Local tissue temperature: a critical factor in the pathogenesis of bovid herpesvirus 2

Abstract

The effect of local tissue temperature on bovid herpesvirus 2 lesions in bovine skin was studied. Two areas of thoracic skin were multiply inoculated with virus and maintained at different temperatures; one above and the other below the rectal temperature of the animal. An entire inoculation site was removed daily from each area and subjected to virus, viral antigen, and interferon titrations and both light and electron microscopic examinations. Lesions in cold skin appeared sooner after inoculation, were larger and deeper, contained more infectious virus, viral antigen, and interferon, and lasted longer than lesions in hot skin. Differences in viral titers greater than 10(9) 50% tissue culture infective doses per gram were measured on postinfection days 5 to 9. These studies have demonstrated for the first time that temperature effects on viral pathogenesis may operate at the local level rather than by systemic modification of immune responses. The results also suggest that despite the presence of virus in internal organs of bovid herpesvirus 2-infected cattle and the ability of bovid herpesvirus 2 to replicate to very high titers in these tissues in vitro, only the skin is cool enough to permit substantial viral replication and dermal lesions in vivo. The observed restriction of bovid herpesvirus 2 skin lesions to the udder and teats of cattle and the restriction of outbreaks of disease to months when the temperature is declining may also be reflections of this temperature sensitivity.

Bovine Alphaherpesvirus 2 infections in Bavaria: an analysis of the current situation - several years after eradicating Bovine Alphaherpesvirus 1

“…Factors like UV radiation or marked temperature fluctuations might favor reactivation of latent infections and thus virus spread and/or the re-stimulation of antibody responses. The effect of skin temperature on BoHV-2 infections has been clearly shown previously, proposing an explanation for the seasonality of BHM-outbreaks [8,35].…”

Pathogenesis of Bovine alphaherpesvirus 2 in calves following different routes of inoculation

“…The localized nature of cutaneous BoHV-2 replication and pathology has been previously attributed to the route of virus penetration/exposure, specific virus tropism and, additionally, to the surface temperature which may favor virus replication (Letchworth et al 1982a). In fact, early studies have demonstrated that BoHV-2 replicates more efficiently at lower temperatures (30-3 o C), comparing to replication at physiological bovine temperatures (38-39 o C) (Letchworth et al 1982a, Letchworth & Carmichael 1984. The preference for replication at low temperatures might also explain the higher incidence and distribution of BoHV-2 in regions of temperate climate (Letchworth & Carmichael 1984).…”

“…In fact, early studies have demonstrated that BoHV-2 replicates more efficiently at lower temperatures (30-3 o C), comparing to replication at physiological bovine temperatures (38-39 o C) (Letchworth et al 1982a, Letchworth & Carmichael 1984. The preference for replication at low temperatures might also explain the higher incidence and distribution of BoHV-2 in regions of temperate climate (Letchworth & Carmichael 1984). On the other hand, systemic viral spread has been demonstrated only after IV inoculation (Castrucci et al 1977(Castrucci et al , 1978.…”

Therapy of malignant ascites in vivo by 211At-labelled microspheres

“…The optimal temperature for BHV-2 replication is lower than the normal body temperature. This might explain why the skin lesions are restricted to the teat and udder and the seasonality of the disease as well (8). The number of clinically affected animals during an outbreak is highly variable and depends on the animals' immune status.…”