Robust gene expression changes in the ganglia following subclinical reactivation in rhesus macaques infected with simian varicella virus.

Varicella zoster virus (VZV) causes varicella during acute infection and establishes latency in the sensory ganglia. Reactivation of VZV results in herpes zoster, a debilitating and painful disease. It is believed that VZV reactivates due to a decline in cell-mediated immunity; however, the roles that CD4 versus CD8 T cells play in the prevention of herpes zoster remain poorly understood. To address this question, we used a well-characterized model of VZV infection where rhesus macaques are intrabronchially infected with the homologous simian varicella virus (SVV). Latently infected rhesus macaques were thymectomized and depleted of either CD4 or CD8 T cells to induce selective senescence of each T cell subset. After T cell depletion, the animals were transferred to a new housing room to induce stress. SVV reactivation (viremia in the absence of rash) was detected in three out of six CD8-depleted and two out of six CD4-depleted animals suggesting that both CD4 and CD8 T cells play a critical role in preventing SVV reactivation. Viral loads in multiple ganglia were higher in reactivated animals compared to non-reactivated animals. In addition, reactivation results in sustained transcriptional changes in the ganglia that enriched to gene ontology and diseases terms associated with neuronal function and inflammation indicative of potential damage as a result of viral reactivation. These studies support the critical role of cellular immunity in preventing varicella virus reactivation and indicate that reactivation results in long-lasting remodeling of the ganglia transcriptome.

Debilitating clinical disease in a wild-born captive western lowland gorilla (Gorilla gorilla gorilla) co-infected with varicella zoster virus (VZV) and simian T-lymphotropic virus (STLV).

A wild-born, 34-yr-old female western lowland gorilla (Gorilla gorilla gorilla) was transferred between zoologic collections in the United Kingdom. Adjustment to its new environment was difficult and a series of health problems ensued. Progressive severe illness of multiple etiologies, and a failure to respond to multiple therapies, led to its euthanasia 5 mo later. Disease processes included severe thoracic and axillary cutaneous ulceration of T2-3 dermatome distribution, gastroenteritis, ulcerative stomatitis, emaciation, hind limb weakness or paresis, and decubitus ulcers of the ankles and elbows. Ante- and postmortem infectious disease screening revealed that this animal was not infected with Mycobacterium tuberculosis, simian varicella virus (SVV), simian immunodeficiency virus (SIV), or hepatitis B virus; but was infected with varicella-zoster virus (VZV) and simian T-lymphotropic virus (STLV). It is hypothesized that recrudescence of VZV and other disease processes described were associated with chronic STLV infection and the end of a characteristically long incubation period.

Asociación serológica de la rinoneumonitis viral equina y la anemia infecciosa equina / Serological association between equine rinoneumonitis and equine infectious anemia viruses

Objetivo. Determinar el nivel de asociación serológica entre los herpesvirus equinos tipos 1 y 4 (HVE-1 y HVE-4) causantes de la rinoneumonitis equina y el virus de la anemia infecciosa equina (VAIE) en caballos de trabajo provenientes de 5 municipios del Meta. Materiales y métodos. Se realizó una encuesta serológica transversal en 68 equinos provenientes de los municipios de San Martín, Guamal, Restrepo, Cumaral y Paratebueno. Para la evaluación de los anticuerpos contra los HVE-1 y HVE-4, se utilizó un ELISA indirecto para detectar la presencia de anticuerpos dirigidos contra la glicoproteína G del HVE-1 y HVE-4 (Svanovir ™ EHV1/EHV4-Ab ELISA); para el diagnóstico de anticuerpos contra el VAIE se utilizó la prueba de inmunodifusión en agar de gel de Coggins. Resultados. No se encontraron reactores al HVE-1; sin embargo, el porcentaje de seropositividad fue de 94.12% (64/68) y 13.2%(9/68) para HVE-4 y VAIE respectivamente. El porcentaje de animales coinfectados HVE-4 y AIE fue 13.23% (9/68). Cuando se discriminaron los resultados por Municipio se encontró un 27.9% (19/68) de reactividad en el municipio de Restrepo, 26.5% (18/68) en Cumaral, 14.7% (10/68) en Paratebueno, 14.7% (10/68) en Guamal, y 10.3% (7/68) en San Martin. El porcentaje de reactores por municipio al VAIE fue Cumaral 5.88% (4/68), Restrepo 4.4% (3/68), Guamal 1.47%(1/68) y San Martín 1.47% (1/68). Conclusión. El alto porcentaje de coinfección entre HVE-4 y VAIE sugiere un efecto importante en la interacción, pues el efecto inmunosupresor del VAIE podría facilitar la reactivación del estado latente del HVE-4.

Simian varicella in old world monkeys.

Simian varicella virus (SVV) causes a natural erythematous disease in Old World monkeys and is responsible for simian varicella epizootics that occur sporadically in facilities housing nonhuman primates. This review summarizes the biology of SVV and simian varicella as a veterinary disease of nonhuman primates. SVV is closely related to varicella-zoster virus, the causative agent of human varicella and herpes zoster. Clinical signs of simian varicella include fever, vesicular skin rash, and hepatitis. Simian varicella may range from a mild infection to a severe and life-threatening disease, and epizootics may have high morbidity and mortality rates. SVV establishes a lifelong latent infection in neural ganglia of animals in which the primary disease resolves, and the virus may reactivate later in life to cause a secondary disease corresponding to herpes zoster. Prompt diagnosis is important for control and prevention of epizootics. Antiviral treatment for simian varicella may be effective if administered early in the course of infection.

Pathologic changes of experimental simian varicella (Delta herpesvirus) infection in African green monkeys (Cercopithecus aethiops).

Gross and microscopic lesions of experimental simian varicella (Delta herpesvirus) infection in African green monkeys (Cercopithecus aethiops) are described. In stratified squamous epithelium, such as the epidermis, tongue, and esophagus, focal areas of epidermal hyperplasia, ballooning degeneration, and blood-filled vesicle formation with ulceration were apparent. Most visceral organs were involved, and the changes included necrosis, hemorrhage, and characteristic intranuclear eosinophilic inclusions in a variety of cells. A generalized vascular involvement was present with intranuclear inclusions in the endothelial and smooth muscle cells in various organs. The nervous system was normal on gross and microscopic examination. Virus titer and serum transferase values were correlated with the clinical signs of infection.