Sharon Lewin

Last updated

Sharon Ruth Lewin
Professor Sharon Lewin.jpg
Lewin in November 2017
Born
Melbourne, Australia
Alma mater Monash University
Known forHIV persistence and latency, HIV/HBV co-infection, COVID-19
SpouseRobert Milstein [1]
Awards
  • Peter Wills Medal (2015)
  • Officer of the Order of Australia (2019)
  • Robert C. Gallo Award for Scientific Excellence and Leadership in Medical Virology (2020)
  • Medal for Outstanding Female Researcher (2022)
Scientific career
FieldsMedicine, immunology, V\virology
InstitutionsThe Peter Doherty Institute for Infection and Immunity, University of Melbourne and Royal Melbourne Hospital
Monash University, Department of Infectious Diseases
Alfred Hospital
Burnet Institute

Sharon Ruth Lewin AO , FAA , FRACP, FAHMS is an Australian physician who is the inaugural Director of The Peter Doherty Institute for Infection and Immunity (Doherty Institute). She is also a Professor of Medicine at The University of Melbourne, a National Health and Medical Research Council (NHMRC) Practitioner Fellow, Director of the Cumming Global Centre for Pandemic Therapeutics, and President of the International AIDS Society (IAS).

Contents

Research and accomplishments

Lewin began her research career just as an antiretroviral treatment emerged for people living with HIV.[ citation needed ] Drawn to study HIV because of its global challenge, along with the complex social issues, Lewin's research interests have developed from questions arising during the clinical care of people living with HIV. Detecting, quantifying and potentially reactivating latent HIV is a central theme of Lewin's research, which spans basic virology, cellular immunology and clinical research. Her research laboratory is run together with immunologist and clinician Paul Cameron.[ citation needed ]

While completing her postdoctoral training with David Ho at the Aaron Diamond AIDS Research Centre, Lewin developed a highly sensitive PCR method to detect unspliced HIV RNA, an early product of viral transcription, in people receiving antiretroviral drugs. [2] Lewin's laboratory has developed models of HIV latency which are used to further tease out the mechanisms involved, and to assess the impact of latency reversal agents.[ citation needed ] Lewin's lab has shown that triggering the CCR7 receptor on resting CD4 T cells can induce latency, [3] acting through the activation of the cellular cytoskeleton, particularly actin remodelling. [4] This chemokine-induced latency model has been used in a comprehensive comparison of in vitro models for evaluating latency reversal agents. [5] Lewin's laboratory has also described the role of myeloid dendritic cells [6] and other antigen-presenting cells [7] in establishing HIV latency.

Lewin's team have made contributions to the knowledge of the HIV reservoir during antiretroviral treatment. This includes studies of naive CD4 T cells, where longitudinal and cross-sectional studies have shown that both CD31+ and CD31- naive CD4 T cells contribute to the ongoing HIV reservoir [8] and that HIV DNA is preferentially found in CD4 T cells expressing the chemokine receptors CXCR3 and CCR6. [9] Lewin's group has also studied immune reconstitution after antiretroviral treatment begins, exposing some of the factors associated with faster reconstitution [10] and has demonstrated a link between immune reconstitution and variants in the IL-7R gene. [11] [12]

Lewin's research has elucidated some of the basic immunology of Hepatitis B infection alone [13] and in co-infection with HIV. [14] Ongoing research is providing a deeper understanding of the clinical consequences of co-infection with Hepatitis B and HIV, both in Australian participants [15] [16] and through a long-standing collaboration with Thai researchers. [17] [18] [19] [20]

