Association between low molecular polypeptide 7 single nucleotide polymorphism and response to therapy in hepatitis C virus infection

Table 1 The demographic data of chronic hepatitis C virus patients infected with hepatitis C virus type 4a (sustained virological response vs non-response) after treatment

	NR (n = 48)	SVR (n = 56)	P value
Age (yr)			0.004
min-max	12-64	7-58
mean ± SD	44.17 ± 10.97	37.91 ± 10.91
Gender			0.9061
Female	9 (18.75)	10 (17.86)
Male	39 (81.25)	46 (82.14)
Weight (kg)	85.05 ± 13.98	78.54 ± 15.10	0.025
ALT	89.15 ± 62.70	48.39 ± 40.52	0.001
AFP	30.56 ± 22.58	11.28 ± 15.33	0.001
Viral load	686 150.38 ± 680 474.25	15 656.09 ± 452 782.09	0.001
Low fibrosis (F0-F1) (n = 39)	7 (17.95)	32 (82.05)	0.001
High fibrosis (F2-F4) (n = 65)	41 (63.08)	24 (36.92)	0.035
A0-A1 (n = 71)	24 (33.8)	47 (66.2)	0.006
A2-A3 (n = 33)	24 (72.73)	9 (27.27)	0.009

Data are expressed as mean ± SD or n (%). NR: Non-response; SVR: Sustained virological response; ALT: Alanine aminotransferase; AFP: Alpha-fetoprotein.

¹Not significant.

Table 2 The percentage of sustained virological response and non-response patients compared with control subjects in various genotypes of low molecular polypeptide-7 gene n (%)

	NR (n = 48)	SVR (n = 56)	All patients (n = 104)	Control (n = 33)
AA (n = 14)	9 (64.29)	5 (35.71)	14 (13.46)	3 (9)
CA (n = 42)	35 (83.33)	7 (16.67)	42 (40.38)	12 (36.5)
CC (n = 48)	4 (8.33)	44 (91.67)	48 (46.15)	18 (54.5)

NR: Non-response; SVR: Sustained virological response.

Table 3 Sustained virological response and non-response frequencies in various low molecular polypeptide-7 genotypes n (%)

	AA (n = 14)	CA (n = 42)	CC (n = 48)	P value
NR (n = 48)	9 (18.75)	35 (72.92)	4 (8.33)	0.001
SVR (n = 56)	5 (8.93)	7 (12.50)	44 (78.57)	0.001

Polymerase chain reaction-restriction fragment length polymorphism analysis were performed on chronic hepatitis C virus patients and the low molecular polypeptide-7 genotype frequencies were calculated as percentages of each group. NR: Non-response; SVR: Sustained virological response.

Table 4 The relationship of the genotypes of low molecular polypeptide-7 gene polymorphism within different liver fibrosis and activity stages in sustained virological response and non-response groups after treatment n (%)

	AA (n = 14)	CA (n = 42)	CC (n = 48)	P value
F0 (n = 10)	1 (10.00)	2 (20)	7 (70)	0.045
F1 (n = 29)	4 (13.79)	7 (24.14)	18 (62.07)	0.004
F2 (n = 36)	4 (11.11)	14 (38.89)	18 (50.00)	0.013
F3 (n = 23)	4 (17.39)	14 (60.87)	5 (21.74)	0.019
F4 (n = 6)	1 (16.67)	5 (83.33)	0 (0)	0.1021
A0 (n = 10)	1 (11.11)	1 (11.11)	7 (77.78)	0.018
A1 (n = 29)	9 (14.52)	19 (30.65)	34 (54.84)	0.001
A2 (n = 36)	3 (11.11)	18 (66.67)	6 (22.22)	0.001
A3 (n = 6)	1 (16.67)	4 (66.67)	1 (16.67)	0.023

¹Not significant.

Table 5 Multivariate analysis of different clinical factors and alleles of low molecular polypeptide-7 gene polymorphism in responders and non-responders hepatitis C virus patients (%)

	Regression coefficient	SE	Odds ratio	95%CI	P value
F0-F1 vs F2-F4	2.0553	0.490	0.128	0.0490-0.3346	0.0001
A0-A1 vs A2-A4	-1.6529	0.465	0.192	0.0771-0.4759	0.0004
AFP (< 5 ng/mL vs > 5 ng/mL)	-1.4800	0.490	0.228	0.0871-0.5948	0.00025
CC vs CA + AA	3.6972	0.616	40.333	12.0719-134.7572	0.0001
C allele vs A allel	1.9298	0.334	6.888	3.5800-13.2519	0.0001