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World J Gastroenterol. Mar 21, 2014; 20(11): 2839-2853
Published online Mar 21, 2014. doi: 10.3748/wjg.v20.i11.2839
Individualization of chronic hepatitis C treatment according to the host characteristics
Nikolaos K Gatselis, Kalliopi Zachou, Asterios Saitis, George N Dalekos, Department of Medicine and Research Laboratory of Internal Medicine, School of Medicine, University of Thessaly, 41110 Larissa, Greece
Maria Samara, Department of Pathology, School of Medicine, University of Thessaly, 41110 Larissa, Greece
Author contributions: Gatselis NK, Zachou K and Dalekos GN had the original idea, designed the chapters and wrote the first draft of the review; Saitis A, Gatselis NK, Samara M and Zachou K collected and summarized the published literature while, made many critical comments on the manuscript; Dalekos GN made the final critical revision of the manuscript for important intellectual content; all authors have seen and approved the final version of the manuscript.
Correspondence to: George N Dalekos, MD, PhD, Professor, Head, Department of Medicine and Research Laboratory of Internal Medicine, School of Medicine, University of Thessaly, Biopolis, 41110 Larissa, Greece. dalekos@med.uth.gr
Telephone: +30-241-3502285 Fax: +30-241-3501557
Received: September 19, 2013
Revised: November 19, 2013
Accepted: January 6, 2014
Published online: March 21, 2014

Abstract

Hepatitis C virus (HCV) infection is a global health problem that affects more than 170 million people worldwide. It is a major cause of cirrhosis and hepatocellular carcinoma, making the virus the most common cause of liver failure and transplantation. The standard-of-care treatment for chronic hepatitis C (CHC) has been changed during the last decade and direct acting antiviral drugs have already been used. Besides, understanding of the pathogenesis of CHC has evolved rapidly during the last years and now several host factors are known to affect the natural history and response to treatment. Recent genome-wide association studies have shown the important role of interleukin-28B and inosine triphosphatase in HCV infection. The present review article attempts to summarize the current knowledge on the role of host factors towards individualization of HCV treatment.

Key Words: Chronic hepatitis C, Hepatitis C virus host factors, Interleukin 28B, Inosine triphosphatase, Single nucleotide polymorphism

Core tip: Hepatitis C virus (HCV) is a major health problem with personal, social and economic implications. In the past few years, advances in HCV molecular virology and host genetics revealed a complex interplay between the virus and the host that influence the natural history of chronic hepatitis C (CHC) and response to treatment. Besides, the management of CHC has evolved with the development of direct acting antiviral agents (DAAs). In this review, we have summarized the knowledge regarding host determinants of HCV treatment outcome and consider how this knowledge might help to individualize clinical management in the era of DAAs.



INTRODUCTION

Chronic hepatitis C (CHC) is one of the most important health issues problem worldwide with more than 170 million people infected and significant personal, social, and economic impact[1]. The long-term sequelae of CHC include cirrhosis, decompensation, hepatocellular carcinoma and liver related death[2,3].

The standard-of-care (SOC) treatment for CHC during the last decade has been the combination therapy of pegylated-interferon-α (PEG-IFN) with ribavirin (RBV), a guanosine analogue that interrupts the viral RNA metabolism[4,5]. However, the rate of sustained virological response (SVR), defined as having undetectable serum hepatitis C virus (HCV) RNA at week 24 after treatment discontinuation, is suboptimal for genotype 1 hepatitis C virus (HCV-1), with less than 50% of patients achieving viral eradication[4,6,7]. Moreover, PEG-IFN/RBV therapy is associated with significant adverse effects, which increase morbidity, while treatment is prolonged ranging from 24 to 48 wk or more, according to EASL and AASLD guidelines[8,9]. As a result clinicians often have to weigh the various viral and host characteristics for each patient before initiating treatment[10].

