Lalita Ramakrishnan

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Lalita Ramakrishnan
FRS FMedSci
Lalita Ramakrishnan Royal Society.jpg
Ramakrishnan in 2018
Born1959 (age 64–65)
Baroda, Gujarat, India
Alma mater Baroda Medical College
Tufts University
SpouseMark Troll
Mother Rajalakshmi Ramakrishnan
Relatives Venki Ramakrishnan (brother)
Awards Member of the National Academy of Sciences (2015)
EMBO Member (2019) [1]
Scientific career
Fields Microbiology
Immunology
Infectious diseases [2]
Institutions University of Cambridge
University of Washington
Thesis Abelson virus-transformed cells as models of early B lymphocyte differentiation  (1990)
Website www.med.cam.ac.uk/ramakrishnan/ OOjs UI icon edit-ltr-progressive.svg

Lalita Ramakrishnan (born 1959) is an Indian-born American microbiologist who is known for her contributions to the understanding of the biological mechanism of tuberculosis. [3] [4] [5] As of 2019 she serves as a professor of Immunology and Infectious Diseases at the University of Cambridge, where she is also a Wellcome Trust Principal Research Fellow and a practicing physician. [6] Her research is conducted at the MRC Laboratory of Molecular Biology (MRC LMB), where she serves as the Head of the Molecular Immunity Unit of the Department of Medicine embedded at the MRC LMB. Working with Stanley Falkow at Stanford, she developed the strategy of using Mycobacterium marinum infection as a model for tuberculosis. [7] [6] Her work has appeared in a number of journals, including Science , Nature , and Cell . [2] [8] [4] In 2018 and 2019 Ramakrishnan coauthored two influential papers [9] in the British Medical Journal (BMJ) arguing that the widely accepted estimates of the prevalence of latent tuberculosis—estimates used as a basis for allocation of research funds—are far too high. [10] [11] She is married to Mark Troll, a physical chemist. [12] [13] [14]

Contents

Early life and education

Ramakrishnan was born in 1959 in Baroda (now Vadodara) [15] and grew up there. [16] Her parents were both scientists as is her brother, Nobel laureate Venki Ramakrishnan. When Ramakrishnan was a child, her mother had three bouts of spinal tuberculosis. [3]

As a high school student, Ramakrishnan excelled at math and physics. [3] Ramakrishnan began attending medical school at age 17, which is "not atypical in India, where specialized training begins shortly after high school." [4] In 1983, she graduated with a Bachelor of Medicine degree in Vadodara [17] from Baroda Medical College. [18]

After taking an elective course in advanced immunology, Ramakrishnan decided to study immunology. In 1990, she graduated from Tufts University with a PhD in Immunology. [17] She then became the first foreign graduate of the medical residency program at Tufts-New England Medical Center. [4] After completing a fellowship in Infectious Diseases at the University of California at San Francisco hospitals, including San Francisco General Hospital (now Zuckerberg San Francisco General Hospital and Trauma Center), [19] Ramakrishnan completed postdoctoral work in Stanley Falkow's lab at Stanford University, where she developed the strategy of using Mycobacterium marinum infection in zebrafish as a model for tuberculosis. [6]

Career and research

In 2001, Ramakrishnan joined the faculty of the University of Washington, [6] where she worked both as a basic scientist and infectious diseases physician. While at the University of Washington, she pioneered the study of tuberculosis in zebrafish as a close approximation to tuberculosis in humans. This strategy led to a fundamental new biological understanding of how disease develops. Zebrafish larvae are optically transparent and lend themselves to genetic manipulation; by infecting them with their natural pathogen, Mycobacterium marinum , a bacterium that causes tuberculosis in fish and is a close genetic relative of the bacteria that cause tuberculosis in humans, she could carefully track the infection while manipulating the genes of both the larvae and the bacteria. This approach "enabled a detailed dissection of granuloma formation" [6] (a granuloma is a structure of the immune system made up principally of cells, called macrophages, that ingest bacteria and other foreign particles). In 2010, Ramakrishnan was the senior author of a study which was published as the cover story of Cell. [20]

