Sunil Kumar Ahuja

Last updated
Sunil K. Ahuja
SunilAhujaMD.jpg
Born13 March 1961
Education
Scientific career
Fields Genetics, immunology, molecular biology
Institutions

Sunil Kumar Ahuja (born March 13, 1961) [1] is a professor of Medicine, Microbiology, Immunology & Biochemistry at the University of Texas Health Science Center at San Antonio and an expert on the role of immunogenetics on HIV pathogenesis. Ahuja is also the Director of the Veterans Administration Research Center for AIDS and HIV-1 Infection. His most recent work, first published in the 2005 issue of Science, involves the ethnic group-specific role of CCR5 haplotype and CCL3L1 gene copy number on the progression of HIV to AIDS. [2]

Contents

Education

Sunil Ahuja received his medical degree from the Armed Forces Medical College India in 1983. [3] Following work towards a M.Sc. degree from the University of Alberta in Canada, Ahuja had his internship and residency at the SUNY Health Science Center at Brooklyn.

Publications

Sunil Ahuja's research has been published in many peer-reviewed journals, including Science, The New England Journal of Medicine, Nature Medicine, Nature Immunology and Proceedings of the National Academy of Sciences .

Honors

Ahuja has been the recipient of many honors and awards, including being named in 2001 the Elizabeth Glaser Scientist and the Burroughs Wellcome Clinical Scientist in Translational Research. [4] [5] In 2005 he also was the recipient of the MERIT award from the National Institutes of Health. Less than 5% of NIH-funded researchers receive this award. [5]

In February 2008, Ahuja was listed as one of "35 People Who Will Shape Our Future" by Texas Monthly magazine. [3]

Scientific disagreements

Some of Sunil Ahuja's work has been questioned by the scientific community. In July 2008, Ahuja's group reported that the DARC gene influenced HIV/AIDS susceptibility. [6] This finding was then questioned by four other groups of scientists, reporting the failure to replicate. [7] [8] [9] [10] Ahuja's group responded in the same issue of Cell Host & Microbe , [11] and also in a subsequent study published in 2011. [12]

Related Research Articles

<span class="mw-page-title-main">HIV</span> Human retrovirus, cause of AIDS

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, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.

<span class="mw-page-title-main">Immune system</span> Biological system protecting an organism against disease

The immune system is a network of biological processes that protects an organism from diseases. It detects and responds to a wide variety of pathogens, from viruses to parasitic worms, as well as cancer cells and objects such as wood splinters, distinguishing them from the organism's own healthy tissue. Many species have two major subsystems of the immune system. The innate immune system provides a preconfigured response to broad groups of situations and stimuli. The adaptive immune system provides a tailored response to each stimulus by learning to recognize molecules it has previously encountered. Both use molecules and cells to perform their functions.

<span class="mw-page-title-main">Inflammation</span> Physical effects resulting from activation of the immune system

Inflammation is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants, and is a protective response involving immune cells, blood vessels, and molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and initiate tissue repair.

<span class="mw-page-title-main">T helper cell</span> Type of immune cell

The T helper cells (Th cells), also known as CD4+ cells or CD4-positive cells, are a type of T cell that play an important role in the adaptive immune system. They aid the activity of other immune cells by releasing cytokines. They are considered essential in B cell antibody class switching, breaking cross-tolerance in dendritic cells, in the activation and growth of cytotoxic T cells, and in maximizing bactericidal activity of phagocytes such as macrophages and neutrophils. CD4+ cells are mature Th cells that express the surface protein CD4. Genetic variation in regulatory elements expressed by CD4+ cells determines susceptibility to a broad class of autoimmune diseases.

<span class="mw-page-title-main">Duffy antigen system</span> Human blood group classification

Duffy antigen/chemokine receptor (DARC), also known as Fy glycoprotein (FY) or CD234, is a protein that in humans is encoded by the ACKR1 gene.

<span class="mw-page-title-main">Chemokine</span> Small cytokines or signaling proteins secreted by cells

Chemokines, or chemotactic cytokines, are a family of small cytokines or signaling proteins secreted by cells that induce directional movement of leukocytes, as well as other cell types, including endothelial and epithelial cells. In addition to playing a major role in the activation of host immune responses, chemokines are important for biological processes, including morphogenesis and wound healing, as well as in the pathogenesis of diseases like cancers.