Antiviral therapy is currently changing and various direct acting antiviral drugs (DAAs) have been developed, which are directed against essential components of viral replication[11,12]. In addition, understanding of the pathogenesis of CHC has evolved rapidly, leading to development of novel compounds, targeting host factors that are potentially modifiable[13]. Given the high cost of treatment and the increased possibility of adverse events, identification of factors predicting SVR and the need to individualize HCV therapy by incorporating new predictive data in clinical decision-making is urgent.

Several host factors such as age, gender, race-ethnicity, fibrosis stage, obesity, hepatic steatosis, low-density lipoprotein cholesterol (LDLc), insulin resistance, and genetic variances of the host[14,15], are known to affect the spontaneous clearance and treatment outcomes (Figure 1).

Figure 1
Figure 1 Host factors associated with treatment outcomes of chronic hepatitis C. SNP: Single nucleotide polymorphism; BMI: Body mass index.

Recently, genome-wide association studies (GWAS) have identified several clinically important genetic determinants of PEG-IFN/RBV treatment outcomes. The most important are single nucleotide polymorphisms (SNPs) in interleukin 28B (IL28B) gene, which is associated with spontaneous clearance and response to anti-HCV treatment[16-18] and in inosine triphosphatase (ITPA) gene, which protects against ribavirin-related hemolytic anaemia and subsequent dose reductions[19,20].

In this review, we present in brief the major host factors that can modify the response to treatment of CHC, focusing on the clinical utility of IL28B and ITPA genotyping for pretreatment counseling and individualization of therapy modalities.

NON-GENETIC HOST FACTORS
Demographic host factors

It is well documented that race is associated with treatment response either with SOC or triple (SOC plus DAAs) therapy[21-31]. In several controlled trials, it was demonstrated that SOC in African-American patients has a reduced likelihood of SVR, ranging between 19% and 28%, compared to non-African-Americans in whom SVR rate was 39%-52%, especially when HCV-1 is taken into account[22,23,25]. The same was true for triple therapy in naïve patients infected with HCV-1; SPRINT-2 trial (boceprevir-based therapy)[30] as well as ADVANCED study (telaprevir-based therapy)[29] showed that Black ethnic origin negatively affected SVR. In addition, HCV infected individuals of Asian origin seem to achieve better SVR rates in comparison to Caucasians[26,31]. Differences in population frequency of the favorable IL28B genotype may explain the recognized ethnic disparity in treatment response rates[16,32]. However, the response to treatment in Black populations was poorer across all IL28B genotypes, suggesting that there may be other viral and/or host factors influencing SVR[27,28]. Hispanics also tended to have poorer SVR rates compared to Caucasian patients[21,24,27].

Although female gender was considered a positive predictor of SVR in IFN plus RBV era[33], in PEG-IFN/RBV trials no statistically significant correlation was found on multivariate analysis between gender and SVR[4,6,34-36]. Age has also been considered a significant factor for predicting response to treatment. In particular, large prospective studies of PEG-IFN/RBV combination therapy showed that patients younger than 40-45 years achieved significantly higher SVR rates compared to older patients[4,6,33,34]. In triple therapy trials with boceprevir, age was also significant[30,37] regarding the achievement of SVR in univariate investigation but not after multivariate analysis, especially when IL28B genotype was taken into account[38].

Metabolic parameters

Obesity is traditionally considered a significant predictor of disease progression in CHC, probably due to increased inflammatory milieu, which promotes liver injury in overweight individuals[39]. In a prospective trial[40], fibrosis progression was associated with body mass index (BMI). A high BMI was also inversely correlated with SVR in both IFN and SOC treated HCV patients[41,42]. Furthermore, a lower baseline body weight was significantly associated with SVR across all genotypes in the era of PEG-IFN/RBV combination therapy[4,6,34,42]. However, when RBV weight-based dosing was implicated, BMI and body weight were no longer significant parameters of SVR[43,44]. On the contrary, in a retrospective analysis of SPRINT-2[30] and RESPOND-2[37] studies by Poordad et al[38], low BMI proved to be one of the significant factors for achieving SVR in boceprevir-based therapy of treatment-naïve patients.

