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 John Ellis, DVM, PhD, Dipl. ACVP, Dipl. ACVM, Western College of Veterinary Medicine, Saskatoon, Saskatchewan. This combination of factors results in variable respiratory disease in uncomplicated infections, and, if viral replication is not controlled, can predispose the lung to secondary bacterial infections typical of BRD.

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.