Peeples, Mark

Education 
               

Selected Publications
Guerrero-Plata A, Casola A, Suarez G, Yu X, Spetch L, Peeples ME, Garofalo RP. 2006. Differential response of dendritic cells to human metapneumovirus and respiratory syncytial virus. Am J Respir Cell Mol Bio 34:(3):320-9.  PubMed ID: 16284360

Moore PE, Cunningham G, Calder MM, DeMatteo AD Jr, Peeples ME, Summar ML, Peebles RS Jr. 2006. Respiratory syncytial virus infection reduces beta2-adrenergic responses in human airway smooth muscle. Am J Respir Cell Mol Biol 35(5):559-64.  PubMed ID: 16763224

Pantua HD, McGinnes LW, Peeples ME, Morrison TG. 2006. Requirements for the assembly and release of Newcastle disease virus-like particles. J Virol 80(22):11062-73.  PubMed ID: 16971425
Laliberte JP, McGinnes LW, Peeples ME, Morrison TG. 2006. Integrity of membrane lipid rafts is necessary for the ordered assembly and release of infectious Newcastle disease virus particles. J Virol 80(21):10652-62.  PubMed ID: 17041223

Gower TL, Pastey MK, Peeples ME, Collins PL, McCurdy LH, Hart TK, Guth A, Johnson TR, Graham BS.  2005.  RhoA signaling is required for respiratory syncytial virus-induced syncytium formation and filamentous virion morphology.  J Virol 9(9)5326-5336.  PubMed ID: 15827147

Zhang L, Bukreyev A, Thompson CI, Watson B, Peeples ME, Collins PL, Pickles RJ.  2005.  Infection of ciliated cells by human parainfluenza virus type 3 in an in vitro model of human airway epithelium.  J Virol 70(2)1113-1124.  PubMed ID: 15613339

Kong X, San Juan H, Behera A, Peeples ME, Wu J, Lockey RF, Mohapatra SS.  2004.  ERK-1/2 activity is required for efficient RSV infection.  FEBS Letters 559:33-38.  PubMed ID: 14960303

Barretto N, Hallak L, and Peeples ME. 2003. Neuraminidase treatment of respiratory syncytial virus-infected cells or virions, but not target cells, enhances cell-cell fusion and infection. Virology, 313:33-43.  PubMed ID: 12951019

Borrego-Diaz E, Peeples ME, Markosyan RM, Melikyan GB, and Cohen FS. 2003. Completion of trimeric hairpin formation of influenza virus hemagglutinin is critical for the transition from hemifusion to fusion. Virology 316:234-244.

Techaarpornkul S, Collins PL, and Peeples ME. 2002 Respiratory syncytial virus containing the fusion protein as its only glycoprotein attaches to cells via either glycosaminoglycans or another molecule. Virology 259, 294:296-304.  PubMed ID: 12009871

Peeples Laboratory
Respiratory syncytial virus (RSV) infections of the airways are the most frequent cause of hospitalization for infants. They are also a cause of death for the elderly, nearly as important as influenza in non-epidemic years. We are working to understand how RSV attacks cells in the airways. We have found that laboratory-adapted strains of RSV use a different mechanism to enter cultured cells than do RSV strains directly from patients, but we have also discovered a cell line that allows us to grow RSV directly from patients without causing this laboratory adaptation. This virus enables us, for the first time, to search for the RSV receptor on the cells lining the airways.

We have found that RSV only infects airway cells that have hair-like projections called cilia on their surface. In cystic fibrosis patients, because these “ciliated” cells are missing the CFTR channel they are unable to maintain the proper water balance in the mucus coating over them. The result is that the mucus that covers the airways becomes very thick. Since RSV naturally infects these ciliated cells, we are attempting to use RSV as a gene therapy vector to treat children with cystic fibrosis. So far, we have been able to make an altered form of RSV that does not kill cells, and to express the CFTR channel from it.