Review on bovine respiratory syncytial virus and bovine parainfluenza - usual suspects in bovine respiratory disease - a narrative review

Abstract

Bovine Respiratory Syncytial virus (BRSV) and Bovine Parainfluenza 3 virus (BPIV3) are closely related viruses involved in and both important pathogens within bovine respiratory disease (BRD), a major cause of morbidity with economic losses in cattle populations around the world. The two viruses share characteristics such as morphology and replication strategy with each other and with their counterparts in humans, HRSV and HPIV3. Therefore, BRSV and BPIV3 infections in cattle are considered useful animal models for HRSV and HPIV3 infections in humans.The interaction between the viruses and the different branches of the host's immune system is rather complex. Neutralizing antibodies seem to be a correlate of protection against severe disease, and cell-mediated immunity is thought to be essential for virus clearance following acute infection. On the other hand, the host's immune response considerably contributes to the tissue damage in the upper respiratory tract.BRSV and BPIV3 also have similar pathobiological and epidemiological features. Therefore, combination vaccines against both viruses are very common and a variety of traditional live attenuated and inactivated BRSV and BPIV3 vaccines are commercially available.

Keywords: BPIV3; BRD; BRSV; Bovine Parainfluenza; Bovine respiratory disease; Bovine respiratory syncytial virus; Review; Vaccines.

Fig. 1

Morphology of BRSV and BPIV3. G: G protein; HN: Haemagglutinase – Neuraminidase; L: Polymerase protein; M: Matrix protein; N: Nucleoprotein; P: Phosphoprotein; F: Fusion protein

Fig. 2

Cytopathic effect caused by BPIV3 virus and haemadsorption of erythrocytes onto the surface of the infected cell layer

Fig. 3

Formation of syncytia and immunostaining of BRSV in mucosal cells in the bronchioli of a calf infected with BRSV

Fig. 4

Interstitial pneumonia in a lung of a calf two weeks after infection with BRSV

Fig. 5

Virus infection and interaction with the innate immune system. a Virus passes the mucous layer, binds to sialic acids on the surface of the cell membrane. b Virus and enters the epithelial cell. c The virus replication in the infected cells leads to damage of the cells and to the formation of syncytia (cytopathic effect). d The virus infection triggers an antiviral innate immune response (production of interferon). The NS1 and NS2 protein of BRSV reduce the interferon response. e Macrophages and natural killer cells are attracted and destroy virus infected cells. f The immune response leads to further tissue damage. BRSV and PI3 both enhance this process

Fig. 6

Role of humoral and cellular immune response in controling virus infection