In two recent meta-analyses, insulin resistance (IR) was strongly associated with the probability of achieving SVR to dual treatment[45,46]. In Spanish[47] as well as Japanese[48] patients, IR seemed to be an independent predictor of response irrespective of the IL28B genotype. Concerning triple therapy, IR did not have any effect on SVR when telaprevir was used in the combination[49].

Recent studies suggest that pretreatment serum lipid levels may be important predictors of treatment response. Several studies indicate that high pretreatment LDLc and total cholesterol levels are associated with higher rates of SVR to dual PEG-IFN/RBV therapy in multivariate analysis[50-56]. In addition, pretreatment triglyceride levels may also play a role in SVR[56]. LDLc remained a significant independent predictor of SVR in post hoc analysis of the telaprevir-based REALIZE study[57] in treatment experienced patients[58]. The abovementioned associations between serum lipids and treatment response are supported by potential biological mechanisms. In vitro studies suggest relationships between lipoproteins and HCV that are important for viral entry into hepatocytes, viral replication and secretion. Indeed, several studies have shown that HCV may combine with lipoproteins in the serum, obscuring the virus from the host immune response, which may in turn help viral entry into the hepatocytes[59-61]. Various receptors involved in lipoprotein-viral particle entry into hepatocytes are posited, including the scavenger receptor B1 (SR-B1) and LDLc receptor[62-65]. IFN therapy leads to down-regulation of SR-B1 expression[66]. Finally, statin use in HCV-1 has been associated with increased SVR to dual PEG-IFN/RBV therapy[55] and in boceprevir-based triple therapy[30]. Taken together the above studies support the notion that decreased lipoprotein expression may in turn impact serum lipoproteins and lipids profile measures affecting SVR. However, these associations need to be interpreted with caution, because the favourable IL28B CC genotype is also associated with increased LDLc[67-69].

Histologic parameters

The presence of advanced liver fibrosis and cirrhosis has long been recognized to be associated with lower SVR rates to IFN-based treatment[33,34,70]. Actually, advanced fibrosis and cirrhosis have been shown to be major independent predictors of non-response to SOC[34,44,70]. Furthermore, in treatment-naïve patients, triple therapies with boceprevir and telaprevir (SPRINT-2[30] and ADVANCE[29] studies, respectively), showed that the severity of liver fibrosis together with IL28B genotype affect treatment outcome. Similar results were found when treatment-experienced patients were taken into account[57,71], although in these patients other factors such as IL28B genotype and pattern of previous response seemed to be the best predictors of response to triple therapy[38].

GENETIC FACTORS OF THE HOST

Host genetic factors have long been suggested that might play an important role for the observed differences in HCV clearance and response to treatment among different ethnic groups. Over 40 genes have been linked to modulation of anti-HCV therapy affecting either response to treatment or side effects to drugs[72,73]. However, only after sequencing of the entire human genome in 2001, major advances have been made in genotyping technologies, with the large-scale discovery of SNPs and the implementation of GWAS.