Lewin's clinical research efforts have focussed on potential HIV cure strategies, particularly those using the epigenetic modifiers including histone deacetylase inhibitors (HDACis). [21] [22] In vitro experiments showed that HDACis such as entinostat, [23] metacept-1 and -3 [24] could activate latent HIV in primary T cells. Following a sabbatical working with Christine Katlama and Brigitte Autran at the Hopital Pitié-Salpêtrière and Université Pierre et Marie Curie (UPMC), Paris, Lewin began to focus more on moving potential cure strategies into clinical trials. [25] Lewin's lab conducted the first multi-dose proof-of-concept HDACi trial in HIV positive participants, administering vorinostat daily over a 14-day period and assessing safety and impact on HIV transcription and reservoirs. [26] The trial and follow-on study [27] showed that while vorinostat was safe and able to increase HIV transcription in most participants, it did not reduce the HIV reservoir. [26] A dose-escalation study conducted in Melbourne, Australia and San Francisco, California, USA of the anti-alcohol compound Disulfiram also showed the ability to increase levels of cell-associated unspliced HIV RNA. [28] Both vorinostat and Disulfiram are now being investigated as part of a combination approach to latency activation ('kick' or 'tickle') followed by a second intervention to remove cells harbouring reactivated virus ('kill' or 'tease').

Lewin gave the opening plenary at the International AIDS Conference in Vienna in 2010.[ citation needed ] Lewin was local co-chair for the International AIDS Conference (AIDS 2014) in Melbourne, a member of WHO and UNAIDS strategic advisory groups and lead co-author of the 2016 International AIDS Society global scientific strategy to achieve an HIV cure. [29] Lewin is a founding council member of the Academy of Health and Medical Sciences, elected member of the Governing Council of the International AIDS Society representing the Asia Pacific region, she became President of the International AIDS Society in 2022 for a two-year tenure, [30] member of the council of the National Health and Medical Research Council (NHMRC) of Australia and chairs the Health Translation Advisory Committee. She chairs the Ministerial Advisory Committee on Blood Borne Viruses and Sexually Transmitted Infections, the peak advisory group to the Minister of Health of Australia.[ citation needed ]

Awards and honours

Related Research Articles

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The management of HIV/AIDS normally includes the use of multiple antiretroviral drugs as a strategy to control HIV infection. There are several classes of antiretroviral agents that act on different stages of the HIV life-cycle. The use of multiple drugs that act on different viral targets is known as highly active antiretroviral therapy (HAART). HAART decreases the patient's total burden of HIV, maintains function of the immune system, and prevents opportunistic infections that often lead to death. HAART also prevents the transmission of HIV between serodiscordant same-sex and opposite-sex partners so long as the HIV-positive partner maintains an undetectable viral load.

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<span class="mw-page-title-main">Lamivudine</span> Chemical compound

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HIV-associated neurocognitive disorders (HAND) are neurological disorders associated with HIV infection and AIDS. It is a syndrome of progressive deterioration of memory, cognition, behavior, and motor function in HIV-infected individuals during the late stages of the disease, when immunodeficiency is severe. HAND may include neurological disorders of various severity. HIV-associated neurocognitive disorders are associated with a metabolic encephalopathy induced by HIV infection and fueled by immune activation of macrophages and microglia. These cells are actively infected with HIV and secrete neurotoxins of both host and viral origin. The essential features of HIV-associated dementia (HAD) are disabling cognitive impairment accompanied by motor dysfunction, speech problems and behavioral change. Cognitive impairment is characterised by mental slowness, trouble with memory and poor concentration. Motor symptoms include a loss of fine motor control leading to clumsiness, poor balance and tremors. Behavioral changes may include apathy, lethargy and diminished emotional responses and spontaneity. Histopathologically, it is identified by the infiltration of monocytes and macrophages into the central nervous system (CNS), gliosis, pallor of myelin sheaths, abnormalities of dendritic processes and neuronal loss.

Virus latency is the ability of a pathogenic virus to lie dormant within a cell, denoted as the lysogenic part of the viral life cycle. A latent viral infection is a type of persistent viral infection which is distinguished from a chronic viral infection. Latency is the phase in certain viruses' life cycles in which, after initial infection, proliferation of virus particles ceases. However, the viral genome is not eradicated. The virus can reactivate and begin producing large amounts of viral progeny without the host becoming reinfected by new outside virus, and stays within the host indefinitely.

<span class="mw-page-title-main">HIV/AIDS</span> Spectrum of conditions caused by HIV infection

HIV is a retrovirus that attacks the immune system. It can be managed with treatment. Without treatment it can lead to a spectrum of conditions including AIDS.

