Thumbi Ndung’u is a Kenyan-born HIV/AIDS researcher. He is the deputy director (Science) and a Max Planck Research Group Leader at the Africa Health Research Institute (AHRI) in Durban, South Africa. He is Professor of Infectious Diseases in the Division of Immunity and Infection, University College London. He is Professor and Victor Daitz Chair in HIV/TB Research and Scientific Director of the HIV Pathogenesis Programme (HPP) at the Nelson R. Mandela School of Medicine, University of KwaZulu-Natal. He holds the South African Research Chair in Systems Biology of HIV/AIDS. He is an adjunct professor of Immunology and Infectious Diseases at the Harvard T.H. Chan School of Public Health. He is the Programme Director of the Sub-Saharan African Network for TB/HIV Research Excellence (SANTHE), a research and capacity building initiative funded by the African Academy of Sciences and the Wellcome Trust.
Ndung’u attended Gathugu Primary School in Kiambu, Kenya and Nyeri High School, Nyeri, Kenya. He graduated with a Bachelor of Veterinary Medicine degree from the University of Nairobi, Kenya, and obtained a PhD in Biological Sciences in Public Health from Harvard University, United States. As a graduate student, he worked with Max Essex at Harvard. He was also a Postdoctoral Fellow in Virology at Harvard Medical School. He is a member of the Academy of Science of South Africa (ASSAf) and a fellow of the African Academy of Sciences (AAS). He has been a member of the External Advisory Board of the HIV Vaccine Trials Network (HVTN), a member of the Scientific Advisory Committee of the Cape Town HVTN Immunology Laboratory (CHIL), a member of the Scientific Advisory Panel of the Poliomyelitis Research Foundation and a member of the advisory board of the Global Health and Vaccination Research Programme (GLOBVAC), The Research Council of Norway. He was co-chair of the Young and Early Career Investigators Committee (YECIC) of the Global HIV Vaccine Enterprise from 2008 to 2010 that worked on the Enterprise's five-year strategic plan.
Ndung’u was the first scientist to clone infectious HIV subtype C and has received numerous awards for his scientific and scholarly contributions. The awards include:
His research interests are host-pathogen interactions, particularly immune mechanisms of HIV and TB control. He has co-authored more than 200 manuscripts in peer-reviewed journals. He has made seminal contributions on our understanding of how virus-host interactions lead to immune-mediated mechanisms of HIV control, which has implications for immune-based prophylactic and therapeutic strategies against the virus. He has received grant funding from the South African National Research Foundation, the South African Medical Research Council, the Bill and Melinda Gates Foundation, the National Institutes of Health, the Howard Hughes Medical Institute, the European Union, the African Academy of Sciences and the Wellcome Trust among others. He is leading a multidisciplinary team of researchers working in the fields of HIV and TB immunopathogenesis, vaccine development and immune-based HIV functional cure strategies. He has special interest in capacity building for biomedical research in Africa.
The human immunodeficiency viruses (HIV) are two species of Lentivirus that infect humans. Over time, they cause acquired immunodeficiency syndrome (AIDS), a condition in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. Without treatment, the average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.
Simian immunodeficiency virus (SIV) is a species of retrovirus that cause persistent infections in at least 45 species of non-human primates. Based on analysis of strains found in four species of monkeys from Bioko Island, which was isolated from the mainland by rising sea levels about 11,000 years ago, it has been concluded that SIV has been present in monkeys and apes for at least 32,000 years, and probably much longer.
Defective interfering particles (DIPs), also known as defective interfering viruses, are spontaneously generated virus mutants in which a critical portion of the particle's genome has been lost due to defective replication or non-homologous recombination. The mechanism of their formation is presumed to be as a result of template-switching during replication of the viral genome, although non-replicative mechanisms involving direct ligation of genomic RNA fragments have also been proposed. DIPs are derived from and associated with their parent virus, and particles are classed as DIPs if they are rendered non-infectious due to at least one essential gene of the virus being lost or severely damaged as a result of the defection. A DIP can usually still penetrate host cells, but requires another fully functional virus particle to co-infect a cell with it, in order to provide the lost factors.
Feline immunodeficiency virus (FIV) is a Lentivirus that affects cats worldwide, with 2.5% to 4.4% of felines being infected.
Following infection with HIV-1, the rate of clinical disease progression varies between individuals. Factors such as host susceptibility, genetics and immune function, health care and co-infections as well as viral genetic variability may affect the rate of progression to the point of needing to take medication in order not to develop AIDS.
The genome and proteins of HIV (human immunodeficiency virus) have been the subject of extensive research since the discovery of the virus in 1983. "In the search for the causative agent, it was initially believed that the virus was a form of the Human T-cell leukemia virus (HTLV), which was known at the time to affect the human immune system and cause certain leukemias. However, researchers at the Pasteur Institute in Paris isolated a previously unknown and genetically distinct retrovirus in patients with AIDS which was later named HIV." Each virion comprises a viral envelope and associated matrix enclosing a capsid, which itself encloses two copies of the single-stranded RNA genome and several enzymes. The discovery of the virus itself occurred two years following the report of the first major cases of AIDS-associated illnesses.
