The aim of this study was to determine if prior heat shock and consequential heat shock protein (HSP) accumulation would inhibit viral infection. Confluent cultures of Madin-Darby bovine kidney cells were subjected to 30 mins of hyperthermia at 42°C then allowed to recover at 37°C for six hrs. During the six hrs, HSP concentrations increased by 232% in heat-shocked cultures. Following the recovery period, six replicates of heat-shocked (HS) and six replicates of non-heat-shocked (CON) cultures were infected with Bovine Herpes virus 1. After 72 hours, severity of infection was assessed by counting formed viral plaques in cell cultures. CON cultures averaged 172.0±34.3 plaques per culture and HS cultures averaged 339.3±96.1 plaques per culture, representing a significant increase in infected cells (p=0.0044). These data provide evidence that physiological stressors related to extreme or exhaustive exercise, specifically hyperthermia, may increase risk of viral infection.