Peste des petits ruminants (PPR) is a highly contagious transboundary viral disease of sheep and goats that causes major economic losses and livelihood disruption across Africa, the Middle East, and Asia. Goats are often more severely affected than sheep, particularly in endemic smallholder systems, where high turnover, nutritional stress, and limited veterinary infrastructure sustain viral transmission. Despite effective live attenuated vaccines and the ongoing FAO–WOAH Global Eradication Programme, PPR remains widely distributed, indicating that vaccination alone is insufficient without understanding of host, viral, and environmental determinants of disease persistence. This review synthesizes current knowledge on three interrelated pillars of PPR prevention and control in goats: epidemiology, immunology, and host genetics. We summarize the epidemiological drivers of PPR transmission and how these factors shape disease burden in endemic settings. We review the immunobiology of PPR virus (PPRV) infection and vaccination, focusing on innate antiviral sensing, adaptive immune protection, virus-induced immunosuppression, and field determinants of vaccine performance. Finally, we examine the emerging evidence for host genetic resilience to PPR, with emphasis on immunogenomic and transcriptomic findings and the relevance of indigenous breeds such as the Black Bengal goat as genomic resources. Current evidence suggests that genetic resilience to PPR is likely polygenic and remains insufficiently characterized, though genomic and transcriptomic tools offer opportunities to identify markers of reduced susceptibility, milder disease, or improved vaccine response. Sustainable control of PPR in goats will require integrated strategies combining mass vaccination, surveillance, improved husbandry, and host-focused immunogenomic research to strengthen herd resilience and accelerate progress toward global eradication.
M. A. Islam, Saifur Rahman, Md. Shafiqul Islam et al.· Viruses· 0 citations
Peripheral blood mononuclear cells (PBMCs) are the most immunologically active and readily accessible fraction of whole blood, and they initiate host immune responses following infection and vaccination. Since PBMC transcriptomes capture diverse host–pathogen interactions, they offer a promising tool to uncover the genetic drivers of viral resistance and tolerance. As a detailed case study of this principle, we examine porcine reproductive and respiratory syndrome (PRRS), which remains one of the most economically important viral diseases of swine worldwide. Following PRRS virus (PRRSV) exposure, pigs rely on two complementary defense strategies: resistance, the capacity to limit viral replication, and tolerance, the capacity to sustain performance despite infection. Since resistance and tolerance phenotypes are difficult to measure directly through experimental challenge, indirect immune-trait measurements collected after vaccination offer a practical alternative. Most transcriptomic studies of the host response to PRRSV have focused on respiratory tissues, reflecting the virus’s tropism for pulmonary macrophages. However, intramuscularly delivered modified-live PRRSV vaccine reaches the bloodstream, bypassing the lung, so PBMCs, as the frontline defense system, mount the earliest measurable innate response. This review synthesizes the current literature on PBMC transcriptome models for deciphering innate resistance and tolerance to viral disease, using PRRS as our principal worked example; presents our own approach to profiling PBMCs after PRRSV vaccination; and outlines how the field has advanced since the original candidate-gene and QTL studies of the 2010s, including the recent FDA approval of the first CD163 gene-edited PRRSV-resistant pig line, and the emergence of single-cell and multi-tissue PBMC atlases, before considering how the same PBMC-based approach could extend to other host–virus interactions.
M. A. Islam, C. Neuhoff, M. Pröll et al.· Viruses· 0 citations
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