The incidence and prevalence of uveitis depends on age, gender, anatomic position of the inflammatory process (anterior, intermediate, posterior uveitis, pan-uveitis), histopathology (granulomatous, non-granulomatous), course of an inflammatory process (acute, chronic, recurrent), and etiology (infectious, non-infectious). The most common anatomic form of uveitis is AU [
1,
2]. Although AU has a diverse spectrum of infectious and non-infectious etiology, approximately 50% remain idiopathic [
1,
2,
7,
8]. The clinical and etiologic patterns of uveitis in Northeastern Iran were evaluated by Hosseini et al. They reported that pan-uveitis is the most common clinical pattern with an idiopathic etiology. Moreover, toxoplasmosis was among the most common infectious causes of uveitis [
9]. Hepatitis viruses are one of the infective agents considered in the pathogenesis of uveitis. The association between viral hepatitis and uveitis has been proposed in a few studies, most of which investigated the role of hepatitis B and C in the pathogenesis of uveitis. These studies noted that deposition of circulating immune complexes, physiologic immune reaction against an infection within the eye, and complement-mediated immune activation may lead to extra-hepatic manifestations such as glomerulonephritis, uveitis, and polyarteritis nodosa [
3‐
5]. Tien at el. in a cohort study on the relationship between uveitis and the different types of viral hepatitis concluded that patients with hepatitis B virus and HCV co-infection have the highest risk of uveitis. Also, They reported only one case of uveitis among 82 cases of isolated HAV infection (rate:19.44 per 10,000 person-years) [
5]. The extra-hepatic manifestations which reported to be associated with HAV infection include glomerulonephritis, acute renal failure (ARF), myositis, acute pancreatitis, arthritis, pleural or pericardial effusion, myocarditis, autoimmune thrombocytopenic purpura, erythematous maculopapular rash, and parotitis. In these conditions, deposition of the immune-complex in various organs such as the skin, joints, kidneys, and muscles leads to immune system activation [
6,
10‐
12]. Bhatt et el. noted that direct invasion of HAV into the kidney tissues as well as immune-related mechanisms may lead to ARF [
11]. In our literature review, previous reports of ophthalmic manifestations associated with HAV infection were not found. Stangos et al. reported a case of multiple evanescent white dot syndrome (an inflammatory chorioretinal disorder) 10 days after receiving simultaneous formalin-inactivated HAV and live-attenuated yellow fever vaccine. They concluded an autoimmune etiology contributing to this ocular inflammation [
13]. The antigen-antibody complex deposition and granulocyte aggregation in the highly vascularized uveal tract and choroid may lead to activation of the immune system. The expression of pro-inflammatory cytokines, (e.g. interleukin 1) and HLAs, (e.g. HLA-DR) in the intraocular tissues secondary to systemic viral infection or inflammation may also result in uveitis [
14‐
16]. However, the primary underlying immune-related mechanisms that compromise the intraocular immune privilege and blood–ocular barrier are not fully understood [
15,
16]. Some studies have shown extra-hepatic manifestations of HAV infection occurred following non-specific symptoms at presentation [
6,
10,
12]. In our study, the patient presented with acute AU 3 days before presentation of typical systemic symptoms of HAV infection. Bhatt at el. reported a 34 year-old man with acute parotitis and facial skin rash as the manifestations of HAV infection 6 days prior to any hepatic presentations [
11] These findings suggest that extra-hepatic manifestations of HAV infection may occur before (during incubation period) or after the presentation of systemic and hepatic signs secondary to deposition of circulating immune-complex in various organs.