In 2014, Ramakrishnan joined the faculty of the University of Cambridge as a principal research fellow for the Wellcome Trust and Professor of Immunology and Infectious Diseases. Work in Seattle, and subsequently in Cambridge, led to the discovery of the molecular and cellular details of mycobacterial and host interactions at each step of infection. This yielded fundamental insights that suggest entirely new approaches to treat tuberculosis. Ramakrishnan and her research group showed that two lipids (a type of fatty molecule) on the surface of the mycobacteria work together to enable the bacteria to initially avoid the macrophages that would kill them and instead enter macrophages that provide them a niche for growth. [21] She found that the bacteria then stimulate the formation of granulomas that provide them a safe harbour, in contrast to the normal role of granulomas in protecting the host from the bacteria. [22] Later the infected macrophages in the granulomas die, and this accelerates bacterial growth and promotes the development of the disease. [23] [24] [25] [26] These findings led to host-targeting therapies that show promise in tuberculosis patients. Ramakrishnan and her group tackled the problem of drug tolerance in tuberculosis, and found a drug that inhibits the development of resistance to the standard drugs used to treat the disease. [27]

Ramakrishnan later exploited the zebrafish to study leprosy, another devastating disease with morbid neurological consequences. She showed that a Mycobacterium leprae lipid causes nerve damage by inciting abnormal responses in the macrophages. [28]

In addition to basic science investigations, Ramakrishnan, along with Marcel Behr and Paul Edelstein, reviewed studies concerning the concept of latent tuberculosis in order to determine whether tuberculosis-infected persons have life-long infection capable of causing disease at any future time. These studies, both published in the British Medical Journal (BMJ), show that the incubation period of tuberculosis is short, usually within months after infection, and very rarely more than 2 years after infection. [29] [30] They also show that more than 90% of people infected with M. tuberculosis for more than two years never develop tuberculosis even if their immune system is severely suppressed. [11] Immunologic tests for tuberculosis infection such as the tuberculin skin test and interferon gamma release assays (IGRA) only indicate past infection, with the majority of previously infected persons no longer capable of developing tuberculosis. Ramakrishnan told the New York Times that researchers "have spent hundreds of millions of dollars chasing after latency, but the whole idea that a quarter of the world is infected with TB is based on a fundamental misunderstanding." [9]

The first BMJ article about latency was accompanied by an editorial written by Soumya Swaminathan, Deputy Director-General of the World Health Organization, who endorsed the findings and called for more funding of TB research directed at the most heavily afflicted parts of the world, rather than disproportionate attention to a relatively minor problem that affects just the wealthy countries. [9] Earlier researchers had warned of a "ticking time bomb" of TB cases in the US and other wealthy countries that should be a focus of attention. [31] The work of Ramakrishnan and her coauthors cast doubt on this warning. Writing in The Atlantic, science journalist Katherine J. Wu commented that "even the world's biggest authorities on TB are dispensing with what was once conventional wisdom." [32]

Awards and honours

Ramakrishnan was elected a Member of the US National Academy of Sciences in 2015. [18] [33] She has received a number of other awards, including a National Institutes of Health (NIH) Director's Pioneer Award and a Burroughs Wellcome Fund Investigators in the Pathogenesis of Infectious Disease Award. [4] She also served on the Life Sciences jury for the Infosys Prize in 2016. In 2018 she was elected a Fellow of the Royal Society (FRS) [34] and Fellow of the Academy of Medical Sciences (FMedSci). [35] [36] She was made a member of the European Molecular Biology Organization (EMBO) in 2019. [1]

Related Research Articles

<span class="mw-page-title-main">Tuberculosis</span> Infectious disease

Tuberculosis (TB), also known colloquially as the "white death", or historically as consumption, is an infectious disease usually caused by Mycobacterium tuberculosis (MTB) bacteria. Tuberculosis generally affects the lungs, but it can also affect other parts of the body. Most infections show no symptoms, in which case it is known as latent tuberculosis. Around 10% of latent infections progress to active disease that, if left untreated, kill about half of those affected. Typical symptoms of active TB are chronic cough with blood-containing mucus, fever, night sweats, and weight loss. Infection of other organs can cause a wide range of symptoms.

