Hepatitis C virus (HCV) infection is a global blood borne disease that affects almost 3% of the world's population with a morbidity and mortality rates that are second only to HIV among the emerging infections [
1]. The highest estimated prevalence of HCV has been reported in Egypt [
2,
3] with 11–14% of the population chronically infected with the virus. This high prevalence has been attributed to using the intravenous tartar emetic injections in a series of well intended countrywide schistosomiasis control campaigns that occurred from the 1950s until 1980 [
2,
3] Only 20% or less of initial HCV infections cause acute viral hepatitis severe enough for the patient to seek medical care, however 60–85% of all infections become persistent [
4,
5]. Individuals with chronic HCV infection usually remain asymptomatic and undiagnosed for decades before chronic hepatitis sometimes leads to severe fibrosis and cirrhosis, hepatic failure, or hepatocellular carcinoma. [
6‐
10]. These long-term complications, along with the large reservoir of infected people, made HCV one of the leading public-health problems. Continuous improvements in transmission prevention and chemotherapeutic regimens are promising, but on their own are unlikely to control this premium cause of chronic liver disease. The current antiviral regimen, a combination of pegylated interferon α and ribavirin, is curative in about half of treated patients depending on the viral and/or host factors. Additionally, this regimen requires prolonged therapy, sometimes with serious side effects, expensive and only a fraction of those with chronic HCV infections meet the criteria for treatment [
11]. Intravenous drug users and certain high-risk groups will continue to have an increased chance of exposure to the virus and are at risk f Manns et al., [
11] or new infections [
12,
13]. HCV transmission is likely to persist in areas with limited access to antiviral drugs and poor needle injection and blood product hygiene. Thus, development of a vaccine capable of preventing chronic HCV infection, if not preventing infection altogether, is essential for the control of HCV disease. Vaccine induced antibodies that interfere with viral entry are the protective correlate of many existing prophylactic vaccines. However, for highly variable RNA viruses such as Human immunodeficiency virus (HIV), the genesis of broadly reactive neutralizing antibody (nAb) responses by vaccination has been very difficult reviewed in Phogat et al., [
14]. Indeed, HIV has evolved several mechanisms to evade antibody-mediated neutralization, including the masking of conserved regions by glycan, quaternary protein interactions and the presence of immune-dominant variable elements. Therefore, several investigators have focused on E2 glycoproteins (gps) for developing HCV vaccines including purified recombinant glycoproteins (gps) [
15,
16], modified viral vectors expressing HCV gps [
17,
18], recombinant virus like particles encoding HCV gp epitopes, and DNA constructs encoding HCV gps [
19]. These studies reported that anti-gp responses can be elicited (reviewed in Lechmann and Liang) [
20]. However, they did not report on the neutralizing activity of the induced antibodies, but rather several of these reports assessed whether anti-gp responses inhibited the binding of recombinant E2 to cells [
15,
19,
21]. On the other hand, several observations support the hypothesis that neutralizing antibodies (nAb) may help control HCV replication. These included (i) immunization of chimpanzees to elicit gp specific Ab responses induced sterilizing immunity against challenge with homologous virus [
22,
23]. (ii) recombinant gps induce a response that modulates infection and reduces the rate of progression to chronic disease in chimpanzees [
24,
25]. (iii) HCV infected patients with antibody deficiencies have accelerated rates of disease progression [
26,
27]. (iv) passive administration of hyperimmune sera containing Abs capable of neutralizing HCVpp reduced HCV viraemia post-liver transplant [
28] and modulated chimpanzee progression rate to chronic disease [
29]. Several studies used synthetic peptides derived from various regions of HCV proteins as vaccine candidates proposing that the elicited antibodies would interfere with the viral life cycle [
30,
31]. In the present study we hypothesize that the sequence motifs located at the amino-terminal region of HVR-1 contains several genetically conserved sequences which may include conformation dependent epitope. The development of antibodies to these motifs may interfere with the mechanisms involved in viral adherence to cell surface or even to viral assembly. We designed and synthesized conserved peptides from this domain used them to immunize goats and purified the goat antibodies for examining their immunogenic and neutralizing properties as candidates for further assessment of HCV peptide vaccine.