Bovine alphaherpesvirus 1 (BoHV-1) is a virus of the family Herpesviridae and the subfamily Alphaherpesvirinae, known to cause several diseases worldwide in cattle, including rhinotracheitis, vaginitis, balanoposthitis, abortion, conjunctivitis, and enteritis. BoHV-1 is also a contributing factor in shipping fever, also known as bovine respiratory disease (BRD). It is spread horizontally through sexual contact, artificial insemination, and aerosol transmission and it may also be transmitted vertically across the placenta. BoHV-1 can cause both clinical and subclinical infections, depending on the virulence of the strain. Although these symptoms are mainly non-life-threatening it is an economically important disease as infection may cause a drop in production and affect trade restrictions. Like other herpesviruses, BoHV-1 causes a lifelong latent infection and sporadic shedding of the virus. The sciatic nerve and trigeminal nerve are the sites of latency. A reactivated latent carrier is normally the source of infection in a herd. The clinical signs displayed are dependent on the virulence of the strain. There is a vaccine available which reduces the severity and incidence of disease. Some countries in Europe have successfully eradicated the disease by applying a strict culling policy. Infection can occur in cattle of any age, but it is most commonly seen between the ages of 6 and 18 months. Transmission BoHV-1 enters the animal through the mucous membrane in the respiratory tract or genital tracts. The main mode of disease transmission is direct nose-to-nose contact between an infected and a susceptible animal. This is made possible because of the virus sloughing off into the mucus. Aerosols have to be exhaled, sneezed, or coughed from an infected animal during viral shedding in order for transmission to occur. Transmission also originates from contaminated semen through use of live breeding or AI; bulls that have been affected genitally may shed the virus in their semen. Once infected it is hard for the animal to get rid of BoHV-1 because it has many mechanisms to evade the hosts’ immune systems involved in both innate immunity and adaptive immunity. The virus degrades interferon regulatory factor 3 (IRF3), effectively halting transcription of interferon type 1. Interferons are a component of innate immunity involved in inhibiting viral replication in a host cell, as well as activating immune cells. BoHV-1 is also able to evade adaptive immune cells by inducing apoptosis in CD4+ cells, which assist in activating T cells when antigens are present. This down regulates the