The ostreid herpesvirus (OsHV-1) was recently detected in San Diego Bay for the first time in naïve juvenile oysters. Due to the virus’ ability to cause mass mortality and transfer between oysters, it is important to determine the factors that instigate infection and the downstream impacts of infection. In this study, the role of temperature in controlling OsHV-1 induced mortality is assessed. Oysters were exposed to the San Diego Bay microvariant of OsHV-1 through bath exposure at 4 different temperatures (15, 18, 21, and 24C) and it was discovered that OsHV-1 did not induce mortality at 15C, but it did at the higher temperatures. However, OsHV-1 was still able to replicate in oyster tissue at all temperatures. These findings are critical for management of oyster stocks in San Diego Bay, but other factors may have additional controls over OsHV-1 proliferation and should continue to be investigated. A second component of this study looks for similarities in bacterial response to OsHV-1 between the San Diego Bay microvariant and others from around the world. Interestingly, this study is similar to others in that it found an increase in bacterial richness and decrease in bacterial evenness following OsHV-1 exposure and 4 taxa linked to OsHV-1 infection were also found in association with the San Diego Bay microvariant, including Arcobacter, Vibrio and Amphritea and Pseudoalteromonas. Although these bacteria were likely not essential in the killing process of the disease, the significant shift in the bacterial community following exposure suggests a weaking of the host defenses and some coordinated activity between select bacteria and OsHV-1.