Pathogenesis

Alphaherpesviruses typically cause localized lesions, particularly of mucosal surfaces of the respiratory and genital tracts or, less commonly, the skin. Progression is characterized by the sequential production ofvesicles, pustules, and shallow ulcers that become covered by a pseudomembrane and heal after 10-14 days, usually without scar formation (Figure 1).

Generalized alphaherpesvirus infections may occur in very young calves or in a fetus prior to abortion. Encephalitis produced by bovine encephalitis herpesvirus (BHV5) occurs as a consequence of spread of virus from the nasal cavity to the brain, via trigeminal nerve branches.

The gammaherpesvirus BHV4 is associated with low-grade clinical infection. MCF is a uniformly fatal disease associated with mucosal erosions, ophthalmia, and encephalitis that appear to be immune mediated. Lesions are characterized by infiltration and proliferation of lymphocytes. It is still not clear which lymphocyte population is the site of latency; both B and T lymphocytes have been implicated for different gammaherpesviruses. Immune complexes of viral antigen are probably also produced and contribute to the pathology.

Latency is a hallmark of bovine herpesviruses. The genome, probably as a circularized episome, persists in ganglion cells, typically the trigeminal and sciatic in the case of alphaherpesviruses, and in white blood cells in the case of gammaherpesviruses. From these sites of latency, virus is periodically shed to give rise to recurrent disease, shedding, and transmission to in-contact animals.

BHV1 establishes latency in sensory neurons oftrigemi-nal ganglia, and in germinal centers ofpharyngeal tonsil and similar sites related to the genital tract. BHV1 reactivates

Figure 1 As examples of alphaherpesvirus genital disease, three naturally occurring cases (a (early case), b, c) of acute, primary, infectious pustular vulvovaginitis in 8-month-old does caused by caprine herpesvirus 1 are shown. The extent of the individual vesicular/ pustular lesions on the vaginal mucosa is not well shown because of the swelling, and the pain associated with closer examination. Reproduced from Piper KL, Fitzgerald CJ, Ficorilli N, and Studdert MJ (2008) Isolation of caprine herpesvirus 1 from a major outbreak of infectious pustular vulvovaginitis in goats. Australian Veterinary Journal 86: 136-138, with permission.

Figure 1 As examples of alphaherpesvirus genital disease, three naturally occurring cases (a (early case), b, c) of acute, primary, infectious pustular vulvovaginitis in 8-month-old does caused by caprine herpesvirus 1 are shown. The extent of the individual vesicular/ pustular lesions on the vaginal mucosa is not well shown because of the swelling, and the pain associated with closer examination. Reproduced from Piper KL, Fitzgerald CJ, Ficorilli N, and Studdert MJ (2008) Isolation of caprine herpesvirus 1 from a major outbreak of infectious pustular vulvovaginitis in goats. Australian Veterinary Journal 86: 136-138, with permission.

periodically from latency, virus is shed, and consequently virus transmission occurs. Two RNA transcripts, the latency-related RNA and ORF-E RNA, are abundantly expressed in trigeminal ganglia of latently infected cattle, and these transcripts probably regulate the BHV1 latency-reactivation cycle.

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