Imperial College London

Dr Michael K.P. Liu

Faculty of MedicineDepartment of Infectious Disease

Research Associate
 
 
 
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Contact

 

+44 (0)20 3315 5986michael.liu Website

 
 
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Location

 

I.02. 03Chelsea and Westminster HospitalChelsea and Westminster Campus

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Summary

 

Publications

Publication Type
Year
to

19 results found

Mandala WL, Liu MKP, 2021, SARS-CoV-2 and HIV-1: Should HIV-1-infected individuals in Sub-Saharan Africa be considered a priority group for the COVID-19 vaccines?, Frontiers in Immunology, Vol: 12, ISSN: 1664-3224

Since its emergence in 2019 SARS-CoV-2 has proven to have a higher level of morbidity and mortality compared to the other prevailing coronaviruses. Although initially most African countries were spared from the devastating effect of SARS-CoV-2, at present almost every country has been affected. Although no association has been established between being HIV-1-infected and being more vulnerable to contracting COVID-19, HIV-1-infected individuals have a greater risk of developing severe COVID-19 and of COVID-19 related mortality. The rapid development of the various types of COVID-19 vaccines has gone a long way in mitigating the devastating effects of the virus and has controlled its spread. However, global vaccine deployment has been uneven particularly in Africa. The emergence of SARS-CoV-2 variants, such as Beta and Delta, which seem to show some subtle resistance to the existing vaccines, suggests COVID-19 will still be a high-risk infection for years. In this review we report on the current impact of COVID-19 on HIV-1-infected individuals from an immunological perspective and attempt to make a case for prioritising COVID-19 vaccination for those living with HIV-1 in Sub-Saharan Africa (SSA) countries like Malawi as one way of minimising the impact of COVID-19 in these countries.

Journal article

Yang H, Rei M, Brackenridge S, Brenna E, Sun H, Abdulhaqq S, Liu MKP, Ma W, Kurupati P, Xu X, Cerundolo V, Jenkins E, Davis SJ, Sacha JB, Frueh K, Picker LJ, Borrow P, Gillespie GM, McMichael AJet al., 2021, HLA-E-restricted, Gag-specific CD8(+) T cells can suppress HIV-1 infection, offering vaccine opportunities, Science Immunology, Vol: 6, Pages: 1-11, ISSN: 2470-9468

Human leukocyte antigen-E (HLA-E) normally presents an HLA class Ia signal peptide to the NKG2A/C-CD94 regulatory receptors on natural killer (NK) cells and T cell subsets. Rhesus macaques immunized with a cytomegalovirus-vectored simian immunodeficiency virus (SIV) vaccine generated Mamu-E (HLA-E homolog)–restricted T cell responses that mediated post-challenge SIV replication arrest in >50% of animals. However, HIV-1–specific, HLA-E–restricted T cells have not been observed in HIV-1–infected individuals. Here, HLA-E–restricted, HIV-1–specific CD8+ T cells were primed in vitro. These T cell clones and allogeneic CD8+ T cells transduced with their T cell receptors suppressed HIV-1 replication in CD4+ T cells in vitro. Vaccine induction of efficacious HLA-E–restricted HIV-1–specific T cells should therefore be possible.

Journal article

Peng BJ, Carlson JM, Liu MKP, Gao F, Goonetilleke N, McMichael AJ, Borrow P, Gilmour J, Heath SL, Hunter E, Bansal A, Goepfert PAet al., 2018, Antisense-Derived HIV-1 Cryptic Epitopes Are Not Major Drivers of Viral Evolution during the Acute Phase of Infection, JOURNAL OF VIROLOGY, Vol: 92, ISSN: 0022-538X

Journal article

Liu D, Wang C, Hora B, Zuo T, Goonetilleke N, Liu MKP, Berrong M, Ferrari G, McMichael AJ, Bhattacharya T, Perelson AS, Gao Fet al., 2017, A strongly selected mutation in the HIV-1 genome is independent of T cell responses and neutralizing antibodies, Retrovirology, Vol: 14, ISSN: 1742-4690

