Ghalib Alkhatib, PhD

Chair, Department of Basic Sciences & Professor of Microbiology

Phone: (916) 686-7944

Ghalib Alkhatib, PhD


  • PhD in Microbiology and Immunology, McGill University, Montreal, Canada
  • B.S. in Biology/Microbiology, Pahlavi University, Shiraz, Iran


Dr. Alkhatib obtained a Ph.D. in Molecular Virology from McGill University in Montreal, Canada in 1989. He completed his postdoctoral work at the Mount Sinai Hospital Research Institute in Toronto, Canada where his research focused on the molecular immunology of natural killer (NK) cells. Subsequently, Dr. Alkhatib served as Visiting Fellow in the Laboratory of Viral Diseases at the National Institutes of Health in Bethesda, Maryland from 1995 to 1998. During his fellowship, he identified and characterized CCR5 as the coreceptor for the macrophage-tropic (M-tropic/R5) HIV-1 isolates. As a result of this groundbreaking research, CCR5 is now the target for the development of drugs that block HIV-1 infection. Dr. Alkhatib has held several academic positions, including Assistant and Associate Professor in the Department of Microbiology and Immunology at the Indiana University School of Medicine in Indianapolis from 1997 to 2010. Dr. Alkhatib joined the Drug Discovery Division of the Southern Research Institute in June 2012, having previously served since 2010 as Professor in the Department of Biomedical Sciences and Center of Excellence for Infectious Diseases in the Paul L. Foster School of Medicine at Texas Tech University Health Sciences Center in El Paso, Texas. Before joining the California Northstate University College of Medicine Dr. Alkhatib served for 2 years as a Medical Educator and HIV researcher at the New York Institute of Technology College of Osteopathic Medicine.

He joined CNUCOM to take a senior position in research and teaching. He loves teaching Medical Microbiology and applying his research experience in the lectures. He is particularly interested in the challenge of working with the diverse population of Faculty and students at CNUCOM. An important factor that attracted him to work at CNUCOM is the state-of-the-art research facility that is equipped with all he needs to continue his research projects.

Research Interest

Studies in Dr. Alkhatib’s laboratory are focused on the molecular determinants involved in retrovirus infection. The research is directed at understanding how interactions of HIV-1 (AIDS virus) and HTLV-1 (human T cell leukemia virus) envelope glycoproteins with host cell receptors lead to membrane fusion and viral entry. Analyzing the mechanisms of retroviral entry is a key step in the development of anti-viral agents. An active area of our HIV research in focuses on the analysis of naturally occurring mutations in CCR5 in HIV-positive and HIV-negative individuals. Our preliminary data indicate a correlation between point mutations in CCR5 and susceptibility to HIV-1 infection.

We have recently joined the scientific community in analyzing the entry mechanism of the virus that caused the Covid-19 pandemic. A reporter gene activation assay, similar to that used to isolate the HIV Coreceptors, has been modified to analyze the interaction of the SARS-CoV-2 spike glycoprotein with the host receptor system. Several reagents have been developed to map the determinants involved in these interactions.

Honors and Awards

  • McGill University Summer Award, June 1985
  • F.C. Harrison Fellowship, Department of Microbiology and Immunology, McGill University, Montreal, Quebec (1985-1988)
  • Multiple Sclerosis Society of Canada Studentship (1985-1988)
  • Dean's Honor List, McGill University, Montreal (11/1988)
  • Yaphy Welfard Award of Excellence, Department of Microbiology and Immunology, McGill University (1989)
  • NSERC post-doctoral fellowship, Biotechnology Research Institute, National Research Council, Canada (1988-1990)
  • Medical Research Council of Canada (MRC) Post-doctoral Fellowship (1991-1993)
  • The NIH FARE Award for Research Excellence (3/1997)
  • Travel award to attend the 7th Coference on Retroviruses and Opportunistic Infections, San Francsico, CA (2000)
  • Travel award to attend the 9th Coference on Retroviruses and Opportunistic Infections, Seattle, WA (2002)
  • Travel Award (to Jeff Altenburg) to attend the ASM meeting on “Viral Immune Evasion” March 8-12, 2005, Acapulco, Mexico
  • Travel award (to Jeff Altenburg) to attend the 25th Annual American Society for Virology Meeting in Madison, Wisconsin (July 14-19, 2006)
  • Travel award (to my graduate student Jeff Altenburg) to attend the 16th Annual AIDS Meeting, Toronto, Canada (August 13-18, 2006)

