Sheep and goats are one of the most important sources of food and income for many people around the world. They are especially important among vulnerable groups in Africa and Asia who may depend solely on them for their livelihood. The disease peste des petits ruminants (PPR) mainly affects domestic sheep and goats, and is caused by the highly contagious PPR virus (PPRV). PPRV is currently the goal of a control and eradication program launched by the Food and Agriculture Organ of the United Nations (FAO) and the World Organization for Animal Health (OIE). This thesis has explored aspects of PPR with the hope of helping the eradication effort. Among other things, the thesis has looked at prevalence and risk factors for PPRV, development of better diagnostic methods, and studied the virus-host interactions.
The prevalence and risk factors for infection among sheep and goats in Tanzania was studied during two years. PPRV circulated with a prevalence of 49.3% in 2014 and 10.0% in 2015. The main risk factors for the animals were being female and increasing age. Interaction with wildlife was also evaluated as a risk factor, but did not lead to increased infection. The transport of serum samples was improved by validating the use of filter papers in a commercial cELISA. By adjusting the cut-off for a positive result, filter papers were a viable option for transport with unreliable cold-chains.
Long transports are also a problem in molecular diagnosis, as the sensitive nucleic acid may degrade. A protocol was developed for a field-adapted full genome sequencing of PPRV. A portable miniPCR and a minION sequencing device, allow analysis at the disease outbreak or in a minimally equipped laboratory. A genetic marker of 255 nucleotides is commonly used for molecular epidemiology, but use of the full genome allows more precise tracing of the infection and viral evolution.
A major symptom of PPR is a severe immunosuppression, mainly produced by the PPRV C and V proteins. The effects of these proteins were studied on the type I and II interferon (IFN) signaling pathways. The V protein was a strong inhibitor of both pathways, whereas the C protein inhibited the type I pathway, but stimulated the type II