Human Immunodeficiency Virus (HIV) and Hepatitis C Virus (HCV) co-infection is a multi-faceted, chronic condition that significantly impacts public health. According to the World Health Organization (WHO), 2 to 15% of those infected with HIV are also affected by HCV, increasing their risk of morbidity and mortality due to accelerated liver disease. The burden of co-infection is especially high in certain high-risk groups, such as intravenous drug users and men who have sex with men. These individuals who are HIV-positive are commonly co-infected with HCV due to shared routes of transmission including, but not limited to, exposure to HIV-positive blood, sexual intercourse, and passage of the Hepatitis C virus from mother to infant during childbirth.

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CD4 immunoadhesin is a recombinant fusion protein consisting of a combination of CD4 and the fragment crystallizable region, similarly known as immunoglobulin. It belongs to the antibody (Ig) gene family. CD4 is a surface receptor for human immunodeficiency virus (HIV). The CD4 immunoadhesin molecular fusion allow the protein to possess key functions from each independent subunit. The CD4 specific properties include the gp120-binding and HIV-blocking capabilities. Properties specific to immunoglobulin are the long plasma half-life and Fc receptor binding. The properties of the protein means that it has potential to be used in AIDS therapy as of 2017. Specifically, CD4 immunoadhesin plays a role in antibody-dependent cell-mediated cytotoxicity (ADCC) towards HIV-infected cells. While natural anti-gp120 antibodies exhibit a response towards uninfected CD4-expressing cells that have a soluble gp120 bound to the CD4 on the cell surface, CD4 immunoadhesin, however, will not exhibit a response. One of the most relevant of these possibilities is its ability to cross the placenta.

Long-term nonprogressors (LTNPs), are individuals infected with HIV, who maintain a CD4 count greater than 500 without antiretroviral therapy with a detectable viral load. Many of these patients have been HIV positive for 30 years without progressing to the point of needing to take medication in order not to develop AIDS. They have been the subject of a great deal of research, since an understanding of their ability to control HIV infection may lead to the development of immune therapies or a therapeutic vaccine. The classification "Long-term non-progressor" is not permanent, because some patients in this category have gone on to develop AIDS.

Diffuse infiltrative lymphocytosis syndrome (DILS) is a rare multi-system complication of HIV believed to occur secondary to an abnormal persistence of the initial CD8+ T cell expansion that regularly occurs in an HIV infection. This persistent CD8+ T cell expansion occurs in the setting of a low CD4+/CD8+ T cell ratio and ultimately invades and destroys tissues and organs resulting in the various complications of DILS. DILS classically presents with bilateral salivary gland enlargement (parotitis), cervical lymphadenopathy, and sicca symptoms such as xerophthalmia and xerostomia, but it may also involve the lungs, nervous system, kidneys, liver, digestive tract, and muscles. Once suspected, current diagnostic workups include (1) confirming HIV infection, (2) confirming six or greater months of characteristic signs and symptoms, (3) confirming organ infiltration by CD8+ T cells, and (4) exclusion of other autoimmune conditions. Once the diagnosis of DILS is confirmed, management includes highly active antiretroviral therapy (HAART) and as-needed steroids. With proper treatment, the overall prognosis of DILS is favorable.

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<span class="mw-page-title-main">Pathophysiology of HIV/AIDS</span>

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<span class="mw-page-title-main">Signs and symptoms of HIV/AIDS</span>

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The Berlin patient is an anonymous person from Berlin, Germany, who was described in 1998 as exhibiting prolonged "post-treatment control" of HIV viral load after HIV treatments were interrupted.

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Human Immunodeficiency Virus (HIV) has the capability to enter a latent stage of infection where it exists as a dormant provirus in CD4+ T-cells. Most latently infected cells are resting memory T cells, however a small fraction of latently infected cells isolated from HIV patients are naive CD4 T cells.