Initial studies investigated candidate genes to identify differences or SNPs between two populations. Several SNPs were identified in genes that are involved in the innate defense against HCV including MxA, OAS1, EIF2AK2, IFNAR1, IL-6, MHC, MAPKAPK3 and KIR receptors[74-82]. In addition, pretreatment hepatic gene expression such as an 8-gene subset (GIP2/IFI15/ISG15, ATF5, IFIT1, MX1, USP18/UBP43, DUSP1, CEB1, and RPS28)[83] and a two-gene signature (IFI27 and CXLC9)[84] predicted the response to treatment with a sufficient predictive accuracy in the majority of patients studied. Interestingly, in a recent paper by Chen et al[85], treatment response was linked to cell-specific activation patterns: interferon-stimulated gene 15 (ISG 15) protein up-regulation was more pronounced in hepatocytes of non-responders but also in Kupffer cells of responders. Even more recently, the same group showed that the gene expression pattern, at either the mRNA or the protein level, is more predictive of treatment outcome than the host (IL28B) or viral genotype[86]. Furthermore, the level of expression of intrahepatic mir-122 has been associated with HCV treatment response[87]. Expression of mir-122 was significantly lower in primary non-responders compared to early responders[86], while 8 other microRNAs (mir-34b, mir-145, mir-143, mir-652, mir-18a, mir-27b, mir-422b, and mir-378) were also found to be differentially expressed in responders and non-responders[88].

However, the validity of the reported associations varies, since a small number of them have repeatedly been reported from several independent large cohorts and have been verified to apply to different ethnicities. For this reason, it is till now IL28B polymorphisms that are considered as ‘‘state of the art’’ in HCV pharmacogenetics, which can potentially tailor future therapies[89].

IL-28B

Independent GWAS have identified genetic variants near the IL28B gene that are strongly associated with treatment response[16-18] and spontaneous HCV clearance[32,90,91]. Two bi-allelic SNPs, in linkage disequilibrium[92], were most strongly associated with favourable response; SNP rs12979860 located 3 kb upstream of the IL28B gene (favourable response CC genotype, and unfavourable CT/TT genotypes) and rs8099917 located 8 kb downstream of the IL28B gene and 16 kb upstream of the IL28A gene (favourable response TT genotype, and unfavourable GT/GG genotypes) (Figure 2A). Subsequently, these treatment response findings were confirmed by many studies in different populations such as HCV-1 patients[27,93-97], HCV-4 patients[98-101], patients with recent HCV infection[102], adults and children with spontaneous HCV clearance[103-105], HCV/HIV co-infected patients[106-108], and patients with recurrent HCV infection after orthotopic liver transplantation[109]. The results were reproduced in five recent meta-analyses in Asian, Caucasian and African patients[110-114].

Figure 2
Figure 2 Single nucleotide polymorphisms of IL28B and ITPA gene location. ITPA: Inosine triphosphatase.

The influence of IL28B on treatment response in genotype 2 or genotype 3 infections is less clinically relevant. Several studies from Europe and Japan have demonstrated an association between IL28B and SVR rates[115,116], while other studies failed to show a clear effect[117,118] although some studies showed that viral elimination within the first weeks of treatment and the achievement of rapid virological response (RVR) was significantly faster in CCrs12979860 and TTrs8099917 patients[118,119]. Thus, determination of IL28B genotype may be more relevant in slow responders to treatment (e.g., non-RVR patients)[120]. Recently, a meta-analysis of 23 studies involving 3042 patients showed that in HCV-2 and HCV-3 patients with favourable IL28B polymorphisms (either CCrs12979860 or TTrs8099917 patients), RVR rates were increased by 13%-15% and SVR rates by 5%[121].

The mechanisms behind these associations are related to the host innate immune response[122,123]. IL28B gene along with IL28A and IL29 belong to the type III IFN family, also named IFN-λ and they are located on the human chromosome 19. In particular, IL28A corresponds to IFN-λ2, IL28B to IFN-λ3 and IL29 to IFN-λ1[124]. The corresponding cytokines are induced by viral infection and their antiviral activity is mediated by triggering the Janus kinase-Signal Transducer and Activator of Transcription (JAK-STAT) pathway, following to their interaction with a heterodimeric class II cytokine receptor that consists of IL-10 and IL-28 receptors[125-127]. The JAK-STAT pathway activates ISGs which are known to cause apoptosis, growth inhibition, and inhibition of viral replication[128]. IL28B genotype has strongly been associated with intrahepatic ISGs expression, with the unfavourable genotypes expressing higher baseline ISGs levels compared with the favourable genotype[129,130]. This finding could indicate an exhaustion of innate immunity prior to treatment in patients with unfavourable IL28B genotype. Raglow et al[131] showed that this relationship is reversed in normal liver tissue, where TTrs12979860 genotype expresses lower levels of ISGs than CCrs12979860 genotype. Recently, two independent studies identified dysregulation in several pathways of innate immunity and natural killer cells activity in patients with unfavourable IL28B genotype, resulting in a muted response to IFN therapy[132,133].

