1Abstract: This is associated with preserved selection pressure at specific viral amino acids (e.g., the T242N polymorphism within the HLA-B*57/5801 restricted TW10 epitope), but with reversion at other sites (e.g., the T186S polymorphism within the HLA-B*8101 restricted TL9 epitope), most notably in Gag and suggestive of ""immune relaxation""."
Abstract: Mutations at HIV Gag T186S and T242N reduced VRC, however, in advanced disease only the T242N mutants demonstrated increasing VRC, and were associated with compensatory mutations (p = 0.013).
Early selection in Gag by protective HLA alleles contributes to reduced HIV-1 replication capacity that may be largely compensated for in chronic infection.
Abstract: Additional mutations in Gag that may modulate the impact of the T242N mutation on RC were identified.
Abstract: However, RC correlated positively with the presence of known compensatory mutations in chronic viruses from B*57-expressing individuals harboring the Gag T242N mutation (n = 50; R = 0.36; P = 0.01), suggesting that the rescue of fitness defects occurred through mutations at secondary sites.
HLA-associated immune pressure on Gag protein in CRF01_AE-infected individuals and its association with plasma viral load.
Result: Both had very high CD4 cell counts of >500 cell/microL and very low viral loads of less than 104 copies/mL, which is in distinct contrast to the remaining six B*57/*58-negative spouses who lacked T242N (median plasma viral load, 5.39 log copies/mL), and supports the results of the recent study by Chopera et al.
Result: However, because the T242N escape mutation is known to emerge within the first three months of infection in B*57-positive subjects, it is unlikely that these six contact cases had acquired the wild-type T242 virus, but instead, the transmitted T242N probably reverted after its transmission to these recipients.
Result: However, the roles of T242N and the compensatory mutations in CRF01_AE infections are unknown.
Result: It was recently reported that the transmission of viruses with attenuating CTL escape mutations,
Dynamics and timing of in vivo mutations at Gag residue 242 during primary HIV-1 subtype C infection.
Abstract: In subjects expressing HLA-B*57/5801 and infected with the wild-type virus, the T242N escape appeared at 203 days (196-231) p/s, reached dominance at 277 days (265-315 days) p/s, and became complete at 323 days (289-373 days) p/s.
Abstract: The study highlights the differential selection of T242N escape by HLA-B*57 and B*5801 and suggests that the presence of HLA-B*57/5801-mediated immune pressure is able to control replication of the wild-type virus encoding Thr at Gag residue 242 but fails to suppress the T242N escape variant.
Clade-specific evolution mediated by HLA-B*57/5801 in human immunodeficiency virus type 1 clade A1 p24.
Abstract: Our data suggest that clade A1 consensus proline at Gag residue 243 might represent an inherent block to T242N escape in clade A1.
Abstract: Whether this T242N pathway is shared by all clades remains unknown.
Abstract: While T242N was ubiquitous in clade D HLA-B*57(+) subjects, this mutation was rare (15%) in clade A1.
Maternal transmission of human immunodeficiency virus escape mutations subverts HLA-B57 immunodominance but facilitates viral control in the haploidentical infant.
Abstract: Associated compensatory mutations within p24-Gag were observed to reverse this impairment and to influence the propensity of T242N to revert after transmission to B57-negative hosts.
Abstract: However, if the B57 advantage is largely mediated by selection for fitness-attenuating viral mutations within B57-restricted epitopes, such as T242N in TW10-Gag, then the transmission of such mutations could facilitate viral control in the haploidentical infant.
Abstract: Moreover, primary failure to control viremia was observed in one infant to whom multiple compensatory mutations were transmitted along with T242N.
Abstract: The presence of T242N led to a reproducible reduction in viral fitness, as demonstrated by in vitro assa
Reduced viral replication capacity of human immunodeficiency virus type 1 subtype C caused by cytotoxic-T-lymphocyte escape mutations in HLA-B57 epitopes of capsid protein.
Abstract: To answer the question, the RRCs were quantified for escape mutations in three immunodominant HLA-B*57/B*5801 epitopes in capsid: A146P in IW9 (RRC(P146) = 0.91), A163G in KF11 (RRC(G163) = 0.89), and T242N in TW10 (RRC(N242) = 0.86).
Transmission of human immunodeficiency virus type 1 from a patient who developed AIDS to an elite suppressor.
Abstract: Isolates from both patients were replication competent and contained the T242N escape mutation in Gag, which is known to decrease viral fitness.
HIV mutation literature information.
PMID: 
2011
PloS one
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