In situ study on the pathogenesis and immune reaction of equine herpesvirus type 1 (EHV‐1) infections in mice

• Published in: Immunology 1998-03, Vol.93 (3), p.329-334
• Main Authors: Bartels, T, Steinbach, F, Hahn, G, Ludwig, H, Borchers, K
• Format: Article
• Language: English
• Subjects: Animals; Disease Models, Animal; Herpesviridae Infections - immunology; Herpesviridae Infections - pathology; Herpesviridae Infections - veterinary; Herpesvirus 1, Equid - pathogenicity; Inflammation; Lung - immunology; Lung - pathology; Lung Diseases - immunology; Lung Diseases - pathology; Lung Diseases - virology; Lymphocytes - immunology; Macrophages - pathology; Mice; Mice, Inbred BALB C; Neutrophils - pathology; Recurrence; Respiratory Tract Infections - immunology; Respiratory Tract Infections - pathology; Respiratory Tract Infections - virology; Rodent Diseases - immunology; Rodent Diseases - pathology; Rodent Diseases - virology
• ISSN: 0019-2805; 1365-2567
• DOI: 10.1046/j.1365-2567.1998.00451.x

The mouse model was used to study the pathogenesis of equine herpesvirus type 1 (EHV‐1) after primary and secondary intranasal infections. Within a few hours after infection, EHV‐1 was found in nasal and olfactorial epithelium and sub‐epithelial cells of the respiratory mucosa, but antigen‐specific immune cells were never detected. Next to the lung, EHV‐1 was transmitted early and directly to the brain, both via the olfactory route and the trigeminal nerve, but traces of degenerative or inflammatory processes were not detected there. In the lung, the immune cells residing or invading the parenchyma did not contain viral DNA or proteins. The primary immune response in the lungs was an alveolar and interstitial inflammation, dominated by the sequential appearance of neutrophils and macrophages, while the number of T and B lymphocytes remained unaltered. Within 24 hr after re‐infection, lymphocytes accumulated around the blood vessels, outnumbering monocytes more than twofold, without neutrophils appearing. The lymphocytes comprised of little more B than T cells and the T cells were predominantly CD8+ cells. Those and B cells infiltrated the parenchyma. These results show the route of virus distribution and demonstrate the lack of antigen‐specific immune cells in the lungs of mice after primary intranasal infection with EHV‐1.