However, it is not clear so far, if there is a direct correlation between IL28B polymorphisms and IL28B expression level. IL28 mRNA in the peripheral blood mononuclear cells (PBMCs) of patients with favourable IL28B genotype was significantly higher, whereas the presence of the risk alleles CT/CCrs8099917 were associated with lower expression of IFN-λ[17,18]. Shi et al[134] demonstrated that mRNA and serum levels of IL28B were lower in patients with CT/TTrs12979860 unfavourable genotypes. Moreover, in the era of liver transplantation, these genetic variations were significantly associated with IL28B mRNA expression in both the resected liver derived from the recipients and the donated liver[109]. On the contrary, other studies have not found such a correlation between IL28B genotype and IL28B gene expression[129,135]. Abe et al[136] showed that the expression levels of IL28B in the liver were lower in patients with the favorable IL28B genotype. This is in discordance with what happens in the periphery (PBMCs).

Knowledge about the impact of IL28B SNPs on the different phases of viral elimination shed light on the functional implications of IL28B variability. The favourable IL28B genotypes enhance the reduction of HCV RNA during the early phases (“first” and “second”) of viral kinetics. This is translated into increased rates of RVR, complete early virological response (EVR) on-treatment and finally SVR[27,133,137-143]. In fact, most RVR patients carry the good-response IL28B genotype. Furthermore, IL28B genotype can be combined with a chemotactic chemokine, the interferon-gamma inducible protein 10 kDa (IP-10), which strongly predicts the HCV RNA decline during the first days of therapy for all HCV genotypes[144]. In fact, it has been shown that the combination of increased baseline plasma IP-10 levels in association with IL28B non-favourable genotypes can accurately predict the first-phase decline of HCV RNA during treatment[135,145,146]. Besides, in acute HCV infection, IL28B genotype together with serum IP-10 levels can identify patients who are most likely to undergo spontaneous clearance and those in need of early antiviral therapy[147].

The new DAAs along with PEG-IFN/RBV combination are the new SOC in HCV-1 patients. Thus, it is necessary to redefine the role of the IL28B genotype in the decision to treat and how to treat these patients. SNPs in the IL28B region are the best baseline predictors of SVR and could be used as independent factors for treatment decision-making. In particular, treatment-naïve HCV-1 patients with genotype CCrs12979860 have the same probability (more than 80%) in achieving SVR either with dual therapy or triple therapy with telaprevir or boceprevir[27,29,30]. So, in these patients, the best therapeutic choice would be the standard PEG-IFN/RBV therapy, in order to avoid the higher costs and significant side effects of triple therapy[148,149]. However, during treatment, monitoring of HCV kinetics with milestones such as RVR and/or EVR, has been proved stronger predictor of treatment outcome[150,151]. Therefore, treatment-naïve HCV-1 patients with favorable IL28B genotype who do not achieve RVR should be considered candidates for more effective therapy with DAAs.