Background: Mutations rapidly accumulate in the HIV-1 genome after infection. Some of those mutations areselected by host immune responses and often cause viral ftness losses. This study is to investigate whether stronglyselected mutations that are not associated with immune responses result in ftness losses.Results: Strongly selected mutations were identifed by analyzing 5′-half HIV-1 genome (gag/pol) sequences fromlongitudinal samples of subject CH0131. The K43R mutation in the gag gene was frst detected at day 91 post screeningand was fxed in the viral population at day 273 while the synonymous N323tc mutation was frst detected at day177 and fxed at day 670. No conventional or cryptic T cell responses were detected against either mutation sites byELISpot analysis. However, when ftness costs of both mutations were measured by introducing each mutation intotheir cognate transmitted/founder (T/F) viral genome, the K43R mutation caused a signifcant ftness loss while theN323tc mutation had little impact on viral ftness.Conclusions: The rapid fxation, the lack of detectable immune responses and the signifcant ftness cost of theK43R mutation suggests that it was strongly selected by host factors other than T cell responses and neutralizingantibodies

Journal article

Song H, Hora B, Bhattacharya T, Goonetilleke N, Liu MKP, Wiehe K, Li H, Iyer SS, McMichael AJ, Perelson AS, Gao Fet al., 2014, Reversion and T Cell Escape Mutations Compensate the Fitness Loss of a CD8(+) T Cell Escape Mutant in Their Cognate Transmitted/Founder Virus, PLOS ONE, Vol: 9, ISSN: 1932-6203

Journal article

Liu MKP, Hawkins N, Ritchie AJ, Ganusov VV, Whale V, Brackenridge S, Li H, Pavlicek JW, Cai F, Rose-Abrahams M, Treurnicht F, Hraber P, Riou C, Gray C, Ferrari G, Tanner R, Ping L-H, Anderson JA, Swanstrom R, Chavi CB, Cohen M, Karim SSA, Haynes B, Borrow P, Perelson AS, Shaw GM, Hahn BH, Williamson C, Korber BT, Gao F, Self S, McMichael A, Goonetilleke Net al., 2013, Vertical T cell immunodominance and epitope entropy determine HIV-1 escape, JOURNAL OF CLINICAL INVESTIGATION, Vol: 123, Pages: 380-393, ISSN: 0021-9738

Journal article

Song H, Pavlicek JW, Cai F, Bhattacharya T, Li H, Iyer SS, Bar KJ, Decker JM, Goonetilleke N, Liu MKP, Berg A, Hora B, Drinker MS, Eudailey J, Pickeral J, Moody MA, Ferrari G, McMichael A, Perelson AS, Shaw GM, Hahn BH, Haynes BF, Gao Fet al., 2012, Impact of immune escape mutations on HIV-1 fitness in the context of the cognate transmitted/founder genome., Retrovirology, Vol: 9

BACKGROUND: A modest change in HIV-1 fitness can have a significant impact on viral quasispecies evolution and viral pathogenesis, transmission and disease progression. To determine the impact of immune escape mutations selected by cytotoxic T lymphocytes (CTL) on viral fitness in the context of the cognate transmitted/founder (T/F) genome, we developed a new competitive fitness assay using molecular clones of T/F genomes lacking exogenous genetic markers and a highly sensitive and precise parallel allele-specific sequencing (PASS) method. RESULTS: The T/F and mutant viruses were competed in CD4+ T-cell enriched cultures, relative proportions of viruses were assayed after repeated cell-free passage, and fitness costs were estimated by mathematical modeling. Naturally occurring HLA B57-restricted mutations involving the TW10 epitope in Gag and two epitopes in Tat/Rev and Env were assessed independently and together. Compensatory mutations which restored viral replication fitness were also assessed. A principal TW10 escape mutation, T242N, led to a 42% reduction in replication fitness but V247I and G248A mutations in the same epitope restored fitness to wild-type levels. No fitness difference was observed between the T/F and a naturally selected variant carrying the early CTL escape mutation (R355K) in Env and a reversion mutation in the Tat/Rev overlapping region. CONCLUSIONS: These findings reveal a broad spectrum of fitness costs to CTL escape mutations in T/F viral genomes, similar to recent findings reported for neutralizing antibody escape mutations, and highlight the extraordinary plasticity and adaptive potential of the HIV-1 genome. Analysis of T/F genomes and their evolved progeny is a powerful approach for assessing the impact of composite mutational events on viral fitness.

