Insights into the Pathogenesis of Viral Haemorrhagic Fever Based on Virus Tropism and Tissue Lesions of Natural Rift Valley Fever

Rift Valley fever phlebovirus (RVFV) infects humans and a wide range of ungulates historically has caused devastating epidemics in Africa the Arabian Peninsula. Lesions naturally infected cases (RVF) have only been described detail sheep with few reports concerning cattle humans. The most frequently observed lesion both ruminants is randomly distributed necrosis, particularly liver. supportive vascular endothelial injury are also present include mild hydropericardium, hydrothorax ascites; marked pulmonary congestion oedema; lymph node haemorrhages many tissues. Although complete understanding RVF pathogenesis still lacking, antigen-presenting cells skin likely early targets virus. Following suppression type I IFN production necrosis dermal cells, RVFV spreads systemically, resulting infection other variety organs. Failure innate adaptive immune responses to control exacerbated by apoptosis lymphocytes. An excessive pro-inflammatory cytokine chemokine response leads microcirculatory dysfunction. Additionally, impairment coagulation system results widespread haemorrhages. Fatal outcomes result from multiorgan failure, oedema organs (including lungs brain), hypotension, circulatory shock. Here, we summarize current cellular tropism as informed lesions natural infections. We specifically examine how extant knowledge informs regarding haemorrhagic form RVF, identifying opportunities for future research.