Haemolymphatic tissues of captive boa constrictor (Boa constrictor): morphological features in healthy individuals and with Boid Inclusion Body Disease.

Knowledge on the structure and composition of the haematopoietic tissue (HT) is essential to understand the basic immune functions of the immune system in any species. For reptiles, it is extremely limited, hence we undertook an in-depth in situ investigation of the HT (bone marrow, thymus, spleen, lymphatic tissue of the alimentary tract) in the common boa (Boa constrictor). We also assessed age- and disease-related changes, with a special focus on Boid Inclusion Body Disease , a highly relevant reptarenavirus-associated disease in boid snakes.

Cell culture co- and superinfection experiments suggest that transmission during captivity contributes to the presence of reptarenavirus S and L segment swarms in boid inclusion body disease-positive snakes.

Boid inclusion body disease (BIBD) caused by reptarenaviruses affects captive constrictor snake collections worldwide. The disease manifests by the formation of cytoplasmic inclusion bodies in various tissues. Curiously, a snake with BIBD nearly always carries a swarm of reptarenavirus small and large segments rather than a single pair, and the composition of the swarm can vary between tissues.

Bovine Gammaherpesvirus 6 Tropism in the Natural Host.

Bovine gammaherpesvirus 6 (BoHV-6) is endemic in cattle in Europe, with a high prevalence. There is evidence that the virus is a commensal and not associated with disease processes. For other gammaherpesviruses, it is known that they have a rather specific target cell spectrum, generally including B cells and, at least in the early phase of infection, the epithelium of the respiratory tract.

Pulmonary SARS-CoV-2 infection leads to para-infectious immune activation in the brain.

Neurological complications, including encephalopathy and stroke, occur in a significant proportion of COVID-19 cases but viral protein is seldom detected in the brain parenchyma. To model this situation, we developed a novel low-inoculum K18-hACE2 mouse model of SARS-CoV-2 infection during which active viral replication was consistently seen in mouse lungs but not in the brain. We found that several mediators previously associated with encephalopathy in clinical samples were upregulated in the lung, including CCL2, and IL-6.