Journal article

Riou C, Treurnicht F, Abrahams M-R, Mlisana K, Liu MKP, Goonetilleke N, Koup R, Roederer M, Karim SA, de Bruyn G, Williamson C, Gray CM, Burgers WAet al., 2012, Increased Memory Differentiation Is Associated with Decreased Polyfunctionality for HIV but Not for Cytomegalovirus-Specific CD8(+) T Cells, JOURNAL OF IMMUNOLOGY, Vol: 189, Pages: 3838-3847, ISSN: 0022-1767

Journal article

Riou C, Ganusov VV, Campion S, Mlotshwa M, Liu MKP, Whale VE, Goonetilleke N, Borrow P, Ferrari G, Betts MR, Haynes BF, McMichael AJ, Gray CMet al., 2012, Distinct Kinetics of Gag-Specific CD4(+) and CD8(+) T Cell Responses during Acute HIV-1 Infection, JOURNAL OF IMMUNOLOGY, Vol: 188, Pages: 2198-2206, ISSN: 0022-1767

Journal article

Ganusov VV, Goonetilleke N, Liu MKP, Ferrari G, Shaw GM, McMichael AJ, Borrow P, Korber BT, Perelson ASet al., 2011, Fitness Costs and Diversity of the Cytotoxic T Lymphocyte (CTL) Response Determine the Rate of CTL Escape during Acute and Chronic Phases of HIV Infection, JOURNAL OF VIROLOGY, Vol: 85, Pages: 10518-10528, ISSN: 0022-538X

Journal article

Brackenridge S, Evans EJ, Toebes M, Goonetilleke N, Liu MKP, di Gleria K, Schumacher TN, Davis SJ, McMichael AJ, Gillespie GMet al., 2011, An Early HIV Mutation within an HLA-B*57-Restricted T Cell Epitope Abrogates Binding to the Killer Inhibitory Receptor 3DL1, JOURNAL OF VIROLOGY, Vol: 85, Pages: 5415-5422, ISSN: 0022-538X

Journal article

Ritchie AJ, Campion SL, Kopycinski J, Moodie Z, Wang ZM, Pandya K, Moore S, Liu MKP, Brackenridge S, Kuldanek K, Legg K, Cohen MS, Delwart EL, Haynes BF, Fidler S, McMichael AJ, Goonetilleke Net al., 2011, Differences in HIV-Specific T Cell Responses between HIV-Exposed and -Unexposed HIV-Seronegative Individuals, JOURNAL OF VIROLOGY, Vol: 85, Pages: 3507-3516, ISSN: 0022-538X

Journal article

Ferrari G, Korber B, Goonetilleke N, Liu MKP, Turnbull EL, Salazar-Gonzalez JF, Hawkins N, Self S, Watson S, Betts MR, Gay C, McGhee K, Pellegrino P, Williams I, Tomaras GD, Haynes BF, Gray CM, Borrow P, Roederer M, McMichael AJ, Weinhold KJet al., 2011, Relationship between Functional Profile of HIV-1 Specific CD8 T Cells and Epitope Variability with the Selection of Escape Mutants in Acute HIV-1 Infection, PLOS PATHOGENS, Vol: 7, ISSN: 1553-7366