<span class="mw-page-title-main">CCR5</span> Immune system protein

C-C chemokine receptor type 5, also known as CCR5 or CD195, is a protein on the surface of white blood cells that is involved in the immune system as it acts as a receptor for chemokines.

<span class="mw-page-title-main">CD4</span> Marker on immune cells

In molecular biology, CD4 is a glycoprotein that serves as a co-receptor for the T-cell receptor (TCR). CD4 is found on the surface of immune cells such as T helper cells, monocytes, macrophages, and dendritic cells. It was discovered in the late 1970s and was originally known as leu-3 and T4 before being named CD4 in 1984. In humans, the CD4 protein is encoded by the CD4 gene.

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.

<span class="mw-page-title-main">CXCR4</span> Protein

C-X-C chemokine receptor type 4 (CXCR-4) also known as fusin or CD184 is a protein that in humans is encoded by the CXCR4 gene. The protein is a CXC chemokine receptor.

Microfold cells are found in the gut-associated lymphoid tissue (GALT) of the Peyer's patches in the small intestine, and in the mucosa-associated lymphoid tissue (MALT) of other parts of the gastrointestinal tract. These cells are known to initiate mucosal immunity responses on the apical membrane of the M cells and allow for transport of microbes and particles across the epithelial cell layer from the gut lumen to the lamina propria where interactions with immune cells can take place.

Chemokine ligands 4 previously known as macrophage inflammatory protein (MIP-1β), is a protein which in humans is encoded by the CCL4 gene. CCL4 belongs to a cluster of genes located on 17q11-q21 of the chromosomal region. Identification and localization of the gene on the chromosome 17 was in 1990 although the discovery of MIP-1 was initiated in 1988 with the purification of a protein doublet corresponding to inflammatory activity from supernatant of endotoxin-stimulated murine macrophages. At that time, it was also named as "macrophage inflammatory protein-1" (MIP-1) due to its inflammatory properties.

<span class="mw-page-title-main">CCL8</span> Mammalian protein found in Homo sapiens

Chemokine ligand 8 (CCL8), also known as monocyte chemoattractant protein 2 (MCP2), is a protein that in humans is encoded by the CCL8 gene.

<span class="mw-page-title-main">CX3C motif chemokine receptor 1</span> Protein-coding gene in the species Homo sapiens

CX3C motif chemokine receptor 1 (CX3CR1), also known as the fractalkine receptor or G-protein coupled receptor 13 (GPR13), is a transmembrane protein of the G protein-coupled receptor 1 (GPCR1) family and the only known member of the CX3C chemokine receptor subfamily.

<span class="mw-page-title-main">CCR2</span> Mammalian protein found in Homo sapiens

C-C chemokine receptor type 2 (CCR2 or CD192 is a protein that in humans is encoded by the CCR2 gene. CCR2 is a CC chemokine receptor.

<span class="mw-page-title-main">CCR3 (gene)</span>

C-C chemokine receptor type 3 is a protein that in humans is encoded by the CCR3 gene.

<span class="mw-page-title-main">CXCR6</span>

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.

<span class="mw-page-title-main">CCL3L1</span> Protein-coding gene in the species Homo sapiens

Chemokine ligand 3-like 1, also known as CCL3L1, is a protein which in humans is encoded by the CCL3L1 gene.

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

HIV is commonly transmitted via unprotected sexual activity, blood transfusions, hypodermic needles, and from mother to child. Upon acquisition of the virus, the virus replicates inside and kills T helper cells, which are required for almost all adaptive immune responses. There is an initial period of influenza-like illness, and then a latent, asymptomatic phase. When the CD4 lymphocyte count falls below 200 cells/ml of blood, the HIV host has progressed to AIDS, a condition characterized by deficiency in cell-mediated immunity and the resulting increased susceptibility to opportunistic infections and certain forms of cancer.

A small proportion of humans show partial or apparently complete innate resistance to HIV, the virus that causes AIDS. The main mechanism is a mutation of the gene encoding CCR5, which acts as a co-receptor for HIV. It is estimated that the proportion of people with some form of resistance to HIV is under 10%.