References

  1. ↑ Monash University Distinguished Alumni Sharon Lewin
  2. ↑ Lewin, S. R.; Vesanen, M.; Kostrikis, L.; Hurley, A.; Duran, M.; Zhang, L.; Ho, D. D.; Markowitz, M. (July 1999). "Use of Real-Time PCR and Molecular Beacons To Detect Virus Replication in Human Immunodeficiency Virus Type 1-Infected Individuals on Prolonged Effective Antiretroviral Therapy". Journal of Virology. 73 (7): 6099–6103. doi:10.1128/JVI.73.7.6099-6103.1999. ISSN   0022-538X. PMC   112674 . PMID   10364365.
  3. ↑ Saleh, Suha; Solomon, Ajantha; Wightman, Fiona; Xhilaga, Miranda; Cameron, Paul U.; Lewin, Sharon R. (15 December 2007). "CCR7 ligands CCL19 and CCL21 increase permissiveness of resting memory CD4+ T cells to HIV-1 infection: a novel model of HIV-1 latency". Blood. 110 (13): 4161–4164. doi: 10.1182/blood-2007-06-097907 . ISSN   0006-4971. PMID   17881634.
  4. ↑ Cameron, Paul U.; Saleh, Suha; Sallmann, Georgina; Solomon, Ajantha; Wightman, Fiona; Evans, Vanessa A.; Boucher, Genevieve; Haddad, Elias K.; Sekaly, Rafick-Pierre (28 September 2010). "Establishment of HIV-1 latency in resting CD4+ T cells depends on chemokine-induced changes in the actin cytoskeleton". Proceedings of the National Academy of Sciences. 107 (39): 16934–16939. Bibcode:2010PNAS..10716934C. doi: 10.1073/pnas.1002894107 . ISSN   0027-8424. PMC   2947912 . PMID   20837531.
  5. ↑ Spina, Celsa A.; Anderson, Jenny; Archin, Nancie M.; Bosque, Alberto; Chan, Jonathan; Famiglietti, Marylinda; Greene, Warner C.; Kashuba, Angela; Lewin, Sharon R. (26 December 2013). "An In-Depth Comparison of Latent HIV-1 Reactivation in Multiple Cell Model Systems and Resting CD4+ T Cells from Aviremic Patients". PLOS Pathogens. 9 (12): e1003834. doi: 10.1371/journal.ppat.1003834 . ISSN   1553-7374. PMC   3873446 . PMID   24385908.
  6. ↑ Evans, Vanessa A.; Kumar, Nitasha; Filali, Ali; Procopio, Francesco A.; Yegorov, Oleg; Goulet, Jean-Philippe; Saleh, Suha; Haddad, Elias K.; Pereira, Candida da Fonseca (5 December 2013). "Myeloid Dendritic Cells Induce HIV-1 Latency in Non-proliferating CD4+ T Cells". PLOS Pathogens. 9 (12): e1003799. doi: 10.1371/journal.ppat.1003799 . ISSN   1553-7374. PMC   3855553 . PMID   24339779.
  7. ↑ Kumar, Nitasha A.; Cheong, Karey; Powell, David R.; da Fonseca Pereira, Candida; Anderson, Jenny; Evans, Vanessa A.; Lewin, Sharon R.; Cameron, Paul U. (11 September 2015). "The role of antigen presenting cells in the induction of HIV-1 latency in resting CD4+ T-cells". Retrovirology. 12: 76. doi: 10.1186/s12977-015-0204-2 . ISSN   1742-4690. PMC   4567795 . PMID   26362311.
  8. ↑ Wightman, Fiona; Solomon, Ajantha; Khoury, Gabriela; Green, Justin A.; Gray, Lachlan; Gorry, Paul R.; Ho, Yung Shwen; Saksena, Nitin K.; Hoy, Jennifer (1 December 2010). "Both CD31+ and CD31- Naive CD4+ T Cells Are Persistent HIV Type 1-Infected Reservoirs in Individuals Receiving Antiretroviral Therapy". The Journal of Infectious Diseases. 202 (11): 1738–1748. doi: 10.1086/656721 . ISSN   0022-1899. PMID   20979453.
