Abstract Introduction Bovine alphaherpesvirus types 1 (BoHV-1) and 5 (BoHV-5) are closely related alphaherpesviruses. BoHV-5 causes non-suppurative meningoencephalitis in calves. BoHV-1 is associated with several syndromes and, occasionally, can cause encephalitis. Although both viruses are neurotropic and they share similar biological properties, it is unknown why these alphaherpesviruses differ in their ability to cause neurological disease. Materials and Methods Neural tissue samples were collected from BoHV-1- and BoHV-5-intranasally inoculated calves during acute infection, latency and reactivation. The levels of cyclins mRNA expression in neural tissue from calves infected with BoHV-1 or BoHV-5 were analyzed by qRT-PCR. Data were analyzed by Relative Expression Software Tool (REST). Results Striking differences in the levels of cyclins mRNA were observed between uninfected and infected tissues, particularly in trigeminal ganglion (TG). During acute infection, higher levels of cyclin A2, E1 and B1 were observed in BoHV-1 and BoHV-5-infected TG compared with uninfected TG. mRNA levels of cyclins A2 and E1 were downregulated in olfactory cortex. During latent infection with BoHV-1 and BoHV-5, cyclin A2 and E1 were downregulated in olfactory cortex and cervical medulla whereas cyclin B1 was upregulated in BoHV-1-infected olfactory and frontal cortex and in cervical medulla after BoHV-5 infection. A marked increase of cyclins A2 and E1mRNA levels was detected in TG of BoHV-5-latently-infected cattle. Unlike in uninfected TG, in BoHV-1 and BoHV-5-infected TG, cyclin B1expression was detectable. During reactivation, the levels of cyclin A2, B1 and E1 mRNA increased in TG. The expression levels of cyclins in TG during BoHV-5 latency suggest that these viruses utilize different strategies to persist in the host. Conclusion Bovine alphaherpesviruses neuropathogenicity might be influenced by the differential control of cell cycle components by these herpesviruses. This is the first report on BoHV-5 modulation of cyclins expression in neural tissues from its natural host.