Reference no: EM13266608

Hepatitis is an endemic infection in many countries around the world including countries in the Middle East [1]. There are several viruses that target primarily the liver and cause hepatitis. These include viral hepatitis type A, B, C, D, E, and G [2]. Hepatitis A and E viruses are transmitted mainly by fecal-oral routes and usually cause acute enteric hepatitis. On the other hand, hepatitis B, C, D, and G viruses are transmitted parentally, and thus they can be transmitted sexually or through contaminated blood, and may cause acute and chronic hepatitis [3,4].

Hepatitis B and C viruses are among the most studied viruses, and they were the predominant types of viral hepatitis in Saudi Arabia between 2000 and 2005, with HBV comprising 49.3% and HCV comprising 40.7% of the identified cases [5]. On the other hand, very little information is available about hepatitis G virus (HGV) infection and pathogenesis. Also, its prevalence in healthy individuals and chronically infected hepatitis patients has not been comprehensively studied.

The hepatitis G virus, which is also known as GB virus C (GBV-C), was initially identified in 1995 and classified under the Flaviviridae family [6-9]. It is an enveloped virus with a 10kb positive-sense single-stranded RNA genome. Although HCV and HGV are structurally similar, it appears that HGV replicates more efficiently in white blood cells [4,9,10]. Studies have shown that HGV infection can occur as a single infection or in combination with other infections such as HCV or HIV [9,11,12]. It is unclear whether HGV has any role in the chronicity of hepatitis B or C infections. Therefore, HGV infection may contribute to the progression of chronic infections or to the development of drug resistance. Some reports have revealed a role of HGV infection in the pathogenesis of rare non-liver diseases such as aplastic anaemia [13,14]. The prevalence of HGV appears to vary between regions. It has been shown that the prevalence

of HGV viremia among healthy donors was high in Africa (17.2%) as compared with Asia (3.4%) or Europe (4.5%) [1]. Other studies have reported that the prevalence of HGV viremia in healthy Saudi donors was between 1%-2%, but this percentage was relatively higher in dialysis patients (5.5%) and cryptogenic hepatitis patients (25%) [15,16]. However, the exposure rate of HGV infection in the Saudi population has never been investigated. Several reports have shown that the prevalence of viral hepatitis infection has changed over time due to multiple factors, including economic and environmental factors [5,17]. For instance, reports from Saudi Arabia have shown that the prevalence of HAV and HCV infections was reduced from 53% and 4.7% to 18.1% and 0.65%, respectively, over a period of 20 years. Further, the prevalence of HBV carriers dropped from 6.7% to 0.3% in 18 years after the subunit HBV vaccine was introduced in 1989 [5,17]. Thus, we hypothesized that the prevalence of HGV infection in Saudi Arabia may have changed over the years.

Screening blood donors for blood-borne pathogens is very critical for the recipient’s safety. Since HGV infection is a disease that can be transmitted via contaminated blood, our objective was to evaluate the exposure rate of the hepatitis G virus among healthy donors and chronically infected hepatitis B and C patients by enzyme-linked immunosorbent assay (ELISA).