The long term goal of this renewal application is to study in detail the involvement of host proteins in the gene expression of the respiratory pathogen human parainfluenza virus type 3 (hPIV3). HPIV3 is a common causative agent for acute respiratory tract disease of infants and children. Effective vaccines to combat hPIV3 infection are not currently available. During the continuing studies of this group in the important area of host-virus interaction, they have discovered a number of cellular proteins that interact either with virus-encoded proteins or cis-regulatory RNA elements. These include cytoskeletal protein actin, involved in transcription of virus genome RNA; cellular protein kinase C, isoform z, which specifically phosphorylated hPIV3 phosphoprotein P to activate it for eventual replication of the virus; cellular La protein and ubiquitous cellular enzyme, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) which specifically interact with cis-regulatory viral RNAs. Additionally they have demonstrated that the cellular MxA protein, an interferon-inducible protein, inhibits hPIV3 replication, setting the stage to study the role of host proteins in cell defense mechanisms. They propose to study in detail the role of these cellular proteins in the hPIV3 life cycle, focussing on their actions on the virus's transcriptive and replicative pathways. They will study the molecular basis underlying such specific interactions between these host proteins and viral components. They also propose experiments to counteract some of these host-virus interactive steps that would help create an opportunity to develop antiviral agents. Understanding in detail the molecular basis of the interplay of viruses and cellular proteins would further our knowledge to understand the role of the host in promoting or abrogating virus replication and develop agents that specifically target certain host-virus interactions.

National Institute of Health (NIH)
National Institute of Allergy and Infectious Diseases (NIAID)
Research Project (R01)
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Virology Study Section (VR)
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Rubin, Fran A
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Cleveland Clinic Lerner
United States
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Chattopadhyay, Santanu; Banerjee, Amiya K (2009) Phosphoprotein, P of human parainfluenza virus type 3 prevents self-association of RNA-dependent RNA polymerase, L. Virology 383:226-36
Mao, Hongxia; Chattopadhyay, Santanu; Banerjee, Amiya K (2009) N-terminally truncated C protein, CNDelta25, of human parainfluenza virus type 3 is a potent inhibitor of viral replication. Virology 394:143-8
Malur, Achut G; Wells, Greg; McCoy, Almedia et al. (2009) Evidence for phosphorylation of human parainfluenza virus type 3 C protein: mutant C proteins exhibit variable inhibitory activities in vitro. Virus Res 144:180-7
Mao, Hongxia; Thakur, Chandar S; Chattopadhyay, Santanu et al. (2008) Inhibition of human parainfluenza virus type 3 infection by novel small molecules. Antiviral Res 77:83-94
Basu, Mausumi; Maitra, Ratan K; Xiang, Yan et al. (2006) Inhibition of vesicular stomatitis virus infection in epithelial cells by alpha interferon-induced soluble secreted proteins. J Gen Virol 87:2653-62
Malur, Achut G; Chattopadhyay, Santanu; Maitra, Ratan K et al. (2005) Inhibition of STAT 1 phosphorylation by human parainfluenza virus type 3 C protein. J Virol 79:7877-82
Bose, Santanu; Banerjee, Amiya K (2004) Beta-catenin associates with human parainfluenza virus type 3 ribonucleoprotein complex and activates transcription of viral genome RNA in vitro. Gene Expr 11:241-9
Bose, Santanu; Basu, Mausumi; Banerjee, Amiya K (2004) Role of nucleolin in human parainfluenza virus type 3 infection of human lung epithelial cells. J Virol 78:8146-58
Malur, Achut G; Hoffman, Michael A; Banerjee, Amiya K (2004) The human parainfluenza virus type 3 (HPIV 3) C protein inhibits viral transcription. Virus Res 99:199-204
Bose, Santanu; Banerjee, Amiya K (2002) Role of heparan sulfate in human parainfluenza virus type 3 infection. Virology 298:73-83

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