Abstract: The most common point-mutations included N/H51Y/T/S/Q/P (30.4%), V68T/S/I (44.9%), T/N87S/T/P (46.2%) on PreS1 gene; T125S/N/P (30.8%), I150T (42.5%) on PreS2 gene; S53L (37.7%), A184V/G (39.3%), S210K/N/R/S (39.3%) on S gene.
Result: The point-mutations on the S gene that owned the rates of >30% of the population were: S53L (37.7%), A184V/G (39.3%), and PMID: 32312174
2020
Emerging microbes & infections
Method: The following mutations were introduced: V190A, V190A + F220L, S204N, S204N + L205P, Result: Notably, for the mutational pairs S204N + L205P, Y206F + S210R, Y206F + S204T and Y206F + M197T, the decrease in HBsAg release was significant also compared to the corresponding single mutation S204N (P < 0.001) or Y206F (P = 0.007, P = 0.001 and <0.0001, respectively) (Figure 4(A)).
High rates of chronic HBV genotype E infection in a group of migrants in Italy from West Africa: Virological characteristics associated with poor immune clearance.
Result: A similar situation was observed also for patients 2 and 3, and it was characterized by specific mutational profiles (L49R+S193L and G102A/G+S193S/L+S210S/R+L216 stop) observed only in plasma and not in liver tissue (Fig 3).
Novel HBsAg mutations correlate with hepatocellular carcinoma, hamper HBsAg secretion and promote cell proliferation in vitro.
Result: The impact of sP203Q, sS210R and sP203Q+sS210R on cell proliferation was then evaluated by flow cytometry (DNA propidium iodide-staining) on transfected GFP+ cells at day 7 post transfection (Figure 3B).|mg
Figure: The graph reports the intra-patient prevalence of sP203Q (white dots), sS210R (grey dots), sP203Q+sS210R (black dots) for each patient in the HCC group (N=13) A.
Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India.
Discussion: Table 1 shows that the mutations found upstream-I86F, I92T, and I110L-and those found downstream-T189I, Y200F, S204R, Y206L, S207N, S210R, L213I, and L213F-were recorded in different studies but were not associated with critical functions (Table 1).
Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil.
Abstract: The mutations detected were as follows: sM133L + sI195T (2.94%), sI195M (2.94%), sP120T (2.94%), sY100S/F (2.94%), sY100C (17.64%), sI/T126P + sQ129P (2.94%), sM198I + sF183C (2.94%) and sS210R (5.88%).
Result:
Core promoter mutant HBV non-responding to adefovir after viral breakthrough on lamivudine: rapid virologic response to tenofovir plus lamivudine in a cirrhotic patient.
PMID: 19008175
2008
European journal of medical research
Abstract: Because of unchanged VL sequence analysis was performed three months later, which showed the mutation (rtS219A) and the concomitant mutation (sS210R) and 2 mutations in core promoter region (A1762T), (G1764A).
HBV mutation literature information.
PMID: 
2022
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