<i>Mycobacterium tuberculosis</i> Species of pathogenic bacteria that causes tuberculosis

Mycobacterium tuberculosis, also known as Koch's bacillus, is a species of pathogenic bacteria in the family Mycobacteriaceae and the causative agent of tuberculosis. First discovered in 1882 by Robert Koch, M. tuberculosis has an unusual, waxy coating on its cell surface primarily due to the presence of mycolic acid. This coating makes the cells impervious to Gram staining, and as a result, M. tuberculosis can appear weakly Gram-positive. Acid-fast stains such as Ziehl–Neelsen, or fluorescent stains such as auramine are used instead to identify M. tuberculosis with a microscope. The physiology of M. tuberculosis is highly aerobic and requires high levels of oxygen. Primarily a pathogen of the mammalian respiratory system, it infects the lungs. The most frequently used diagnostic methods for tuberculosis are the tuberculin skin test, acid-fast stain, culture, and polymerase chain reaction.

<i>Mycobacterium</i> Genus of bacteria

Mycobacterium is a genus of over 190 species in the phylum Actinomycetota, assigned its own family, Mycobacteriaceae. This genus includes pathogens known to cause serious diseases in mammals, including tuberculosis and leprosy in humans. The Greek prefix myco- means 'fungus', alluding to this genus' mold-like colony surfaces. Since this genus has cell walls with a waxy lipid-rich outer layer containing high concentrations of mycolic acid, acid-fast staining is used to emphasize their resistance to acids, compared to other cell types.

<span class="mw-page-title-main">Granuloma</span> Aggregation of immune cells in response to chronic inflammation

A granuloma is an aggregation of macrophages that forms in response to chronic inflammation. This occurs when the immune system attempts to isolate foreign substances that it is otherwise unable to eliminate. Such substances include infectious organisms including bacteria and fungi, as well as other materials such as foreign objects, keratin, and suture fragments.

<span class="mw-page-title-main">Asymptomatic carrier</span> Organism which has become infected with a pathogen but displays no symptoms

An asymptomatic carrier is a person or other organism that has become infected with a pathogen, but shows no signs or symptoms.

<span class="mw-page-title-main">Diagnosis of tuberculosis</span> Methods for diagnosing tuberculosis

Tuberculosis is diagnosed by finding Mycobacterium tuberculosis bacteria in a clinical specimen taken from the patient. While other investigations may strongly suggest tuberculosis as the diagnosis, they cannot confirm it.

<span class="mw-page-title-main">Miliary tuberculosis</span> Medical condition

Miliary tuberculosis is a form of tuberculosis that is characterized by a wide dissemination into the human body and by the tiny size of the lesions (1–5 mm). Its name comes from a distinctive pattern seen on a chest radiograph of many tiny spots distributed throughout the lung fields with the appearance similar to millet seeds—thus the term "miliary" tuberculosis. Miliary TB may infect any number of organs, including the lungs, liver, and spleen. Miliary tuberculosis is present in about 2% of all reported cases of tuberculosis and accounts for up to 20% of all extra-pulmonary tuberculosis cases.

Latent tuberculosis (LTB), also called latent tuberculosis infection (LTBI) is when a person is infected with Mycobacterium tuberculosis, but does not have active tuberculosis (TB). Active tuberculosis can be contagious while latent tuberculosis is not, and it is therefore not possible to get TB from someone with latent tuberculosis. The main risk is that approximately 10% of these people will go on to develop active tuberculosis. This is particularly true, and there is added risk, in particular situations such as medication that suppresses the immune system or advancing age.

Tuberculosis (TB) vaccines are vaccinations intended for the prevention of tuberculosis. Immunotherapy as a defence against TB was first proposed in 1890 by Robert Koch. As of 2021, the only effective tuberculosis vaccine in common use is the Bacillus Calmette-Guérin (BCG) vaccine, first used on humans in 1921. It consists of attenuated (weakened) strains of the cattle tuberculosis bacillus. It is recommended for babies in countries where tuberculosis is common.

rBCG30 is a prospective Bacillus Calmette-Guérin vaccine against tuberculosis. It is a live vaccine, consisting of BCG, which has been evaluated as a tuberculosis vaccination. It is genetically modified to produce abundant amounts of mycolyl transferase, a 30kDa antigen that has been shown to produce a strong immune response in animals and humans. rBCG30 had been in human clinical trials, but no clinical development has been reported since 2007.

