Discussion: Ma and Wang reported that eight mutations (P120T, T126S, Q129H, G130N, S143L, D144A, and G145A/R) are associated with diagnostic failure and mutations in the positions 120, 126, 129, 130, 133, 134, 137, 140, 143, 144, and 145 are recorded in escape variants hat evade vaccine or immunoglobulin therapy.
In silico functional and structural characterization of hepatitis B virus PreS/S-gene in Iranian patients infected with chronic hepatitis B virus genotype D.
Introduction: Also, mutations may occur in association with either vaccine-induced immune-escape (P120T, K122R, T126S, Q129H, G130N, M133L, and M133T) or in relation to the patients with occult HBV infection (Y100C, C124R, C124Y, K141E, and D144A).
Analysis of HBsAg mutations in the 25 years after the implementation of the hepatitis B vaccination plan in China.
Abstract: HBV strains with internal stop codons of HBsAg (e.g., sC69*) and additional N-glycosylation (e.g., sG130N) mutations should be studied extensively to prevent them from becoming dominant circulating strains.
Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic.
PMID: 31682960
2020
International journal of infectious diseases
Discussion: Many studies (Protzer-Knolle et al.,; Beckebaum et al.,; Cheung et al.,) have demonstrated that M133T itself is frequently associated with occult HBV infection and is also often associated with some mutations in the 'a' determinant such as G130N, F134L, D144A, D144G, G145A, G145K, and G145R or failed hepatitis B immune globulin (HBIG) prophylaxis.
Occult HBV infection in Chinese blood donors: role of N-glycosylation mutations and amino acid substitutions in S protein transmembrane domains.
Discussion: Mutations T116N, T123N, G130N, and T131N + M133 T have been reported to reduce antigenicity and immunogenicity and rescue virion secretion in N146 mutants.
Molecular characterization of hepatitis B virus in blood donors in Botswana.
Method: We determined the prevalence of 29 immune-associated escape mutations (sQ101K, sT114R, s Result: Conversely, the immune-associated escape mutation G130 N occurred more frequently in genotype-A than D (2%[5/255] vs 0.2%[1/573], P = 0.012).
Result: These results were confirmed also when the analysis was focused on LAM-treated patients, thus limiting the impact of anti-HBV drugs on the selection of these mutations (sA128V: 4.4%[16/362] vs 0.5%[2/209], P = 0.008; sP120S: 5.5%[20/362] vs 1%[2/209], P = 0.006; sG130N: 0.3%[1/362] vs 1.9%[4/209], P = 0.063).
Impact of immune escape mutations and N-linked glycosylation on the secretion of hepatitis B virus virions and subviral particles: Role of the small envelope protein.
Method: Mutations creating novel N-linked glycosylation, such as 112NG113, 114NT115, T115N, and G130N, were introduced to the 0.7mer construct b
Result: The M133T mutation was most efficient at rescuing virion secretion of the G145R mutant, followed by G115N and G130N.
Result: To characterize their biological properties, we generated 0.7mer expression construct containing T115N, G130N, 112NG113 (insertion of the NG dipeptide between residues 112 and 113.
Discussion: In the current work we also performed limited study on four additional mutants creating novel N-linked glycosylation sites: T115N, G130N, 112NG113, and 114NT115.
Naturally occurring hepatitis B virus reverse transcriptase mutations related to potential antiviral drug resistance and liver disease progression.
PMID: 29713126
2018
World journal of gastroenterology
Method: Notably, these authors also found that RT mutations in the A-B interdomain could lead to simultaneous AA substitutions sI126A/N/S/, sG130N, sT131N/P, and sG145R of the overlapped 'a' determinant of HBsAg, including the most frequently described immune-escape mutation sG145R (1/192, 0.52%).
Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection.
Result: Moreover, three patients in the non-HSCT group had predominant variants with sT116N, sT123N, and sG130N changes, which resulted in the addition of NLG sites by substitutions of threonine or glycine with asparagine.