Infections with hepatitis A virus (HAV) are estimated to affect tens of millions of individuals each year.1 The vast majority of individuals spontaneously eradicate the infection and develop lifelong antiviral immunity that protects from reinfection. However, HAV infection can also cause fulminant hepatitis, which may even lead to acute liver failure, requirement for transplantation, or death.2 Despite the high seroprevalence of HAV and the successful generation of sterile immunity after exposure, the individual components of the adaptive immune system and their specific role during acute HAV infection (AHA) are incompletely understood.