Andrew Stanley Pekosz, PhD
Center & Institute Affiliation(s):
PhD , University of Pennsylvania , 1997
My research interests lie in understanding the interaction of viruses with the respiratory epithelium. Our efforts are focused on influenza A virus, the severe, acute respiratory syndrome coronavirus (SARS-CoV) and Andes virus, a South American hantavirus responsible for Hanatavirus Pulmonary Syndrome (HPS).
There are two main focuses to our research program. The first is in how viral proteins target to sites of assembly and identifying the viral and cellular factors that are important for the production of infectious virus particles. For these studies we use influenza A virus to study virus assembly at the plasma membrane and Andes and SARS-CoV to study virus assembly at intracellular sites.
The second research focus of the laboratory is in understanding how viruses can counteract antiviral innate and adaptive immune responses. For these studies we utilize animal models of infection, as well as primary cell cultures of respiratory epithelial cells. By identifying the viral proteins that control the host immune response, we hope to gain a better understanding of how the virus can establish an infection and identify the key host proteins that play a role in controlling virus replication and the immune response to viral infection. In a related line of research, we are investigating how influenza A viruses can adapt to productively infect a new host. Of particular interest is the identification of viral and cellular factors that are important for efficient replication of canine, equine and avian influenza A virus strains to human respiratory epithelial cells.
Honors and Awards
1989 Selman A. Waksman/David H. Struymeyer Award for Achievement in Biochemistry, Rutgers University 1995 Joel M. Dalrymple Memorial Award, American Society for Virology 2001 National Foundation for Infectious Diseases New Investigator Grant 2001-03 Whitaker Foundation, Young Investigator Award 2001-03 Infectious Diseases Society of America, Wyeth-Lederle Vaccines New Investigator Award 2007 Diversity Leadership Award – Faculty, Washington University in St. Louis
virus, virus assembly, virus-host interactions, respiratory infections, receptors, cell tropism, vaccines, flu, influenza, SARS-CoV, hantavirus
Stewart SM, Pekosz A. The influenza C virus CM2 protein can alter intracellular pH, and its transmembrane domain can substitute for that of the influenza A virus M2 protein and support infectious virus production. J Virol. 2012 Jan;86(2):1277-81. Epub 2011 Sep 14. PMID:21917958
Stewart SM, Pekosz A.Mutations in the membrane-proximal region of the influenza A virus M2 protein cytoplasmic tail have modest effects on virus replication. J Virol. 2011 Dec;85(23):12179-87. Epub 2011 Sep 14. PMID: 21917980
Stewart SM, Wu WH, Lalime EN, Pekosz A. The cholesterol recognition/interaction amino acid consensus motif of the influenza A virus M2 protein is not required for virus replication but contributes to virulence. Virology. 2010 Sep 30;405(2):530-8. Epub 2010 Jul 24.PMID:20655564
Grandea AG 3rd, Olsen OA, Cox TC, Renshaw M, Hammond PW, Chan-Hui PY, Mitcham JL, Cieplak W, Stewart SM, Grantham ML, Pekosz A, Kiso M, Shinya K, Hatta M, Kawaoka Y, Moyle M. Human antibodies reveal a protective epitope that is highly conserved among human and nonhuman influenza A viruses. Proc Natl Acad Sci U S A. 2010 Jul 13;107(28):12658-63. Epub 2010 Jul 1.PMID:20615945
Grantham ML, Stewart SM, Lalime EN, Pekosz A. Tyrosines in the influenza A virus M2 protein cytoplasmic tail are critical for production of infectious virus particles. J Virol. 2010 Sep;84(17):8765-76. Epub 2010 Jun 23.PMID:20573832