Lipoarabinomannan, also called LAM, is a glycolipid, and a virulence factor associated with Mycobacterium tuberculosis, the bacteria responsible for tuberculosis. Its primary function is to inactivate macrophages and scavenge oxidative radicals.

T-SPOT.TB is a type of ELISpot assay used for tuberculosis diagnosis, which belongs to the group of interferon gamma release assays. The test is manufactured by Oxford Immunotec in the UK. It is available in most European countries, the United States as well as various other countries. It was developed by researchers at the University of Oxford in England.

Type IV hypersensitivity, in the Gell and Coombs classification of allergic reactions, often called delayed-type hypersensitivity, is a type of hypersensitivity reaction that can take a day or more to develop. Unlike the other types, it is not humoral but rather is a type of cell-mediated response. This response involves the interaction of T cells, monocytes, and macrophages.

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

Cord factor, or trehalose dimycolate (TDM), is a glycolipid molecule found in the cell wall of Mycobacterium tuberculosis and similar species. It is the primary lipid found on the exterior of M. tuberculosis cells. Cord factor influences the arrangement of M. tuberculosis cells into long and slender formations, giving its name. Cord factor is virulent towards mammalian cells and critical for survival of M. tuberculosis in hosts, but not outside of hosts. Cord factor has been observed to influence immune responses, induce the formation of granulomas, and inhibit tumor growth. The antimycobacterial drug SQ109 is thought to inhibit TDM production levels and in this way disrupts its cell wall assembly.

The co-epidemic of tuberculosis (TB) and human immunodeficiency virus (HIV) is one of the major global health challenges in the present time. The World Health Organization (WHO) reported that TB is the leading cause of death in those with HIV. In 2019, TB was responsible for 30% of the 690,000 HIV/AIDS related deaths worldwide and 15% of the 1.4 million global TB deaths were in people with HIV or AIDS. The two diseases act in combination as HIV drives a decline in immunity, while tuberculosis progresses due to defective immune status. Having HIV makes one more likely to be infected with tuberculosis, especially if one's CD4 T-cells are low. CD4 T-cells below 200 increases one's risk of tuberculosis infection by 25 times. This condition becomes more severe in case of multi-drug (MDRTB) and extensively drug resistant TB (XDRTB), which are difficult to treat and contribute to increased mortality. Tuberculosis can occur at any stage of HIV infection. The risk and severity of tuberculosis increases soon after infection with HIV. Although tuberculosis can be a relatively early manifestation of HIV infection, the risk of tuberculosis progresses as the CD4 cell count decreases along with the progression of HIV infection. The risk of TB generally remains high in HIV-infected patients, remaining above the background risk of the general population even with effective immune reconstitution and high CD4 cell counts with antiretroviral therapy.

<span class="mw-page-title-main">Universal stress protein</span>

The universal stress protein (USP) domain is a superfamily of conserved genes which can be found in bacteria, archaea, fungi, protozoa and plants. Proteins containing the domain are induced by many environmental stressors such as nutrient starvation, drought, extreme temperatures, high salinity, and the presence of uncouplers, antibiotics and metals.

Amit Singh is an Indian microbiologist and an associate professor at the Department of Microbiology and cell biology of the Indian Institute of Science. A Wellcome-DBT Senior Fellow, Singh is known for his studies on the pathogenesis of Mycobacterium tuberculosis. His research focuses on exploring the mechanisms behind the persistence of human pathogens like disease and HIV.

<span class="mw-page-title-main">Henry Mwandumba</span> African professor of medicine

Henry Charles Mwandumba is an African Professor of Medicine and the Director of the Malawi-Liverpool-Wellcome Programme. He works on the tuberculosis phagosome in the University of Malawi College of Medicine, and serves as President of the Federation of African Immunological Societies. In 2019 Mwandumba was awarded the Royal Society Africa Prize.

