DNA polymerase domain.
20 EVIDENCE FOR A ROLE OF THE Q151L MUTATION AND THE VIRAL BACKGROUND IN THE DEVELOPMENT OF MULTIPLE DIDEOXYNUCLEOSIDE-RESISTANT HIV-1
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):17
JG García Lerma1, PJ Gerrish2, AC Wright1, SH Qari1 and W Heneine1
HIV-1151L was found to be less fit than HIV-1151M, which may explain the preferential selection of HIV-1151M observed in vivo. The demonstrated ability of HIV-1151L/68G to replicate and the associated zidovudine resistance suggest that 151L is a potential intermediate of Q151M. The dependence of HIV-1151L on other mutations such as S68G for replication may explain the low frequency of the Q151M-mediated pathway of resistance.
21 PRESSURE TO MAINTAIN THE M184V MUTATION IN TISSUE CULTURE CAN MORE EFFICIENTLY BE EXERTED BY LAMIVUDINE AND ABACAVIR THAN BY DIDANOSINE
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):18
MA Wainberg, M Götte and M Oliveira
These data suggest that didanosine may not be able to exert selective pressure to maintain the 184V substitution as adequately as other drugs that can also select for this mutation. The M184V mutation may disappear even faster in the presence of other drugs, such as zidovudine, that are able to impair replication of mutated viruses more efficiently than of wild-type viruses.
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Session 3: New resistance technologies
Abstracts 62 thru 83, Pages 49 to 63
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Session 4: Drug resistance and treatment response
Abstracts 84 thru 110, Pages 67 to 85
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Session 5: Genotype/phenotype relationship: modelling and algorithms
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C Piketty1, A Trylesinski2, A Hill3, G Peytavin4, E Race4, A Si-Mohamed1, F Clavel4 and MD Kazatchkine1
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Abstract not available at this time.
142
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):110

Abstract not available at this time.
143
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):111

Abstract not available at this time.
144
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):112

Abstract not available at this time.
145
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):112

Abstract not available at this time.
146
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):113

Abstract not available at this time.
147
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):114

Abstract not available at this time.
148
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):114

Abstract not available at this time.
149
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):115

Abstract not available at this time.
150
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):116

Abstract not available at this time.
151
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):116

Abstract not available at this time.
152
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):117

Abstract not available at this time.
153
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):118

Abstract not available at this time.
154a
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):119

Abstract not available at this time.
154b
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):119

Abstract not available at this time.
154c
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):120

Abstract not available at this time.
Session 6: Epidemiology and transmission of drug-resistant HIV
Abstracts 155 thru 187, Pages 121 to 144
155
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):123

Abstract not available at this time.
156
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):123

Abstract not available at this time.
157
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):124

Abstract not available at this time.
158
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):125

Abstract not available at this time.
159
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):125

Abstract not available at this time.
160
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):126

Abstract not available at this time.
161
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):127

Abstract not available at this time.
162
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):127

Abstract not available at this time.
163
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):128

Abstract not available at this time.
164
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):128

Abstract not available at this time.
165
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):129

Abstract not available at this time.
166
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):130

Abstract not available at this time.
167
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):130

Abstract not available at this time.
168
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):131

Abstract not available at this time.
169
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):132

Abstract not available at this time.
170
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):132

Abstract not available at this time.
171
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):133

Abstract not available at this time.
172
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):134

Abstract not available at this time.
173
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):134

Abstract not available at this time.
174
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):135

Abstract not available at this time.
175
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):136

Abstract not available at this time.
176
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):136

Abstract not available at this time.
177
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):135

Abstract not available at this time.
178
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):138

Abstract not available at this time.
179
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):139

Abstract not available at this time.
180
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):139

Abstract not available at this time.
181
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):140

Abstract not available at this time.
182
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):141

Abstract not available at this time.
183
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):142

Abstract not available at this time.
184
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):142

Abstract not available at this time.
185
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):143

Abstract not available at this time.
186
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):144

Abstract not available at this time.
187
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):144

Abstract not available at this time.
Session 7: Immune reconstitution
Abstracts 188 thru 197, Pages 149 to 154
188
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):149

Abstract not available at this time.
189
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):149

Abstract not available at this time.
190
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):150

Abstract not available at this time.
191
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):151

Abstract not available at this time.
192
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):152

Abstract not available at this time.
193
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):152

Abstract not available at this time.
194 RAPID REBOUND OF VIRAL REPLICATION, T CELL ACTIVATION, PROLIFERATION AND DYSFUNCTION AFTER DISCONTINUATION OF HAART WITH OR WITHOUT INTERLEUKIN 2
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):153
J van Lunzen1, N Frahm1, C Hoffmann2, B Meyer1, J Lauer1, O Degen1 and HJ Stellbrink1
The rapid rebound of viral replication after discontinuation of therapy is associated with an inversion of CD4/CD8 ratio due to increased T cell turnover and activation. Functional defects reappear in parallel despite profound and sustained suppression of viral replication. Adjuvant IL-2 did not influence these parameters.
195 RECONSTITUTION OF NAÏVE T CELLS DURING TREATMENT OF HIV-INFECTED ADULTS IS DEPENDENT ON AGE
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):154
J Cohen Stuart1, N Back1, D Hamann2, JCC Borleffs1, M Roos2, F Miedema2, R de Boer3 and CAB Boucher1
The finding that the rate of naïve T cell regeneration during HAART is equal for the CD4 and CD8 compartment, combined with the inverse correlation between age and recovery rate of naïve T cells, indicates that the thymus plays an important role in the regeneration of naïve T cells in adults on HAART.
196 ASSOCIATION BETWEEN AN EARLY THYMIC VOLUME INCREASE AND T CELL REPOPULATION AFTER HAART
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):154
A Rubio1, M Martínez-Moya2, M Leal1, JM Franco1, J Macías1, J Antonio Pineda1, J Fernández-Cruz2, A Sanchez-Quijano1 and E Lissen1
These data suggest that early thymic volume increases might predict the later T cell repopulation after HAART, supporting the postulated role of the thymus on the immune reconstitution after treatment of adult HIV-1-infected patients.
197 IS PRIMARY HIV INFECTION A MEDICAL EMERGENCY? A PROSPECTIVE STUDY OF IMMUNE RECONSTITUTION AND VIRAL SUPPRESSION IN EARLY AND LATE STAGES OF PRIMARY HIV-1 INFECTION
Antivir Ther. 2000 Jun 12-16; 5 (Suppl. 3):155
DE Smith1, F Hecht2, G Kaufmann1, J Zaunders1, P Cunningham1, P Grey1, J Kahn2 and DA Cooper1
Despite having poorer baseline markers, treatment of patients with very early primary HIV-1 infection results in a similar viral decay rate and immunological recovery compared to patients in later stages of primary HIV infection.

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