Response-guided therapy has become standard practice for HCV-1 patients and guidelines recommend shortening or prolongation of treatment duration, based on-treatment virological response. However, since the discovery of its significance, the incorporation of IL28B genotype in HCV management algorithms is intensively investigated. Huang et al[152] showed that IL28B genotype combined with baseline viral load might help in identifying HCV-1 patients who will or will not benefit from a shortened 24-wk regimen. The positive predictive value of these two factors (TTrs8099917 and lower baseline viral load) was 80% and the negative predictive value 91%. In the same line, Liu et al[153] showed that HCV-1 patients with the TTrs8099917 genotype and low baseline viral load (HCV RNA < 600000 IU/mL) could benefit from a shorter duration of combination therapy. Sarrazin et al[154] in a following study showed that the CCrs12979860 polymorphism was significantly associated with SVR, but in patients with on-treatment virologic response, SVR rates were similar for different IL28B genotypes. This finding indicates that virological response during therapy seems to determine the chance to achieve an SVR in an IL28B-independent way. In addition, two cohorts[155,156] have analyzed the efficacy of prolongation of treatment duration in HCV-1 slow-responders up to 72 wk and demonstrated that the benefits of extended therapy were restricted only to patients with CT/TTrs12979860 genotype.

Despite the fact that DAAs clearly attenuates the association between IL28B genotype and HCV treatment response, there are studies suggesting that the favourable IL28B alleles could also predict response to triple therapy in treatment-naïve and treatment-experienced HCV-1 patients[157-160]. In SPRINT-2[30] and RESPOND-2[37], where treatment-naïve or prior relapsers/non-responders were included respectively, CCrs12979860 genotype was significantly associated with increased SVR rates and could be used as a predictor for shortening therapy[161]. However, the sub-analysis of the REALISE study[57] failed to prove a significant association[162]. Further studies with DAAs are needed to identify whether the predictive role of IL28B genotype remains.

For the time being, studies with new DAAs and/or IFN-free therapy regimens are being conducted. In INFORM-1 study, where 83 patients were treated with mericitabine plus danoprevir or placebo, CCrs12979860 was associated with an increased second phase decline of HCV RNA[163]. In parallel, PROPEL[164] and JUMP-C[165] studies showed higher SVR rates in IL28B CCrs12979860 genotype patients receiving mericitabine plus PEG-IFN/RBV. The efficacy of interferon-free combination of faldaprevir and deleobuvir with RBV for the treatment of HCV-1 patients was also associated with IL28B genotype[166] though in other IFN-free regimens[167,168] the effect of IL28B genotype was unclear. For example, the ATOMIC study[169], where the efficacy of treatment with sofosbuvir along with PEG-IFN/RBV was investigated, showed promising results in shortening the duration of treatment to 12 wk, independently of the IL28B genotype. The importance of IL28B genotype on response to future interferon-free combination DAA regimens remains to be determined with larger and longer duration studies.

ITPA

RBV is a main component in the currently available antiviral regimens for the treatment of CHC. One of the most common side effects of RBV therapy is anemia that may result in dose reduction or discontinuation in up to 15% of patients[4,7,10], which may have deleterious impact on SVR.

The mechanisms of hemolytic anemia induced by RBV administration are complex. RBV causes a relative deficiency of ATP in human erythrocytes by depleting guanosine triphosphate (GTP) and subsequently leading to inhibition of the ATP-dependent oxidative metabolism. This causes oxidative damage to the erythrocyte membranes and leads to extravascular hemolysis by the reticuloendothelial system[170-172]. ITPA gene, which encodes a protein that hydrolyses inosine triphosphate (ITP), has been found to play a significant role in RBV-induced anemia. A reduced ITPA activity leads to the accumulation of ITP in erythrocytes, which allows for the substitution of ITP for GTP in ATP biosynthesis. This substitution reduces ATP depletion and protects against hemolytic anemia[173-177].

