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  • CONUT score is an effective detector


    CONUT score is an effective detector of predicting OS and RFS in HCC patients. We found that patients with a damaged immune-nutrition status had significantly poor OS and RFS. Our initial literature review also retrieved other studies evaluating the survival of HCC patients using CONUT score [36,48,49]. Takagi et al. found that high CONUT score was an independent prognostic risk factor associated with OS, mortality and complications [36,49]. Similarly, Harimoto et al. also reported that HCC patients with high CONUT score had worse survival outcomes [48]. However, not all enrolled HCC patients in above studies were HBV infected. Knowing that HBV infection is the major risk factor of HCC and PHR is an independent prognostic factor of HCC in Asia-Pacific regions [9], our study focused on HBV-related HCC patients and highlighted the relation between immune-nutritional function and PHR. According to the guidelines, antiviral therapy is not recommended in patients with HBV-DNA less than 1000 copies/ml. Nevertheless, our previous study observed that a certain number of patients with low HBV-DNA levels were still at risk of developing PHR. Similarly, Huang et al. also pointed out that PHR was common after partial hepatectomy for HBV-related HCC with a preoperative low HBV-DNA level of less than 1000 copies/ml [30]. However, they Cepharanthine synthesis recommended that routine prophylactic antiviral treatment should be given before partial hepatectomy. In consequence, whether antiviral therapy is available for patients with HBV-DNA less than 1000 copies/ml still remains controversial. Our results indicated that PHR was associated with hepatectomy-induced immunosuppression. Furthermore, COUNT score could well predict the immune-nutrition status of HCC patients and was strongly correlated with PHR. The incidence of PHR was significantly higher in patients with high COUNT score. Based on this finding, we should care more about the low HBV-DNA patients with an impaired immune-nutrition status, and further antiviral therapy might be needed, other than patients with a better immune-nutrition status. In our center, the lower limit detection of HBV-DNA is 500 copies/ml. We divided patients into 2 subgroups (patients with HBV-DNA levels less than 500 copies/ml and patients with HBV-DNA 500–1000 copies/ml) and the results further proved that COUNT score was more effective to predict PHR in patients with HBV-DNA levels<500 copies/ml than patients with HBV-DNA 500–1000 copies/ml.
    Conflicts of interest
    Grant support This work was supported by the National Nature Science Foundation of China (81260088 and 81160262).
    Introduction Hepatitis B virus (HBV) is a strictly hepatotropic DNA virus that belongs to the Hepadnaviridae family [1]. At present, around 364 million people are chronically infected by this distinctive pathogen, about 90% infection occurs perinatally up to age of 6 months and 20–60% infection occurs between 6 months and 5 years old [[2], [3], [4], [5], [6]]. It is estimated that 25% people who infected with HBV in childhood will turn to cirrhosis or even HCC. Each year, almost 1 million persons die from cirrhosis and HCC secondary to HBV infection [5,7,8]. Although vaccines and drugs, interferons and nucleos(t)ide analogues, have been developed to treat HBV infection, the chronic HBV infection prevalence in East Asia and Africa is still assessed at 5–10% [6,9,10]. Meanwhile, drug resistance and side effects cannot be overlooked [11]. Thus, HBV infection representing a major public health problem. New therapeutic methods for HBV infection and its related diseases must be urgently developed. Autophagy is an evolutionarily conserved membrane system which is known to engulf long-lived proteins and damaged organelles and keep homeostasis in cells [11,12] (Fig. 1). The progression of autophagy begins with autophagy-related genes (ATG)-required isolated membranes accumulation called phagophores [13]. The phagophores undergo nucleation and elongation with Beclin-1(BECN1)-class III phosphatidylinositol 3-kinase (PI3K) complex and light chain 3 (LC3) lipidation and formed a double-membraned vacuoles, autophagosomes [13].The autophagosomes then go through a maturation process by docking and fusing with lysosomes [14,15]. Previous studies showed that viruses, such as hepatitis virus, poliovirus or rhinoviruses, can hijack components in the autophagic pathway to promote their survival [13,[16], [17], [18]] (Fig. 1). This is crucial in viruses-mediated chronic infection and tumor development (Fig. 1).