Host cellular responses in Nipah virus infection
Abstract number: P768
Chang L.Y., Hassan S.S., AbuBakar S.
Objectives: Nipah virus (NiV) is a zoonotic infectious virus that causes severe to fatal central nervous system infection in human during an outbreak in Malaysia in 1998. During the outbreak, NiV also causes disease in pigs. Unlike the infection in human, infected pigs normally present with respiratory distress syndrome and the disease is less severe in comparison to human infection. The present study was undertaken to investigate and understand the possible molecular mechanisms that may contribute to the difference in pathogenicity of NiV infection in the two hosts, human and pigs.
Methods: We examined NiV infection and replication in selected cell culture systems representing the two hosts, human and pigs. The state of dysfunction of the NiV-infected cells was then examined using proteomic approaches.
Results: Infection of four different cell types representing the two host organisms using NiV shows that the virus establishes productive infection in all the cell types examined. There are no differences in the capacity to support NiV replication between fully susceptible porcine stable kidney cells (PS) and human lung fibroblasts cells (MRC-5), respectively. However, there are differences between these cells, and human neuronal cells (SK-N-MC) and monocytes (THP-1), in the ability to support NiV replication and virus release. The SK-N-MC cells are less able to support NiV infection when compared to the PS cells. Subsequent examination of the changes in cellular host response as a result of NiV infection in both human and pig cells identified a total of 15 differentially expressed proteins. Most of these proteins are involved in virus replication or RNA synthesis, and proteins associated with the cellular functions of the mitochondria or the induction of apoptosis. The potential importance of these differentially expressed proteins includes the regulation of NiV replication in the two hosts as well as the manifestation of cellular cytopathic responses to the infection.
Conclusion: The proteomic analysis of NiV-infected cells of human and pigs identified differences in the key cellular pathways and events occurring during NiV infection in the two hosts, respectively, that could contribute to the differences in manifestation and severity of NiV infection.
|Session name:||18th European Congress of Clinical Microbiology and Infectious Diseases|
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