Quasispecies structure, cornerstone of hepatitis B virus infection: Mass sequencing approach

Table 1 Main amino acid variants described in the hepatitis B virus genome and its effect

ORF	Amino acid variant	Effect
P	A181T and M204 I/V (compensatory: L80I/V, T128N , R153Q, V173L L180M, A200V1, V207I1)	LMV resistance
	N236T (compensatory: A181 T/V/S. Low sensitivity: V84M, S85A, L217R, I233V)	ADV resistance
	I169T, T184S, S202C/I/G, M250I	ETV resistance2
	A194T1	TDF resistance
S	G145R W156Stop, W163Stop, W172Stop, W196Stop	Immune therapy failure
	D144A, P142S, K141E, Q129H, I/T126N, T131I, M133L	HBsAg structural alterations
X	I130M, V131I, F132Y	Contribution to HCC development
C
preCore	A1762T and G1764A	HBeAg negative forms
Core	G1896A and G1899A	Disease progression
	P5H/L/T, D32N/H, C/E43K, cP50A/H/Y, E83D, I97F/L, L100I, A131G/N/P, S181H/P and C/Q182K/stop	HCC development
	Regions 50-69 and 74-84	Immune scape variants

¹Antiviral treatment resistances not completely defined[58];

²Linked to lamivudine (LMV) signature (L180M + M204V). ORF: Open reading frames; ADV: Adefovir; ETV: Entecavir; TDF: Tenofovir; HBsAg: Hepatitis B virus (HBV) surface antigen; HBeAg: HBV e antigen; HCC: Hepatocellular carcinoma.