Journal article

Kramer HB, Lavender KJ, Qin L, Stacey AR, Liu MKP, di Gleria K, Simmons A, Gasper-Smith N, Haynes BF, McMichael AJ, Borrow P, Kessler BMet al., 2010, Elevation of Intact and Proteolytic Fragments of Acute Phase Proteins Constitutes the Earliest Systemic Antiviral Response in HIV-1 Infection, PLOS PATHOGENS, Vol: 6, ISSN: 1553-7366

Journal article

Goonetilleke N, Liu MKP, Salazar-Gonzalez JF, Ferrari G, Giorgi E, Ganusov VV, Keele BF, Learn GH, Turnbull EL, Salazar MG, Weinhold KJ, Moore S, Letvin N, Haynes BF, Cohen MS, Hraber P, Bhattacharya T, Borrow P, Perelson AS, Hahn BH, Shaw GM, Korber BT, McMichael AJet al., 2009, The first T cell response to transmitted/founder virus contributes to the control of acute viremia in HIV-1 infection, JOURNAL OF EXPERIMENTAL MEDICINE, Vol: 206, Pages: 1253-1272, ISSN: 0022-1007

Journal article

MacLennan CA, Liu MKP, White SA, van Osterhout JJG, Simukonda F, Bwanali J, Moore MJ, Zijlstra EE, Drayson MT, Molyneux MEet al., 2007, Diagnostic accuracy and clinical utility of a simplified low cos method of counting CD4 cells with flow cytometry in Malawi diagnostic accuracy study, BRITISH MEDICAL JOURNAL, Vol: 335, Pages: 190-194, ISSN: 0959-8146

Journal article

Sweenie CH, Mackenzie KJ, Rone-Orugboh A, Liu M, Anderton SMet al., 2007, Distinct T cell recognition of naturally processed and cryptic epitopes within the immunodominant 35–55 region of myelin oligodendrocyte glycoprotein, Journal of Neuroimmunology, Vol: 183, Pages: 7-16, ISSN: 0165-5728

Journal article

Manzotti CN, Liu MKP, Burke F, Dussably L, Zheng Y, Sansom DMet al., 2006, Integration of CD28 and CTLA-4 function results in differential responses of T cells to CD80 and CD86., Eur J Immunol, Vol: 36, Pages: 1413-1422, ISSN: 0014-2980

CD80 and CD86 have the capacity to either stimulate or inhibit T cell responses through their receptors CD28 and cytotoxic T lymphocyte-associated antigen 4 (CTLA-4). Blockade of CD80 and CD86 in autoimmune disease settings has revealed distinct outcomes, yet the differential functions of CD80 and CD86 are still unclear. We have studied the ability of individual ligands to stimulate primary responses in human CD4(+) T cells. Our data reveal both quantitative and qualitative differences between the ligands. Both CD80 and CD86 demonstrated the capacity to costimulate T cell proliferation. However, CD80 committed a greater number of T cells to divide with faster kinetics, consistent with it being a superior ligand for CD28. Once cell division had been initiated, all T cells undergoing cell division expressed CTLA-4, irrespective of whether CD80 or CD86 costimulation was used. However, only in the presence of CD80 was evidence of CTLA-4 engagement and inhibitory function observed. Finally, differences between CD80 and CD86 costimulation extended to the T cell phenotype, in particular the levels of CD40 ligand expression.

Journal article

Mead KI, Zheng Y, Manzotti CN, Perry LCA, Liu MKP, Burke F, Powner DI, Wakelam MJO, Sansom DMet al., 2005, Exocytosis of CTLA-4 is dependent on phospholipase D and ADP ribosylation factor-1 and stimulated during activation of regulatory T cells, JOURNAL OF IMMUNOLOGY, Vol: 174, Pages: 4803-4811, ISSN: 0022-1767

Journal article

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