Hepatitis E virus (HEV), belonging to the Orthohepevirus genus in the family Hepeviridae, causes liver diseases in humans [1]. The virus was first described in the early 1980s as a non-A and non-B hepatitis virus and was subsequently cloned in 1991 [2,3]. HEV contains a small nonenveloped, positive-sense single-stranded RNA genome approximately 7,200 nucleotides long [4]. Similar to hepatitis A, the vast majority of HEV infections are asymptomatic (especially in children) or cause self-limiting acute liver inflammation, which can resolve within a few weeks without any need for specific treatment [4]. However, immunosuppressed individuals, organ-transplant recipients, and pregnant women are at an increased risk of developing life-threatening diseases, including chronic hepatitis and acute liver failure, after HEV infection [5,6]. It has been estimated that the mortality rates for HEV infections in pregnant women and young people are about 20% and 3%, respectively [7]. The incubation period, which occurs during the prodromal phase, can vary from 2 to 8 weeks, and common symptoms of HEV infection during this period are usually nonspecific and include fever, nausea, vomiting, and malaise [8]. HEV is now recognized as a major public health issue, causing over 20 million infections every year worldwide and accounting for approximately 70,000 deaths [1]. Currently, there are eight known HEV genotypes from only one serotype that can infect humans and other animal taxa (HEV-1 to HEV-8), of which HEV-1 and HEV-2 are restricted to humans and are associated with most outbreaks in developing countries in parts of Asia and Africa [9]. Genotypes 3 and 4 are typically identified in developed countries, including the USA, New Zealand, Japan, and most countries in Europe, and can be isolated from a broader range of taxa, including humans, pigs, deer, and rabbits. Genotypes 5 and 6 are found in wild boars [8,10]. More recently, a new genotype of camelid HEV (HEV-7) was isolated from dromedary camels in the UAE and some African countries, including Sudan and Egypt [11,12].
Fecal-oral transmission is considered the main route of HEV transmission, but other transmission routes have been suggested. This includes person-to-person transmission, such as vertical transmission (mother-to-infant) during delivery. In particular, blood transfusion transmission has become one of the main routes, especially in some low-income countries in Asia [4]. Several studies have reported transfusion-transmitted HEV from blood components in many industrialized countries, including European countries, Australia, and the United States [13-18]. In the Gulf and other neighboring countries, few studies have evaluated the HEV seroprevalence in healthy blood donors. A recent study has indicated that the HEV seroprevalence in Qatar is high among blood donors, i.e., approximately 21% [19]. To the best of our knowledge, the first study of HEV in Saudi Arabia was conducted in 1994 in Riyadh and Gizan, with anti-HEV antibody detection frequencies of 8.4% and 14.9%, respectively [20]. Two additional studies of HEV in Saudi Arabia reported seroprevalences in blood donation samples of 18.7% and 16.9% in Makkah and Jeddah, respectively [21,22]. In most countries, screening for HEV in blood donors is not conducted. However, screening was introduced in several European countries, and in Japan [4]. In addition, the United States is now considering HEV screening for blood donors [4]. In this study, we estimated the HEV seroprevalence among blood donors in the Qassim Region, Saudi Arabia. These results provide a basis for evaluating whether routine screening is necessary in Saudi Arabia.