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 the need for specific treatment [4]. However, immunosuppressed individuals, organ-transplant recipients, hemodialysis patients, and pregnant women are at a high risk of developing life-threatening diseases, including chronic hepatitis and acute liver failure, after infection with HEV [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, Central America, and Africa [9]. Genotypes 3 and 4 are typically identified in developed countries, including the USA, New Zealand, Japan, and some 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 is not available for HEV in blood donors. However, in the Netherlands, screening was introduced in 2017, and 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.