The murine leukemia viruses are retroviruses named for their ability to cause cancer in murine (mouse) hosts. Some MLVs may infect other vertebrates. MLVs include both exogenous and endogenous viruses. Replicating MLVs have a positive sense, single-stranded RNA (ssRNA) genome that replicates through a DNA intermediate via the process of reverse transcription.
HIV superinfection is a condition in which a person with an established human immunodeficiency virus infection acquires a second strain of HIV, often of a different subtype. These can form a recombinant strain that co-exists with the strain from the initial infection, as well from reinfection with a new virus strain, and may cause more rapid disease progression or carry multiple resistances to certain HIV medications.
HIV-1 protease or PR is a retroviral aspartyl protease (retropepsin), an enzyme involved with peptide bond hydrolysis in retroviruses, that is essential for the life-cycle of HIV, the retrovirus that causes AIDS. HIV-1 PR cleaves newly synthesized polyproteins at nine cleavage sites to create the mature protein components of an HIV virion, the infectious form of a virus outside of the host cell. Without effective HIV-1 PR, HIV virions remain uninfectious.
HLA-A*02 (A*02) is a human leukocyte antigen serotype within the HLA-A serotype group. The serotype is determined by the antibody recognition of the α2 domain of the HLA-A α-chain. For A*02, the α chain is encoded by the HLA-A*02 gene and the β chain is encoded by the B2M locus. In 2010 the World Health Organization Naming Committee for Factors of the HLA System revised the nomenclature for HLAs. Before this revision, HLA-A*02 was also referred to as HLA-A2, HLA-A02, and HLA-A*2.
C-X-C chemokine receptor type 6 is a protein that in humans is encoded by the CXCR6 gene. CXCR6 has also recently been designated CD186.
The subtypes of HIV include two main subtypes, known as HIV type 1 (HIV-1) and HIV type 2 (HIV-2). These subtypes have distinct genetic differences and are associated with different epidemiological patterns and clinical characteristics.
The primate T-lymphotropic viruses (PTLVs) are a group of retroviruses that infect primates, using their lymphocytes to reproduce. The ones that infect humans are known as human T-lymphotropic virus (HTLV), and the ones that infect Old World monkeys are called simian T-lymphotropic viruses (STLVs). PTLVs are named for their ability to cause adult T-cell leukemia/lymphoma, but in the case of HTLV-1 it can also cause a demyelinating disease called tropical spastic paraparesis. On the other hand, newer PTLVs are simply placed into the group by similarity and their connection to human disease remains unclear.
Stuart C. Ray is an American physician. He is Vice Chair of Medicine for Data Integrity and Analytics, Associate Director of the Infectious Diseases Fellowship Training Program at the Johns Hopkins School of Medicine, and a Professor in the Department of Medicine, Division of Infectious Diseases. Ray also holds appointments in Viral Oncology and the Division of Health Sciences Informatics. He is affiliated with the Institute for Computational Medicine at Johns Hopkins and is licensed to practice medicine in Maryland.
Anna-Lise WilliamsonMASSAf is a Professor of Virology at the University of Cape Town. Williamson obtained her PhD from the University of the Witwatersrand in 1985. Her area of expertise is human papillomavirus, but is also known on an international level for her work in developing vaccines for HIV. These vaccines have been introduce in phase 1 of clinical trial. Williamson has published more than 120 papers.
M. Juliana “Julie” McElrath is a senior vice president and director of the vaccine and infection disease division at Fred Hutchinson Cancer Research Center and the principal investigator of the HIV Vaccine Trials Network Laboratory Center in Seattle, Washington. She is also a professor at the University of Washington.
Bruce D. Walker is an American physician and scientist whose infectious disease research has produced many findings regarding HIV/AIDS. He became interested in studying HIV/AIDS after practicing on the front lines of the epidemic in the early 1980s, prior to the identification of HIV as the etiologic agent and prior to the availability of viable treatment options.
Susan Zolla-Pazner is an American research scientist who is a Professor of Medicine in the Division of Infectious Diseases and the Department of Microbiology at Mount Sinai School of Medicine and a guest investigator in the Laboratory of Molecular Immunology at The Rockefeller University, both in New York City. Zolla-Pazner's work has focused on how the immune system responds to the human immunodeficiency virus (HIV) and, in particular, how antibodies against the viral envelope develop in the course of infection.
Eric Murnane Poeschla is an American infectious disease physician, virologist, and innate immunologist.
Catherine Blish is a translational immunologist and professor at Stanford University. Her lab works on clinical immunology and focuses primarily on the role of the innate immune system in fighting infectious diseases like HIV, dengue fever, and influenza. Her immune cell biology work characterizes the biology and action of Natural Killer (NK) cells and macrophages.
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