Phosphorothioate Oligodeoxynucleotides Bind to the Third Variable Loop Domain (v3) of Human Immunodeficiency Virus Type 1 gp120

1993 ◽  
Vol 3 (1) ◽  
pp. 19-31 ◽  
Author(s):  
C.A. STEIN ◽  
AILEEN M. CLEARY ◽  
LEONID YAKUBOV ◽  
SETH LEDERMAN
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
The Third ◽  
Variable Loop ◽  
Loop Domain ◽  
Immunodeficiency Virus ◽  
Phosphorothioate Oligodeoxynucleotides

scholarly journals Lowered Rilpivirine Exposure During the Third Trimester of Pregnancy in Human Immunodeficiency Virus Type 1–Infected Women

2017 ◽  
Vol 65 (8) ◽  
pp. 1335-1341 ◽  
Author(s):  
Stein Schalkwijk ◽  
Angela Colbers ◽  
Deborah Konopnicki ◽  
Andrea Gingelmaier ◽  
John Lambert ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Third Trimester ◽  
The Third ◽  
Immunodeficiency Virus

scholarly journals Selection of T1249-Resistant Human Immunodeficiency Virus Type 1 Variants

2008 ◽  
Vol 82 (13) ◽  
pp. 6678-6688 ◽  
Author(s):  
Dirk Eggink ◽  
Christopher E. Baldwin ◽  
Yiqun Deng ◽  
Johannes P. M. Langedijk ◽  
Min Lu ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Cross Resistance ◽  
Fusion Inhibitor ◽  
Third Generation ◽  
The Third ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT Human immunodeficiency virus type 1 (HIV-1) entry is an attractive target for therapeutic intervention. Two drugs that inhibit this process have been approved: the fusion inhibitor T20 (enfuvirtide [Fuzeon]) and, more recently, the CCR5 blocker maraviroc (Selzentry). T1249 is a second-generation fusion inhibitor with improved antiviral potency compared to the first-generation peptide T20. We selected T1249-resistant HIV-1 variants in vitro by serial virus passage in the presence of increasing T1249 doses after passage with wild-type and T20-resistant variants. Sequence analysis revealed the acquisition of substitutions within the HR1 region of the gp41 ectodomain. The virus acquired mutations of residue V38 to either E or R in 10 of 19 cultures. Both E and R at position 38 were confirmed to cause resistance to T1249, as well as cross-resistance to T20 and C34, but not to the third-generation fusion inhibitor T2635. We also observed substitutions at residues 79 and 90 (Q79E and K90E), which provide modest resistance to T1249 and, interestingly, T2635. Thus, the gp41 amino acid position implicated in T20 resistance (V38 replaced by A, G, or W) is also responsible for T1249 resistance (V38 replaced by E, R, or K). These results indicate that T20 and T1249 exhibit very similar inhibition modes that call for similar but not identical resistance mutations. All T1249-resistant viruses with changes at position 38 are cross resistant to T20, but not vice versa. Furthermore, substitutions at position 38 do not provide resistance to the third-generation inhibitor T2635, while substitution at positions 79 and 90 do, suggesting different resistance mechanisms.

scholarly journals Primary Human Immunodeficiency Virus Type 1 (HIV-1) Infection during HIV-1 Gag Vaccination

2008 ◽  
Vol 82 (6) ◽  
pp. 2784-2791 ◽  
Author(s):  
Arumugam Balamurugan ◽  
Martha J. Lewis ◽  
Christina M. R. Kitchen ◽  
Michael N. Robertson ◽  
John W. Shiver ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Dna Vaccine ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Natural Immunity ◽  
The Third ◽  
Immunodeficiency Virus ◽  
Hiv 1 ◽  
Ctl Responses

ABSTRACT Vaccination for human immunodeficiency virus type 1 (HIV-1) remains an elusive goal. Whether an unsuccessful vaccine might not only fail to provoke detectable immune responses but also could actually interfere with subsequent natural immunity upon HIV-1 infection is unknown. We performed detailed assessment of an HIV-1 gag DNA vaccine recipient (subject 00015) who was previously uninfected but sustained HIV-1 infection before completing a vaccination trial and another contemporaneously acutely infected individual (subject 00016) with the same strain of HIV-1. Subject 00015 received the vaccine at weeks 0, 4, and 8 and was found to have been acutely HIV-1 infected around the time of the third vaccination. Subject 00016 was a previously HIV-1-seronegative sexual contact who had symptoms of acute HIV-1 infection approximately 2 weeks earlier than subject 00015 and demonstrated subsequent seroconversion. Both individuals reached an unusually low level of chronic viremia (<1,000 copies/ml) without treatment. Subject 00015 had no detectable HIV-1-specific cytotoxic T-lymphocyte (CTL) responses until a borderline response was noted at the time of the third vaccination. The magnitude and breadth of Gag-specific CTL responses in subject 00015 were similar to those of subject 00016 during early chronic infection. Viral sequences from gag, pol, and nef confirmed the common source of HIV-1 between these individuals. The diversity and divergence of sequences in subjects 00015 and 00016 were similar, indicating similar immune pressure on these proteins (including Gag). As a whole, the data suggested that while the gag DNA vaccine did not prime detectable early CTL responses in subject 00015, vaccination did not appreciably impair his ability to contain viremia at levels similar to those in subject 00016.

Sign in / Sign up

Export Citation Format

Share Document