Bernard Moss, M.D., Ph.D.Building 33, Room 1E13C.133 North DriveBethesda, MD 20892-3210Phone: 301-496-9869Fax: email@example.com
Chief, Laboratory of Viral DiseasesChief, Genetic Engineering Section, LVD
The goals are to determine the mechanisms used by viruses to infect cells, express and replicate their genomes, assemble infectious particles, and evade the host immune response. Basic information obtained from these studies is used to design antiviral agents and live and subunit recombinant vaccines. In addition, viruses are engineered as expression vectors for biotechnology.
Poxviruses have provided unique opportunities to combine molecular, genetic, microscopic, and immunologic approaches to achieve many of the above goals. Recent studies have also been directed to the characterization and testing of candidate vaccines for human and simian immunodeficiency viruses.
Virions—containing a double-stranded DNA genome, enzymes, and transcription factors—attach to cells and fuse with the cell membrane, releasing cores into the cytoplasm. The cores synthesize early mRNAs that are translated into a variety of proteins, including growth factors, immune defense molecules, enzymes, and factors for DNA replication and intermediate transcription. Uncoating occurs, and the DNA is replicated to form concatemeric molecules. Intermediate genes in the progeny DNA are transcribed, and the mRNAs are translated to form late transcription factors. The late genes are transcribed and the mRNAs are translated to form virion structural proteins, enzymes, and early transcription factors. Assembly begins with the formation of discrete membrane structures. The concatemeric DNA intermediates are resolved into unit genomes and packaged in immature virions. Maturation proceeds to the formation of infectious intracellular mature virions (MVs). The virions are wrapped by modified trans-Golgi and endosomal cisternae, and the wrapped virions (WVs) are transported to the periphery of the cell via microtubules. Fusion of the wrapped virions with the plasma membrane results in release of extracellular enveloped virions (EVs).
Dr. Moss received his M.D. from the New York University School of Medicine, interned at the Children's Hospital Medical Center (Boston), and then earned a Ph.D. in biochemistry from the Massachusetts Institute of Technology. He became interested in viruses after joining NIH and is well known for studies on the cap structure of mRNAs, regulation of gene expression, replication cycle of poxviruses, virus defense molecules, and development and application of virus vectors.
Dr. Moss has received numerous awards and prizes, including the Dickson Prize for Medical Research, the Invitrogen Eukaryotic Expression Award, the ICN International Prize in Virology, the Taylor International Prize in Medicine, the Bristol-Myers Squibb Award for Distinguished Achievement in Infectious Disease Research, and the International Poxvirus, Asfarvirus and Iridovirus Lifetime Achievement Award. He was elected to the National Academy of Sciences, American Academy of Microbiology, Fellow of the American Association for the Advancement of Science, and president of the American Society for Virology.
Dr. Moss is currently an editor of Virology and a member of the editorial boards of the Journal of Virology, AIDS Research and Human Retroviruses, Current Opinion in Biotechnology, Advances in Virus Research, and the NIH Catalyst. He is an adjunct professor at George Washington University and the University of Maryland.
Special Interest Groups: Cell Biology, Virology, Vaccine Research
From left to right:
Row 1: Sharon Melamed, Visiting Scientist; Pat Earl, Staff Scientist; Bernie Moss, Section Head; Jerry Sisler, Microbiologist; Jeffrey Americo, Biologist; Catherine Cotter, Biologist.Row 2: Linda Wyatt, Staff Scientist; Wei Xiao, Biologist; Sara Reynolds, Graduate Student.Row 3: George Katsafanas, Biologist; Liliana Maruri-Avidal, Postdoctoral Fellow; Jorge Mendez-Rios, Graduate student; Shin-Wu Liu, postdoctoral fellow.Row 4: Cindy Wolfe, Postdoctoral Fellow; Andrea Weisberg, Electron Microscopist; Gilad Sivan, Postdoctoral Fellow; Robin Kastenmeyer, Veterinarian; Zhilong Yang, Postdoctoral Fellow.Row 5: Karl Erlandson, Postdoctoral Fellow; Tatiana (Senkevich) Koonin; Staff Scientist; Amanda Howard; Postdoctoral Fellow; P.S. Satheshkumar, Postdoctoral Fellow; Jason Laliberte, Postdoctoral Fellow.
Yang Z, Martens CA, Bruno DP, Porcella SF, Moss B. Pervasive initiation and 3' end formation of poxvirus post-replicative RNAs. J Biol Chem. 2012 July 24. 2012 Sep 7;287(37):31050-60.
Earl PL, Americo JL, Moss B. Lethal monkeypox virus infection of CAST/EiJ mice is associated with a deficient interferon-gamma response. J Virol. 2012 Jun 13. 2012 Sep;86(17):9105-12.
Howard AR, Moss B. Formation of orthopoxvirus cytoplasmic A-type inclusion bodies and embedding of virions are dynamic processes requiring microtubules. J Virol. 2012 May;86(10):5905-14.
Laliberte JP, Weisberg AS, Moss B. The membrane fusion step of vaccinia virus entry is cooperatively mediated by multiple viral proteins and host cell components. PLoS Pathog. 2011 Dec;7(12):e1002446.
Satheshkumar PS, Moss B. Sequence-divergent chordopoxvirus homologs of the o3 protein maintain functional interactions with components of the vaccinia virus entry-fusion complex. J Virol. 2012 Feb;86(3):1696-705.
Wolfe CL, Ojeda S, Moss B. Transcriptional repression and RNA silencing act synergistically to demonstrate the function of the eleventh component of the vaccinia virus entry-fusion complex. J Virol. 2012 Jan;86(1):293-301.
Visit PubMed for a complete publication listing.
At 12 hours after infection, images were collected at 1 frame/sec for a period of 110 sec.
From Ward BM, Moss B. Visualization of intracellular movement of vaccinia virus virions containing a green fluorescent protein-B5R membrane protein chimera. J Virol. 2001 May; 75(10):4802-13.
At 12 h after infection, images were collected at 1 frame/sec.
From Ward BM, Moss B. Vaccinia virus intracellular movement is associated with microtubules and independent of actin tails. J Virol. 2001 Dec;75(23):11651-63.
The IMARIS Surfaces feature was used to define the ATI as a region of interest, which is depicted visually in the model as a red shell. The virions fluorescing green are within and outside the ATI shell.
From Howard A, Moss B. Formation of orthopoxvirus cytoplasmic A-type inclusion bodies and embedding of virions are dynamic processes requiring microtubules. J Virol. 2012 May;86(10):5905-14.
Infected cells were imaged as Z-stacks at 20 minute intervals for 4 hours. IMARIS Surfaces was used to track an individual ATI (dragontail) and measure virion embedment as fluorescence within the defined surface over time. ATIs, red; Virions, green.
Saltatory movement of virions to ATIs
Video shows a virion tracked using the IMARIS Spots feature move to and associate with an ATI.
Last Updated September 21, 2012
Last Reviewed September 21, 2012