BHV-1 and BRSV are very different viruses with very different lifestyles within infected cells. Yet, both viruses cause necrosis and/or programmed death in infected cells, stimulate the innate immune system to secrete proinflammatory cytokines, and mediate potentially immunosuppressive effects, says
A characteristic feature of BHV-1 (an alphaherpesvirus) is latency, primarily in neurons in sensory ganglia of the head, notably the trigeminal ganglion, but also probably in other tissues, such as tonsils. Reactivation of latent virus is thought to be a critical event in the transmission of the virus and maintenance of the virus in cattle populations. This phenomenon accounts for BHV-1 outbreaks in the absence of acute infection, i.e. in a “closed herd” or in a pen of feedlot cattle derived from the same ranch.
Cattle with uncomplicated BHV-1 infections have upper respiratory disease of variable severity that can resolve in 7 to 10 days. In many, if not most BHV-1-associated BRD cases, there is a mixed infection with bacteria, notably M. hemolytica and/or P. multocida, that results in severe lower respiratory tract disease.
BRSV is a representative of the Pneumoviriane (Paramyxoviridae) group that cause similar lower respiratory tract diseases in a wide range of host species. There is evidence of persistence, or long term carriage of the virus in some animals.
As with BHV-1, loss of ciliated cells in BRSV-infected airways could account for the disruption of the normal non-specific defense mechanism of mucocilary escalator function, and result in deposition of bacteria in the lower respiratory tract. This could contribute significantly to secondary bacterial bronchopneumonia typical BRD.