Rabbit hemorrhagic disease (RHD) is a highly contagious viral infection in rabbits that can occur in acute, subacute, chronic, or peracute forms and is not fatal. It is caused by RHD virus (RHDV), a member of the genus Lagovirus in the family Caliciviridae, with variants including RHDV1, RHDV1a, and RHDV2. First identified in 1984 in domestic rabbits (Oryctolagus cuniculus) in China, RHD has since been reported in Asia, Europe, Africa, Central America, and North America. Both innate and adaptive immune responses contribute to host defense, although rapid disease progression can limit adaptive immunity. Carcasses of affected rabbits often retain adequate fat reserves, indicating that death occurs before the development of cachexia. The liver and spleen are the most frequent gross lesions, with hepatic necrosis as the predominant finding. Diagnosis is confirmed through postmortem examination and laboratory testing, with reverse transcription polymerase chain reaction (RT-PCR) being the most sensitive method for detecting viral RNA. Transmission occurs via direct contact, aerosol inhalation, contaminated food or water ingestion, ocular exposure, and contact with fomites. The virus is shed in respiratory secretions, feces, and urine, thereby enabling its rapid spread. Mortality rates range from 70% to 90%, leading to a significant decline in wild rabbit populations. No specific antiviral treatment exists, and control relies on strict biosecurity, quarantine, environmental disinfection, and vaccination. Strain-specific and bivalent vaccines remain the most effective preventive measures, particularly in regions where RHDV2 is endemic. Continuous surveillance is essential for mitigating ecological and economic impacts.