The human parainfluenza viruses (HPIVs) and respiratory syncytial virus (RSV) are the causative agents of lower respiratory tract infections in infants, children and the elderly leading to bronchiolitis, pneumonia and croup. It is estimated that HPIV infection in children aged 2 and 4 years account for nearly 60% and 80%, respectively, of all outpatients with respiratory illness. Almost all children will have been infected with RSV by the age of 2 years with nearly 50% reinfection rate. These respiratory pathogens belong to the order Mononegavirales which also includes other well known viruses like measles, mumps, Ebola and Marburg viruses. Currently there are no vaccines available to combat these respiratory pathogens, although, recently "reverse genetics" approaches have hastened the generation of several recombinant viruses as vaccine candidates.

Work in my laboratory utilizes recombinant molecular approaches towards understanding the mechanisms of transcription and replication of these non-segmented, negative-sense RNA viruses, in particular, human parainfluenza virus type 3 (HPIV 3). A major area of the research focuses on elucidating the structural and functional relationship of the various viral proteins, especially the polymerase complex (L-P), comprising of the phosphoprotein (P), and the large, multifunctional, RNA-dependent RNA polymerase (L). Current studies in the laboratory are aimed towards understanding the role of yet another unique class of viral proteins, namely, the "accessory proteins", which are synthesized from the polycistronic P mRNA and play an important role in regulating viral transcription and interferon signaling pathways.

The long-term goal of this laboratory is aimed towards the development of novel, and effective strategies primarily using molecular and antiviral approaches to combat these pathogens.

Malur, A.G., Wells, G., McCoy, A. and Banerjee, A.K. (2009).  Evidence for phosphorylation of human parainfluenza virus type 3 C protein:  mutant C proteins exhibit variable inhibitory activities in vitro.  Virus Res. 144:  180-187.

Malur, A., McCoy, M.J., Arce, S., Barna, B.P., Kavuru, M.S., Malur, A.G. and Thomassen, M.J. (2009).  Deletion of PPARg in alveolar macrophages in associated with a Th-1 pulmonary inflammatory response.  J. Immunol. 182:  5816-5822. 

Wells, G and Malur A. (2008).  Expression of human parainfluenza virus type 3 PD protein and intracellular localization in virus infected cells.  Virus Genes 37: 358-367.

Thomassen, M.J., Barna, B.P., Malur, A.G., Bonfield, T.L., Carver, C.F., Malur, A., Dalrymple, H., Kavuru, M.S. and Febbraio, M. (2007).  ABCG1 is deficient in alveolar macrophages of Gm-CSF knockout mice and patients with pulmonary alveolar proteinosis.  J. Lipid Res.  48:  2762-2768. 

Malur, A.G., Chattopadhyay, S., Maitra, R.K. and Banerjee, A.K. (2005). Inhibition of STAT 1 phosphorylation by human parainfluenza virus type 3 C protein. J. Virol. 79: 7877-7882.

Malur, A.G., Hoffman, M. A. and Banerjee, A.K. (2004). The human parainfluenza virus type 3 (HPIV 3) C protein inhibits viral transcription. Virus Res. 99: 199-204.

Choudhary, S.K., Malur, A.G., Huo, Y., De, B.P. and Banerjee, A.K. (2002). Characterization of the oligomerization domain of the phosphoprotein of human parainfluenza virus type 3. Virology 302: 373-382.

Malur, A.G., Choudhary, S.K., De, B.P. and Banerjee, A.K. (2002). Role of a highly conserved NH2-terminal domain of the human parainfluenza virus type 3 RNA polymerase. J. Virol. 76: 8101-8109.

Malur, A.G., Gupta, N.K., De, B.P. and Banerjee, A.K. (2002). Analysis of the mutations in the active site of the RNA-dependent RNA polymerase of human parainfluenza virus type 3 (HPIV 3). Gene Expression 10: 93-100.

Bose, S., Malur, A. and Banerjee, A.K. (2001). Polarity of human parainfluenza virus type 3 infection in polarized human lung epithelial A549 cells: role of microfilament and microtubule. J. Virol. 75: 1984-1989.