In two large GWAS[19,20], two functional SNPs, rs1127354 and rs7270101, within the ITPA gene were strongly associated with protection from RBV treatment-related hemolytic anemia and decreased the need for RBV dose reduction. The rs1127354 SNP is a missense variant in exon 2 of ITPA gene, while rs7270101 is located in ITPA intron 2 and alters splicing (Figure 2B). The AA/ACrs1127354 protective genotypes, as well as the CC/CArs7270101 protective genotypes, are associated with decreased ITPase activity and as a consequence decreased hemolytic side effects from RBV therapy (Figure 3). Following studies steadily reproduces the finding that polymorphic variation of the ITPA gene leads to enzymatic deficiency, which in turn is a major determinant of RBV-induced hemolytic anemia in HCV-1 patients[178-191]. However, ITPA SNPs effect on therapeutic outcome is unclear. Some studies have shown no association[19,178,180,186,191], and others have reported a possible association with treatment outcomes in CHC patients[20,181,182,192]. These discrepancies could be attributed to the geographic variance of ITPA SNPs and different inclusion/exclusion criteria used for patient recruitment. Taking into account that anemia is one of the main adverse events leading to premature termination of therapy, any marker able to predict the risk of severe anemia before treatment would be of outmost importance. For this purpose, Tsubota et al[193] and Kurosaki et al[192] constructed predictions models incorporating ITPA genotype along with baseline hemoglobin, creatinine clearance and quantitative hemoglobin decline at week 2 of treatment. We need of course, further validation before entering these algorithms into clinical practice

Figure 3
Figure 3 Inosine triphosphatase activity according to ITPA genotype. ITPA: Inosine triphosphatase; RBV: Ribavirin.

Prediction of anemia remains important in the era of DAAs, because these newer therapies still require RBV and PEG-IFN in combination, while in addition increases the frequency as well as the severity, and hence, clinical relevance of this adverse event[30,194-197]. Suzuki et al[198] studied 61 patients receiving triple telaprevir-based therapy and showed that decreases in haemoglobin levels were greater in patients with unfavourable (CCrs1127354) than favourable (CA/AArs1127354) genotypes in the ITPA gene, especially during the first 12 wk of treatment. Mean RBV dose during the first 12 wk was lower in patients with CCrs1127354 than CA/AArs1127354 genotypes, but the total dose of RBV and SVR rates were not different. Similar results obtained by Chayama et al[158] in a study of 94 Japanese HCV-1 patients treated with PEG-IFN/RBV and telaprevir. Patients with the anemia-susceptible ITPA SNP CCrs1127354 typically required ribavirin dose reduction earlier than did patients with other genotypes. However, this polymorphism was not proved to be a predictive marker of SVR. Recently, Ogawa et al[199] in a prospective multicenter study with 292 Japanese patients showed that CCrs1127354 genotype along with baseline hemoglobin less than 13.5 g/dL and estimated glomerular filtration rate < 80 mL/min per 1.73 m2 were independent pretreatment predictors for developing severe anemia (Hb < 8.5 g/dL) during the treatment period. No effect on treatment outcome was proved.

In sum, ITPA genotyping is able to detect HCV-infected patients who are at higher risk of developing anaemia. These patients should be monitored more closely in order to avoid premature withdrawals from treatment.

CONCLUSION

Prediction of SVR, which is translated in stopping disease progression, is the main requirement in CHC. Factors that predict SVR in turn have impact on treatment decision making, treatment duration and planning for the individual patient. Major advances in genetics during the last decade allow the identification of specific markers associated with viral response. Among them, IL-28B has been strongly associated with response to current treatment for HCV-1, in all reports, including large cohorts of patients. However, for the single patient, the use of IL-28B alone as a predictive factor of treatment outcome and decision to treat is not sufficient. An important question arising and needing an urgent answer is how host and viral factors could be integrated in clinical practice. However, since in the same patient various host and viral factors interact, predictive analysis should be cautious, considering all these factors in combination. In the upcoming years of personalized medicine, the comprehension of HCV pathogenesis based on the knowledge of both host and viral genotypes could lead to individually tailored HCV therapies.

Footnotes

P- Reviewers: Arain SA, Muratori L S- Editor: Zhai HH L- Editor: A E- Editor: Ma S

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