  9. ↑ Khoury, Gabriela; Anderson, Jenny L.; Fromentin, Rémi; Hartogenesis, Wendy; Smith, Miranda Z.; Bacchetti, Peter; Hecht, Frederick M.; Chomont, Nicolas; Cameron, Paul U. (19 June 2016). "Persistence of integrated HIV DNA in CXCR3 + CCR6 + memory CD4+ T cells in HIV-infected individuals on antiretroviral therapy". AIDS. 30 (10): 1511–1520. doi:10.1097/qad.0000000000001029. ISSN   0269-9370. PMC   4889535 . PMID   26807971.
  10. ↑ Rajasuriar, Reena; Gouillou, Maelenn; Spelman, Tim; Read, Tim; Hoy, Jennifer; Law, Matthew; Cameron, Paul U.; Petoumenos, Kathy; Lewin, Sharon R. (2 June 2011). "Clinical Predictors of Immune Reconstitution following Combination Antiretroviral Therapy in Patients from the Australian HIV Observational Database". PLOS ONE. 6 (6): e20713. Bibcode:2011PLoSO...620713R. doi: 10.1371/journal.pone.0020713 . ISSN   1932-6203. PMC   3107235 . PMID   21674057.
  11. ↑ Rajasuriar, R.; Booth, D. R.; Gouillou, M.; Spelman, T.; James, I.; Solomon, A.; Chua, K.; Stewart, G.; Deeks, S. (January 2012). "The role of SNPs in the α-chain of the IL-7R gene in CD4+ T-cell recovery in HIV-infected African patients receiving suppressive cART". Genes and Immunity. 13 (1): 83–93. doi: 10.1038/gene.2011.65 . ISSN   1466-4879. PMID   21938017.
  12. ↑ Rajasuriar, Reena; Booth, David; Solomon, Ajantha; Chua, Kyra; Spelman, Tim; Gouillou, Maelenn; Schlub, Timothy E.; Davenport, Miles; Crowe, Suzanne (15 October 2010). "Biological Determinants of Immune Reconstitution in HIV-Infected Patients Receiving Antiretroviral Therapy: The Role of Interleukin 7 and Interleukin 7 Receptor α and Microbial Translocation". The Journal of Infectious Diseases. 202 (8): 1254–1264. doi: 10.1086/656369 . ISSN   0022-1899. PMID   20812848.
  13. ↑ Chang, J. Judy; Thompson, Alexander J. V.; Visvanathan, Kumar; Kent, Stephen J.; Cameron, Paul U.; Wightman, Fiona; Desmond, Paul; Locarnini, Stephen A.; Lewin, Sharon R. (1 November 2007). "The phenotype of hepatitis B virus–specific T cells differ in the liver and blood in chronic hepatitis B virus infection". Hepatology. 46 (5): 1332–1340. doi: 10.1002/hep.21844 . ISSN   1527-3350. PMID   17924445. S2CID   9902334.
  14. ↑ Chang, J. Judy; Wightman, Fiona; Bartholomeusz, Angeline; Ayres, Anna; Kent, Stephen J.; Sasadeusz, Joseph; Lewin, Sharon R. (1 March 2005). "Reduced Hepatitis B Virus (HBV)-Specific CD4+ T-Cell Responses in Human Immunodeficiency Virus Type 1-HBV-Coinfected Individuals Receiving HBV-Active Antiretroviral Therapy". Journal of Virology. 79 (5): 3038–3051. doi:10.1128/jvi.79.5.3038-3051.2005. ISSN   0022-538X. PMC   548440 . PMID   15709024.
  15. ↑ Lewin, Sharon R.; Ribeiro, Ruy M.; Walters, Tomos; Lau, George K.; Bowden, Scott; Locarnini, Stephen; Perelson, Alan S. (1 November 2001). "Analysis of hepatitis B viral load decline under potent therapy: Complex decay profiles observed". Hepatology. 34 (5): 1012–1020. doi: 10.1053/jhep.2001.28509 . ISSN   1527-3350. PMID   11679973. S2CID   206249432.
  16. ↑ Audsley, Jennifer; Robson, Christopher; Aitchison, Stacey; Matthews, Gail V.; Iser, David; Sasadeusz, Joe; Lewin, Sharon R. (1 January 2016). "Liver Fibrosis Regression Measured by Transient Elastography in Human Immunodeficiency Virus (HIV)-Hepatitis B Virus (HBV)-Coinfected Individuals on Long-Term HBV-Active Combination Antiretroviral Therapy". Open Forum Infectious Diseases. 3 (1): ofw035. doi:10.1093/ofid/ofw035. PMC   4800457 . PMID   27006960.
