Nafees Ahmad

Nafees Ahmad

Professor, Immunobiology
Professor, Applied BioSciences - GIDP
Member of the Graduate Faculty
Professor, BIO5 Institute
Primary Department
(520) 626-7022

Research Interest

Nafees Ahmad, Ph.D., Professor of ImmunobiologyResearch Interests:1. Molecular mechanisms of HIV-1 vertical transmission2. Molecular mechanisms of HIV-1 pathogenesis in infants and children 3. Molecular mechanisms of HIV-1 infection in immature and mature mononuclear cells4. Identification and characterization of cellular factors involved in HIV-1 replication in immature and mature mononuclear cells5. Biological activity of anti-HIV compoundsThe main focus of my laboratory is understanding the molecular mechanisms of human immunodeficiency virus type 1 (HIV-1) mother-to-infant transmission and pathogenesis of pediatric AIDS (HIV-1 infection in children). Areas of investigation include: Molecular and biological characterization of HIV-1 isolates involved in maternal-fetal transmission; Genetic variability of HIV-1 following mother-to-infant transmission; Viral determinants, including viral heterogeneity, functional conservation/divergence of various HIV-1 genes, presence/absence of motifs in HIV-1 genes, replication efficiency, cell tropism, and cytopathic effects associated with HIV-1 maternal-fetal transmission; Viral and host factors associated with HIV-1 evolution, replication, pathogenesis and disease progression in infected infants and children; Molecular mechanisms of HIV-1 infection in immature and mature mononuclear cells; Kinetics of HIV-1 replication in immature hosts (infants) primary lymphocytes and monocytes/macrophages; Mechanisms of HIV-1 infection in immature and mature mononuclear cells, including entry and post-entry events, HIV-1 gene expression and T-cell development, Biological activity of anti-HIV compounds in tissue culture system of T-cell lines, primary lymphocytes and monocytes/macrophages and receptor/coreceptor cell lines, Characterization of cellular factors in immature and mature mononuclear cells that may influence HIV replication differentially.


Ahmad, N. (2017). Characterization of HIV quasispecies in virologically controlled HIV-infected older patients receiving antiretroviral therapy. Journal of Virology.
Ahmad, N. (2017). Recovery of HIV-mediated Immune Aging of T Cells in Virologically Controlled HIV-Infected Aging Patients on Antiretroviral Therapy. Proceedings of National Academy of Sciences.
Bashyal, B. P., Wellensiek, B. P., Ramakrishnan, R., Faeth, S. H., Ahmad, N., & Gunatilaka, A. A. (2014). Altertoxins with potent anti-HIV activity from Alternaria tenuissima QUE1Se, a fungal endophyte of Quercus emoryi. Bioorganic & medicinal chemistry, 22(21), 6112-6.
BIO5 Collaborators
Nafees Ahmad, Leslie Gunatilaka

Screening of a small library of natural product extracts derived from endophytic fungi of the Sonoran desert plants in a cell-based anti-HIV assay involving T-cells infected with the HIV-1 virus identified the EtOAc extract of a fermentation broth of Alternaria tenuissima QUE1Se inhabiting the stem tissue of Quercus emoryi as a promising candidate for further investigation. Bioactivity-guided fractionation of this extract led to the isolation and identification of two new metabolites, altertoxins V (1) and VI (2) together with the known compounds, altertoxins I (3), II (4), and III (5). The structures of 1 and 2 were determined by detailed spectroscopic analysis and those of 3-5 were established by comparison with reported data. When tested in our cell-based assay at concentrations insignificantly toxic to T-cells, altertoxins V (1), I (3), II (4), and III (5) completely inhibited replication of the HIV-1 virus at concentrations of 0.50, 2.20, 0.30, and 1.50 μM, respectively. Our findings suggest that the epoxyperylene structural scaffold in altertoxins may be manipulated to produce potent anti-HIV therapeutics.

Ahmad, N. (2017). HIV infection and bone abnormalities. The Open Orthopaedics Journal, 11, 777-784.
Badowski, M., Shultz, C. L., Eason, Y., Ahmad, N., & Harris, D. T. (2014). The influence of intrinsic and extrinsic factors on immune system aging. Immunobiology, 219(6), 482-5.

Sex and age-matched wild-type and TCR transgenic mice were infected with cytomegalovirus (CMV) at 6 months of age and followed for 12 additional months to examine aging of the immune system. It was found that viral infection of C57Bl/6 mice resulted in accelerated aging of the immune system as shown by a loss of CD8(+)28(+) cells and an accumulation of KLRG1(+) T cells. CMV infection of OT-1 transgenic mice had no influence on immune aging of these mice which nonetheless demonstrated an accumulation of CD8(+)28(-) and KLRG1(+) T cells with time. CD4(+) T cells were unaffected in either strain of mice. Thus, immunological aging was found to be due to both cell-intrinsic and cell-extrinsic factors. Persistent viral infections may accelerate immunological aging but consideration must be given to individual variation in the aging process.