Timares L                
Associate Professor

Hematology & Oncology
CFAR Center For AIDS Research

Campus Address:


Mailing Address:
1720 2nd Avenue South, LHRB 613A
Birmingham, AL 35294-3300

(205) 975-4157

E-mail Address:

Departmental Affiliation(s):
Primary: Medicine, Hematology/Oncology


Laura Timares is an Associate Professor in the Division of Hematology-Oncology in the School of Medicine who recently transferred (2017) from Department of Dermatology at the University of Alabama at Birmingham (UAB). She obtained both her undergraduate (BA Biology) and graduate degrees (Ph.D., Microbiology and Immunology School of Medicine) from the University of California at Los Angeles (UCLA). Her postdoctoral training at the California Institute of Technology (1991-1993) and Cedars Sinai Medical Center/UCLA (1993-1996) developed her interest in genetic engineering of transplantable cells and their translational application in treating liver diseases and diabetes.  After joining the University of Texas, Southwestern Medical Center at Dallas (UTSW) (1996), she became faculty in the Department of Medicine in the Center for Biomedical Inventions.  There she studied the role of transfected dendritic cells in skin generated by topical genetic immunization and characterized their role as inducers of vaccine immunity.  She was recruited to the University of Alabama in Birmingham (UAB) in the Department of Dermatology (1999) where she continued her research on cutaneous immunology with a focus on the development of prophylactic skin cancer vaccines. In the Division of Heme-Onc, she is currently applying her expertise toward understanding the role of human mucosal immunology in heterosexual HIV transmission.

Research/Interest Description:

To address the urgent need to halt the spread of heterosexual HIV transmission, we must understand how HIV infects immune cells that are normally present in the female reproductive tract.  Drs. John Kappes and Christina Oschenbauer and colleagues revealed that blood-derived monocyte/macrophages engulf not only dead and dying T cells, but also viable T cells that are infected with HIV (but not uninfected viable T cells). This was shown to be dependent on the surface expression of the HIV envelope on T cells.  Furthermore, a significant portion of engulfed infected T cells remained viable over days, during which HIV replicated in the T cell and spread to the macrophage cytoplasm.  We hypothesize that macrophages in the female reproductive tract are also capable of engulfing infected T cells during the earliest phases of HIV infection. Normally,  T cells and macrophages are present as resident cells in the stroma that underlies the transitional epithelium of the cervix, a site that may be a favored portal for heterosexual HIV transmission. Thus, we are interested in knowing whether engulfment of HIV-infected T cells is attributed to a certain subset of tissue resident macrophages, whether the HIV-infected T cell type impacts engulfment, whether this process represents an early form of HIV immune evasion, whether cell-to cell transmission efficiency of surrounding mucosal T cells is enhanced, and whether this process plays an important role in generating cellular reservoirs of hidden HIV.  Both molecular and cellular techniques / assays are employed to elucidate early events of HIV infection. Informative panels of HIV-reporter viruses, representing a variety of relevant infectious virus strains (generated in the Kappes-Oschenbaur lab) are used to investigate infection in ex-vivo culture systems and purified cell populations isolated from remnant tissues of human female reproductive tract surgeries.     

Publications: See a listing of publications on PubMed , a service of the National Library of Medicine.