Hazel Marguerite Dockrell is an Irish-born microbiologist and immunologist whose research has focused on immunity to the human mycobacterial diseases, leprosy and tuberculosis. She has spent most of her career at the London School of Hygiene and Tropical Medicine, where as of 2020 she is a professor of immunology. She was the first female president of the Royal Society of Tropical Medicine and Hygiene. Jimmy Whitworth of the Wellcome Trust describes her as "a marvellous ambassador for global health and research."

Shabaana A. Khader is an Indian-American microbiologist who is the Bernard and Betty Roizman Professor of Microbiology at the University of Chicago. She is also the Chair of the Department of Microbiology. In an effort to design new vaccines and therapeutic strategies, Khader studies host-pathogen interactions in infectious disease.

References

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  6. 1 2 3 4 5 Sheffield, University of. "Professor Lalita Ramakrishnan - Faculty Events - Faculty of Medicine, Dentistry and Health - Faculties - The University of Sheffield". sheffield.ac.uk. Retrieved 24 April 2016.
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  8. ↑ Lalita Ramakrishnan publications indexed by the Scopus bibliographic database. (subscription required)
  9. 1 2 3 McNeil, Donald G. Jr. (20 September 2018). "'Latent' tuberculosis? It's not that common, experts find". The New York Times.
  10. ↑ Marcel A Behr; Paul H Edelstein; Lalita Ramakrishnan (23 August 2018). "Revisiting the timetable of tuberculosis". The BMJ . 362: k2738. doi:10.1136/BMJ.K2738. ISSN   0959-8138. PMC   6105930 . PMID   30139910. Wikidata   Q58716327.
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  15. ↑ "Venkatraman Ramakrishnan - Biographical". www.nobelprize.org. Retrieved 24 April 2016.
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  17. 1 2 "About | Lalita Ramakrishnan Lab". depts.washington.edu. Retrieved 24 April 2016.
  18. 1 2 "- BSI Inflammation Affinity Group Speakers Bio - Lalita Ramakrishnan - British Society for Immunology". immunology.org. Retrieved 24 April 2016.
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  21. ↑ Cambier, C. J.; O'Leary, Seónadh M.; O'Sullivan, Mary P.; Keane, Joseph; Ramakrishnan, Lalita (19 September 2017). "Phenolic Glycolipid Facilitates Mycobacterial Escape from Microbicidal Tissue-Resident Macrophages". Immunity. 47 (3): 552–565.e4. doi:10.1016/j.immuni.2017.08.003. ISSN   1097-4180. PMC   5610147 . PMID   28844797.
  22. ↑ Conrad, William H.; Osman, Morwan M.; Shanahan, Jonathan K.; Chu, Frances; Takaki, Kevin K.; Cameron, James; Hopkinson-Woolley, Digby; Brosch, Roland; Ramakrishnan, Lalita (7 February 2017). "Mycobacterial ESX-1 secretion system mediates host cell lysis through bacterium contact-dependent gross membrane disruptions". Proceedings of the National Academy of Sciences of the United States of America. 114 (6): 1371–1376. Bibcode:2017PNAS..114.1371C. doi: 10.1073/pnas.1620133114 . ISSN   1091-6490. PMC   5307465 . PMID   28119503.
  23. ↑ Tobin, David M.; Vary, Jay C.; Ray, John P.; Walsh, Gregory S.; Dunstan, Sarah J.; Bang, Nguyen D.; Hagge, Deanna A.; Khadge, Saraswoti; King, Mary-Claire; Hawn, Thomas R.; Moens, Cecilia B. (5 March 2010). "The lta4h locus modulates susceptibility to mycobacterial infection in zebrafish and humans". Cell. 140 (5): 717–730. doi:10.1016/j.cell.2010.02.013. ISSN   1097-4172. PMC   2907082 . PMID   20211140.
