Division of Infection and Pathway Medicine

Dr Richard Sloan

We aim to identify and characterise host encoded antiviral factors that inhibit HIV and other retroviruses.

Dr Richard Sloan

Principal Investigator

  • The Chancellor's Building
  • 49 Little France Crescent
  • EH16 4SB

Contact details

Research focus 

We aim to understand how cell intrinsic innate immunity inhibits HIV and similar viruses. Host cells express a variety of antiviral factors that directly inhibit viral infection, these are often inducible by type-I interferons, or may be basally expressed. By identifying and understanding these antiviral factors we can develop new paradigms in antiviral therapy and understand viral disease susceptibility within individuals and populations.

We identify factors through screening technologies, typically in collaboration with other groups, such as Chen Liang (McGill University, Montreal) and Áine McKnight (Barts and The London School of Medicine).

A particular current focus are interferon induced transmembrane proteins (IFITM) that inhibit cell entry of a number of clinically important viruses such as HIV-1, influenza A virus, Ebola virus and Dengue virus. More recently we have started work on RNA-associated early-stage Anti-viral Factor (REAF), which potently inhibits HIV reverse transcription.


My primary teaching responsibility is in the areas of immunology and infectious disease for Biomedical Sciences undergraduate students at the Zhejiang University and Edinburgh University joint institute (ZJU-UoE Institute) in Haining, China.

I also contribute to our online Clinical Microbiology & Infectious Diseases MSc, and other undergraduate infection and immunology courses based in Edinburgh. While our research group hosts a number of masters, undergraduate, and summer student research projects.

Selected publications

  • RNA-Associated Early-Stage Antiviral Factor Is a Major Component of Lv2 Restriction. Marno KM, O'Sullivan E, Jones CE, Díaz-Delfín J, Pardieu C, Sloan RD, McKnight Á. (2017). Journal of Virology. 91(10). e01228-16
  • Latent HIV-1 can be reactivated by cellular superinfection in a Tat-dependent manner, which can lead to the emergence of multidrug-resistant recombinant viruses. (2013). Donahue DA, Bastarache SM, Sloan RD, Wainberg MA. Journal of Virology. 87(17):9620-32.
  • Harnessing the therapeutic potential of host antiviral restriction factors that target HIV. Sloan RD, Wainberg MA. Expert Rev Anti Infect Ther. 2013 11(1):1-4.
  • Productive entry of HIV-1 during cell-to-cell transmission via dynamin-dependent endocytosis. (2013). Sloan RD, Kuhl BD, Mesplede TM, Donahue DA, Munch J, Wainberg MA. Journal of Virology. 87(14):8110-23.
  • The Viral Protein Tat Can Inhibit the Establishment of HIV-1 Latency. Donahue DA, Kuhl BD, Sloan RD, Wainberg MA. (2012). Journal of Virology. 86(6):3253-63.
  • The HIV-1 Vpu viroporin inhibitor BIT225 does not antagonize tetherin-mediated inhibition of virus release. Kuhl BD, Cheng V, Donahue DA, Sloan RD, Liang C, Wainberg MA. (2011). PLoS One 6(11) e26670.
  • Transcription of preintegrated HIV-1 cDNA modulates expression of cell surface major histocompatibility complex class-I via Nef. Sloan RD, Kuhl BD, Donahue DA, Roland A, Bar-Magen T, Wainberg MA. (2011). Journal of Virology. 85(6):2828-36.
  • Tetherin restricts direct cell-to-cell infection of HIV-1. Kuhl BD, Sloan RD, Donahue DA, Bar-Magen T, Liang C, Wainberg MA. (2010). Retrovirology. 24;7:115.
  • Identification of Novel Mutations Responsible for Resistance to MK-2048, a Second-Generation HIV-1 Integrase inhibitor. Bar-Magen T, Sloan RD, Donahue DA, Kuhl BD, Zabeida A, Oliveira M, Hazuda DJ, Wainberg MA. (2010). Journal of Virology. 84(18):9210-6.
  • Expression of Nef from unintegrated HIV-1 DNA downregulates cell surface CXCR4 and CCR5 on T-lymphocytes. Sloan RD, Donahue DA, Kuhl BD, Bar-Magen T, Wainberg MA. (2010). Retrovirology. 13;7:44. Genotyping of acute HBV isolates from England, 1997-2001. Sloan RD*, Strang AL, Ramsay ME, Teo CG. (2009). J Clin Virol. 44(2):157-60. (*Corresponding author).
  • Antiviral resistance mutations potentiate hepatitis B virus immune evasion through disruption of its surface antigen a determinant. Sloan RD, Ijaz S, Moore PL, Harrison TJ, Teo CG, Tedder RS. (2008). Antivir Ther. 13(3):439-47. (Subject of commentary in Antivir Ther. 2008; 13(3):337-40.)