John H. Connor, Ph.D.

Associate Professor of MicrobiologyConnor
620 Albany Street
Office: NEIDL 401V; 617-358-9155
Lab: NEIDL 4; 617-638-0338; 617-358-9132
jhconnor@bu.edu

B.A. Swarthmore College
Ph.D. (Pharmacology) Duke University

BU Profile
Connor Lab Website

My laboratory studies viruses and how they dominate their cellular hosts. Viruses are parasites, incapable of reproducing on their own. Thus, to make copies of themselves they have to co-opt host functions, ranging from protein synthesis to DNA or RNA synthesis. Understandably, the infected host is not at all happy about viral infection and has evolved a dense array of tactics to sense and stop virus replication. This situation sets up a pitched battle between the virus (the invader) and the potential invaded host cell. We know that this battle is joined in every viral infection, but since we still get sick, our immune systems are clearly being beaten. Therefore, we need a greater understanding of how viruses overwhelm or disarm the host defenses so that we can develop new antiviral molecules and vaccines that will effectively augment our antiviral defenses.

To obtain a picture of how the virus-host interaction works and to identify how we can tip the balance in favor of the host, we ask two basic questions:

1) How do viruses hijack the cells that they infect?

2) How do cells defend themselves against viral infection?

To ask these questions we apply molecular biology, microscopy, biochemistry, genetic, high throughput screening and systems biology approaches. Existing projects in the lab include:

Determining how viruses inactivate cellular signaling networks to both promote their replication and short-circuit the host response

Identifying host responses that block virus infection

Determining the response of the circulating immune system to infection by hemorrhagic fever viruses such as Ebola, Marburg and Lassa fever viruses

Selected recent publications

  1. Yurt A, Daaboul GG, Connor JH, Goldberg BB, Selim Ünlü M. (2012) Single nanoparticle detectors for biological applications. Nanoscale. [Epub ahead of print]
  2. Dower K, Filone CM, Hodges EN, Bjornson ZB, Rubins KH, Brown LE, Schaus S, Hensley L, Connor JH. (2011) Identification of a pyridopyrimidinone inhibitor of orthopoxviruses from a diversity-oriented synthesis library. J Virol. 2011 Dec 28. [Epub ahead of print]
  3. Yen JY, Garamszegi S, Geisbert JB, Rubins KH, Geisbert TW, Honko A, Xia Y, Connor JH, Hensley LE. (2011) Therapeutics of Ebola hemorrhagic fever: whole-genome transcriptional analysis of successful disease mitigation. J Infect Dis. 204 Suppl 3:S1043-52.
  4. Yanik AA, Cetin AE, Huang M, Artar A, Mousavi SH, Khanikaev A, Connor JH, Shvets G, Altug H. (2011) Seeing protein monolayers with naked eye through plasmonic Fano resonances. Proc Natl Acad Sci U S A. 108(29):11784-9. Epub 2011 Jun 29.
  5. Dower K, Rubins KH, Hensley LE, Connor JH. (2011) Development of Vaccinia reporter viruses for rapid, high content analysis of viral function at all stages of gene expression. Antiviral Res. 91(1):72-80. Epub 2011 May 5.
  6. Simpson-Holley M, Kedersha N, Dower K, Rubins KH, Anderson P, Hensley LE, Connor JH. (2011) Formation of antiviral cytoplasmic granules during orthopoxvirus infection. J Virol. 85(4):1581-93. Epub 2010 Dec 8.
  7. Dunn EF, Connor JH. (2011) Dominant inhibition of Akt/protein kinase B signaling by the matrix protein of a negative-strand RNA virus.  J Virol. 85(1):422-31.
  8. Smith DR, McCarthy S, Chrovian A, Olinger G, Stossel A, Geisbert TW, Hensley LE, Connor JH. (2010) Inhibition of heat-shock protein 90 reduces Ebola virus replication.  Antiviral Res. 87(2):187-94.
  9. Dunn EF, Fearns R, Connor JH. (2009) Akt inhibitor Akt-IV blocks virus replication through an Akt-independent mechanism. J Virol. 83(22):11665-72.

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