References

  1. "Dr. Ahuja, Sunil K, MD". Archived from the original on 2012-09-05. Retrieved 2008-05-07.
  2. Gonzalez, Enrique; Kulkarni, Hemant; Bolivar, Hector; Mangano, Andrea; Sanchez, Racquel; Catano, Gabriel; Nibbs, Robert J.; Freedman, Barry I.; Quinones, Marlon P.; Bamshad, Michael J.; Murthy, Krishna K.; Rovin, Brad H.; Bradley, William; Clark, Robert A.; Anderson, Stephanie A.; O'Connell, Robert J.; Agan, Brian K.; Ahuja, Seema S.; Bologna, Rosa; Sen, Luisa; Dolan, Matthew J.; Ahuja, Sunil K. (6 January 2005). "The Influence of CCL3L1 Gene-Containing Segmental Duplications on HIV-1/AIDS Susceptibility". Science. 307 (5714): 1434–1440. Bibcode:2005Sci...307.1434G. doi:10.1126/science.1101160. PMID   15637236. S2CID   8815153.
  3. 1 2 "Sunil K. Ahuja: Texas Monthly February 2008". Archived from the original on 2008-07-04. Retrieved 2008-04-12.
  4. "Awards". www.uthscsa.edu. Archived from the original on 17 June 2004. Retrieved 12 August 2017.
  5. 1 2 "News - UT Health Science Center San Antonio - UT Health Science Center News". UT Health Science Center News. Retrieved 12 August 2017.
  6. He W, Neil S, Kulkarni H, Wright E, Agan BK, Marconi VC, Dolan MJ, Weiss RA, Ahuja SK (2008). "Duffy Antigen Receptor for Chemokines Mediates trans-Infection of HIV-1 from Red Blood Cells to Target Cells and Affects HIV-AIDS Susceptibility". Cell Host Microbe. 4 (1): 52–62. doi:10.1016/j.chom.2008.06.002. PMC   2562426 . PMID   18621010.
  7. Walley NM, Julg B, Dickson SP, et al. (2009). "The Duffy Antigen Receptor for Chemokines Null Promoter Variant Does Not Influence HIV-1 Acquisition Or Disease Progression". Cell Host Microbe. 5 (5): 408–410. doi:10.1016/j.chom.2009.04.011. PMC   2720554 . PMID   19454339.
  8. Winkler CA, An P, Johnson R, Nelson GW, Kirk G (2009). "Expression of Duffy antigen receptor for chemokines (DARC) has no effect on HIV-1 acquisition or progression to AIDS in African Americans". Cell Host Microbe. 5 (5): 411–413. doi:10.1016/j.chom.2009.04.010. PMC   7241868 . PMID   19454340.
  9. Julg B, Reddy S, van der Stok M, et al. (2009). "Lack of Duffy Antigen Receptor for Chemokines: No Influence on HIV Disease Progression in an African Treatment Naïve Population". Cell Host Microbe. 5 (5): 413–415. doi:10.1016/j.chom.2009.04.009. PMC   2749504 . PMID   19454341.
  10. Horne KC, Li X, Jacobson LP, et al. (2009). "Duffy antigen polymorphisms do not alter progression of HIV in African Americans in the MACS cohort". Cell Host Microbe. 5 (5): 415–417. doi: 10.1016/j.chom.2009.04.013 . PMID   19454342.
  11. He, Weijing; Marconi, Vincent C.; Castiblanco, John; Kulkarni, Hemant; Clark, Robert A.; Dolan, Matthew J.; Weiss, Robin A.; Ahuja, Sunil K. (2009). "Author reply". Cell Host Microbe. 5 (5): 418–419. doi: 10.1016/j.chom.2009.05.007 .
  12. Ramsuran, V; Kulkarni, H; He, W; Mlisana, K; Wright, EJ; Werner, L; Castiblanco, J; Dhanda, R; Le, T; Dolan, MJ; Guan, W; Weiss, RA; Clark, RA; Karim, SS; Ahuja, SK; Ndung'u, T (May 2011). "Duffy-null-associated low neutrophil counts influence HIV-1 susceptibility in high-risk South African black women". Clinical Infectious Diseases. 52 (10): 1248–56. doi:10.1093/cid/cir119. PMC   3115278 . PMID   21507922.