  17. ↑ Matthews, Gail V.; Avihingsanon, Anchalee; Lewin, Sharon R.; Amin, Janaki; Rerknimitr, Rungsun; Petcharapirat, Panusit; Marks, Pip; Sasadeusz, Joe; Cooper, David A. (1 October 2008). "A randomized trial of combination hepatitis B therapy in HIV/HBV coinfected antiretroviral naïve individuals in Thailand". Hepatology. 48 (4): 1062–1069. doi: 10.1002/hep.22462 . ISSN   1527-3350. PMID   18697216.
  18. ↑ Crane, Megan; Sirivichayakul, Sunee; Chang, J. Judy; Avihingsanon, Anchalee; Ubolyam, Sasiwimol; Buranapraditkun, Supranee; Thantiworasit, Pattarawat; Wightman, Fiona; Locarnini, Stephen (15 March 2010). "No Increase in Hepatitis B Virus (HBV)-Specific CD8+ T Cells in Patients with HIV-1-HBV Coinfections following HBV-Active Highly Active Antiretroviral Therapy". Journal of Virology. 84 (6): 2657–2665. doi:10.1128/jvi.02124-09. ISSN   0022-538X. PMC   2826062 . PMID   20053751.
  19. ↑ Crane, Megan; Avihingsanon, Anchalee; Rajasuriar, Reena; Velayudham, Pushparaj; Iser, David; Solomon, Ajantha; Sebolao, Baotuti; Tran, Andrew; Spelman, Tim (1 September 2014). "Lipopolysaccharide, Immune Activation, and Liver Abnormalities in HIV/Hepatitis B Virus (HBV)–Coinfected Individuals Receiving HBV-Active Combination Antiretroviral Therapy". The Journal of Infectious Diseases. 210 (5): 745–751. doi: 10.1093/infdis/jiu119 . ISSN   0022-1899. PMID   24585898.
  20. ↑ Punyawudho, Baralee; Thammajaruk, Narukjaporn; Thongpeang, Parawee; Matthews, Gail; Lewin, Sharon R.; Burger, David; Ruxrungtham, Kiat; Avihingsanon, Anchalee (2015). "Population pharmacokinetics of tenofovir in HIV/HBV co-infected patients". International Journal of Clinical Pharmacology and Therapeutics. 53 (11): 947–954. doi:10.5414/cp202386. PMID   26308175.
  21. ↑ Rasmussen, Thomas Aagaard; Søgaard, Ole Schmeltz; Brinkmann, Christel; Wightman, Fiona; Lewin, Sharon R.; Melchjorsen, Jesper; Dinarello, Charles; Østergaard, Lars; Tolstrup, Martin (14 May 2013). "Comparison of HDAC inhibitors in clinical development". Human Vaccines & Immunotherapeutics. 9 (5): 993–1001. doi:10.4161/hv.23800. ISSN   2164-5515. PMC   3899169 . PMID   23370291.
  22. ↑ Wightman, Fiona; Ellenberg, Paula; Churchill, Melissa; Lewin, Sharon R. (January 2012). "HDAC inhibitors in HIV". Immunology and Cell Biology. 90 (1): 47–54. doi: 10.1038/icb.2011.95 . ISSN   0818-9641. PMID   22083528. S2CID   21811612.
  23. ↑ Wightman, Fiona; Lu, Hao K.; Solomon, Ajantha E.; Saleh, Suha; Harman, Andrew N.; Cunningham, Anthony L.; Gray, Lachlan; Churchill, Melissa; Cameron, Paul U. (2013). "Entinostat is a histone deacetylase inhibitor selective for class 1 histone deacetylases and activates HIV production from latently infected primary T cells". AIDS. 27 (18): 2853–2862. doi:10.1097/qad.0000000000000067. PMC   4079759 . PMID   24189584.
  24. ↑ Shehu-Xhilaga, Miranda; Rhodes, David; Wightman, Fiona; Liu, Hong B; Solomon, Ajantha; Saleh, Suha; Dear, Anthony E; Cameron, Paul U; Lewin, Sharon R (2009). "The novel histone deacetylase inhibitors metacept-1 and metacept-3 potently increase HIV-1 transcription in latently infected cells". AIDS. 23 (15): 2047–2050. doi: 10.1097/qad.0b013e328330342c . PMID   19609198. S2CID   39280869.
