Bovine herpesvirus type 1 (BHV-1) mutant lacking U(L)49.5 luminal domain residues 30-32 and cytoplasmic tail residues 80-96 induces more rapid onset of virus neutralizing antibody and cellular immune responses in calves than the wild-type strain Cooper.

Bovine herpesvirus type 1 (BHV-1) envelope protein U(L)49.5 inhibits transporter associated with antigen processing (TAP) and down-regulates cell-surface expression of major histocompatibility complex (MHC) class I molecules to promote immune evasion. Earlier, we have constructed a BHV-1U(L)49.5Δ30-32 CT-null virus and determined that in the infected cells, TAP inhibition and MHC-I down regulation properties of the virus are abolished. In this study, we compared the pathogenicity and immune responses in calves infected with BHV-1U(L)49.5Δ30-32 CT-null and BHV-1 wt viruses. Following primary infection, both BHV-1 wt and BHV-1U(L)49.5Δ30-32 CT-null virus replicated in the nasal epithelium with very similar yields. BHV-1 antigen-specific CD8+ T cell proliferation as well as CD8+ T cell cytotoxicity in calves infected with the BHV-1U(L)49.5Δ30-32 CT-null virus peaked by 7 dpi (P<0.05) which is 7 days earlier than that of BHV-1 wt-infected calves. Further, virus neutralizing antibody (VN Ab) titers and IFN-γ producing peripheral blood mononuclear cells (PBMCs) in the U(L)49.5 mutant virus-infected calves, also peaked 7 days (IFN-γ; P<0.05) and 14 days (VN Ab; P<0.05) earlier, respectively. Therefore, relative to wt in the BHV-1U(L)49.5 mutant virus-infected calves, primary neutralizing antibody and cellular immune responses were induced significantly more rapidly.
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