  24. ↑ Tobin, David M.; Roca, Francisco J.; Oh, Sungwhan F.; McFarland, Ross; Vickery, Thad W.; Ray, John P.; Ko, Dennis C.; Zou, Yuxia; Bang, Nguyen D.; Chau, Tran T. H.; Vary, Jay C. (3 February 2012). "Host genotype-specific therapies can optimize the inflammatory response to mycobacterial infections". Cell. 148 (3): 434–446. doi:10.1016/j.cell.2011.12.023. ISSN   1097-4172. PMC   3433720 . PMID   22304914.
  25. ↑ Tobin, David M.; Roca, Francisco J.; Ray, John P.; Ko, Dennis C.; Ramakrishnan, Lalita (2013). "An enzyme that inactivates the inflammatory mediator leukotriene b4 restricts mycobacterial infection". PLOS ONE. 8 (7): e67828. Bibcode:2013PLoSO...867828T. doi: 10.1371/journal.pone.0067828 . ISSN   1932-6203. PMC   3708926 . PMID   23874453.
  26. ↑ Thuong, Nguyen T. T.; Heemskerk, Dorothee; Tram, Trinh T. B.; Thao, Le T. P.; Ramakrishnan, Lalita; Ha, Vu T. N.; Bang, Nguyen D.; Chau, Tran T. H.; Lan, Nguyen H.; Caws, Maxine; Dunstan, Sarah J. (1 April 2017). "Leukotriene A4 Hydrolase Genotype and HIV Infection Influence Intracerebral Inflammation and Survival From Tuberculous Meningitis". The Journal of Infectious Diseases. 215 (7): 1020–1028. doi:10.1093/infdis/jix050. ISSN   1537-6613. PMC   5426373 . PMID   28419368.
  27. ↑ Adams, Kristin N.; Takaki, Kevin; Connolly, Lynn E.; Wiedenhoft, Heather; Winglee, Kathryn; Humbert, Olivier; Edelstein, Paul H.; Cosma, Christine L.; Ramakrishnan, Lalita (1 April 2011). "Drug tolerance in replicating mycobacteria mediated by a macrophage-induced efflux mechanism". Cell. 145 (1): 39–53. doi:10.1016/j.cell.2011.02.022. ISSN   1097-4172. PMC   3117281 . PMID   21376383.
  28. ↑ Madigan, Cressida A.; Cambier, C. J.; Kelly-Scumpia, Kindra M.; Scumpia, Philip O.; Cheng, Tan-Yun; Zailaa, Joseph; Bloom, Barry R.; Moody, D. Branch; Smale, Stephen T.; Sagasti, Alvaro; Modlin, Robert L. (24 August 2017). "A Macrophage Response to Mycobacterium leprae Phenolic Glycolipid Initiates Nerve Damage in Leprosy". Cell. 170 (5): 973–985.e10. doi:10.1016/j.cell.2017.07.030. ISSN   1097-4172. PMC   5848073 . PMID   28841420.
  29. ↑ Behr, Marcel A.; Edelstein, Paul H.; Ramakrishnan, Lalita (23 August 2018). "Revisiting the timetable of tuberculosis". BMJ (Clinical Research Ed.). 362: k2738. doi:10.1136/bmj.k2738. ISSN   1756-1833. PMC   6105930 . PMID   30139910.
  30. ↑ Behr, Marcel A.; Edelstein, Paul H.; Ramakrishnan, Lalita (2024). "Rethinking the burden of latent tuberculosis to reprioritize research". Nature Microbiology. 9 (5): 1157–1158. doi:10.1038/s41564-024-01683-0. PMID   38671272.
  31. ↑ Maugh II, Thomas H. (17 May 2011). "Shorter treatment found for latent tuberculosis". Los Angeles Times. Although TB control measures in the United States have brought the incidence of the disease to an all-time low of 11,181 cases in 2010, it is estimated that at least 11 million Americans have latent TB. 'The 11 million Americans with latent TB represent a ticking time bomb,' Dr. Kenneth Castro, director of the Centers for Disease Control and Prevention's division of tuberculosis elimination, said at a news conference Monday. 'They're the source of future TB cases.'
  32. ↑ Wu, Katherine J. (2023). "A big misconception about the world's greatest infectious killer". The Atlantic.
  33. ↑ "National Academy of Sciences Elects New Members for 2015". India West. Retrieved 24 April 2016.
  34. ↑ "Lalita Ramakrishnan". royalsociety.org.
  35. ↑ "New Fellows for 2018 announced". acmedsci.ac.uk. Academy of Medical Sciences.
  36. ↑ Anon (2018). "Distinguished scientists elected as Fellows and Foreign Members of the Royal Society". Royal Society . Retrieved 10 May 2018.

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