  25. ↑ Lewin, Sharon R; Rouzioux, Christine (2011). "HIV cure and eradication: how will we get from the laboratory to effective clinical trials?". AIDS. 25 (7): 885–897. doi: 10.1097/qad.0b013e3283467041 . PMID   21422987. S2CID   23266836.
  26. 1 2 Elliott, Julian H.; Wightman, Fiona; Solomon, Ajantha; Ghneim, Khader; Ahlers, Jeffrey; Cameron, Mark J.; Smith, Miranda Z.; Spelman, Tim; McMahon, James (13 November 2014). "Activation of HIV Transcription with Short-Course Vorinostat in HIV-Infected Patients on Suppressive Antiretroviral Therapy". PLOS Pathogens. 10 (11): e1004473. doi: 10.1371/journal.ppat.1004473 . ISSN   1553-7374. PMC   4231123 . PMID   25393648.
  27. ↑ Mota, Talia M.; Rasmussen, Thomas A.; Rhodes, Ajantha; Tennakoon, Surekha; Dantanarayana, Ashanti; Wightman, Fiona; Hagenauer, Michelle; Roney, Janine; Spelman, Tim (15 May 2017). "No adverse safety or virological changes 2 years following vorinostat in HIV-infected individuals on antiretroviral therapy". AIDS. 31 (8): 1137–1141. doi:10.1097/qad.0000000000001442. ISSN   0269-9370. PMC   5496768 . PMID   28301423.
  28. ↑ Elliott, Julian H; McMahon, James H; Chang, Christina C; Lee, Sulggi A; Hartogensis, Wendy; Bumpus, Namandje; Savic, Rada; Roney, Janine; Hoh, Rebecca (2015). "Short-term administration of disulfiram for reversal of latent HIV infection: a phase 2 dose-escalation study". The Lancet HIV. 2 (12): e520–e529. doi:10.1016/s2352-3018(15)00226-x. PMC   5108570 . PMID   26614966.
  29. ↑ Deeks, Steven G; Lewin, Sharon R; Ross, Anna Laura; Ananworanich, Jintanat; Benkirane, Monsef; Cannon, Paula; Chomont, Nicolas; Douek, Daniel; Lifson, Jeffrey D (2016). "International AIDS Society global scientific strategy: towards an HIV cure 2016" (PDF). Nature Medicine. 22 (8): 839–850. doi:10.1038/nm.4108. hdl:10044/1/45370. PMC   5322797 . PMID   27400264.
  30. ↑ "Sharon Lewin assumes IAS Presidency". www.iasociety.org. Retrieved 11 May 2023.
  31. ↑ Natoli, Andrea (6 April 2016). "2015 Peter Wills Medal: Prof Sharon Lewin". RESEARCH AUSTRALIA. Retrieved 15 March 2024.
  32. ↑ "Australia Day 2019 Honours List" (PDF). Governor General of the Commonwealth of Australia. 26 January 2019. Retrieved 27 January 2019.
  33. ↑ "Professor Sharon Lewin presented with GVN Robert C Gallo Award". www.doherty.edu.au. The Doherty Institute. 22 September 2020. Retrieved 15 March 2024.
  34. ↑ "Sharon Lewin AO, FRACP PhD FAHMS and RMIT University win 2020 Melbourne Achiever Award". Committee For Melbourne. Retrieved 15 March 2024.
  35. ↑ "PROFESSOR SHARON LEWIN AO". rotaryclubofmelbourne.org.au. Retrieved 15 March 2024.
  36. ↑ Rowney, Katie (6 September 2022). "Professor Sharon Lewin awarded Medal for Outstanding Female Researcher - AAHMS". aahms.org. Retrieved 15 March 2024.
  37. ↑ "Sharon Lewin". www.science.org.au. Retrieved 25 May 2023.
  38. ↑ "La Trobe awards Hon Docs to global health pioneers". La Trobe University. 25 October 2023. Retrieved 1 November 2023.
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