Grant Support

  1. American Foundation for AIDS Research (amFAR), Grant #02709-28-RG, $ 72,000. Effective period: 4/1/00-3/31/02. Grant title: Molecular analysis of MDC antiviral activity. Role: PI
  2. 1R21CA98095-01(NIH/NCI); 4/1/2002 – 3/31/2005; $200,000 (Direct costs); Grant Title: Host Cell Determinants in Retroviral Infection. Role: PI
  3. Co-PI, 5U01 AI25859-13 (Joseph Wheat, PI); 1/1/00-12/31/04; NIAID PI Wheat, L. J. Title: Adult ACTG Central Group
  4. Member of a T32 training grant awarded to Dr. Janice Blum, Project Number: 5T32AI060519-07 Title: immunology and infectious diseases, PI: Blum, Janice
  5. Member of a T32 training grant awarded to Dr. Stan Spinola, Project Number: 5T32AI007637-10. Title: Training in sexually transmitted diseases including HIV, PI: Stan Spinola
  6. Grant# 107768-47-RGNT (Co-PI (7.5%FTE); 3/2010-3/2012 ($150,000), PI Lung-Ji Chang (UFL, Gainsville, FL). Grant title: Combination of CCR5∆32 and siRNAs targeting HIV-1 infection
  7. 2R01AI052019-06A2 (Alkhatib, PI); 9/2002-09/01/2015; $250,000/year (Direct costs) Title: Host Cell Factors and AIDS Pathogenesis
  8. U19-AI-109680; NIAID; 3/1/14-2/28/19; Project #4 (Alkhatib, PI) Annual total Costs: $773,573. Title of Project: Identification and characterization of small molecules that target the influenza virus RNA dependent RNA polymerase.
  9. Scored/unfunded: NIH R21 application entitled: “Antiviral activity of a chemokine-like protein”. Reviewed at the AIDS Immunology and Pathogenesis (AIP) Study Section Priority score: 188

Selected Publications

Bashar Alkhatib, Mary Jabari, Shymaa Bilasy, Husni Abdul-Rahman, Kamal Sandhu, Stephen Lai, and Ghalib Alkhatib. 2023. Resistance to Human Immunodeficiency Virus 1 Infection Conferred by a Compound CCR5Δ32 and CCR5 C20S Heterozygote. The Journal of Infectious Diseases, 13 March 2023

Gorry, P, Ahmad, F., Mohl, J., and Alkhatib, G. 2018. Low levels of HIV-1 envelope-mediated fusion are associated with long-term survival of an infected CCR5-/- patient. AIDS, 32(16): 2269-2278.

Qingwen, J., Altenburg, J., Hossain, M. and Alkhatib, G. 2011. Role for the conserved N-terminal cysteines in the anti-chemokine activities by the chemokine-like protein MC148R1 encoded by Molluscum Contagiosum Virus. Virology 417: 449-456

Qingwen, J., Alkhatib, B., Cornetta, K., and Alkhatib, G. 2010. Alternate receptor usage of glucose transporter protein 1 and neuropilin 1 by the human T cell leukemia virus type 1. Virology 396 (2): 203-12

Altenburg, J., Qingwen, J., Alkhatib, B., and Alkhatib, G. 2010. The potent anti-HIV activity of CXCL12γ correlates with efficient binding and internalization of CXCR4. Journal of Virology 84(5): 2563-72

Qingwen Jin, Marsh, J., Kornetta, K., and Alkhatib, G. 2008. Resistance to Human Immunodeficiency Virus Type 1 (HIV-1) generated by Lentivirus vector-mediated delivery of the CCR5Δ32 gene despite detectable expression of the HIV coreceptors. Journal of General Virology 89: 2611-2621.

Agrawal, L., Jin, Q., Meyers, L., Tubiana. R., Theodore, I., and Alkhatib, G. 2007. CCR5Δ32 protein expression and stability are critical for resistance to HIV-1 in vivo. Journal of Virology 81(15): 8041-8049.

Altenburg, J.D., Broxmeyer, H. Jin, Q., Cooper, S., Basu, S. and Alkhatib, G. 2007. A naturally occurring splice variant of CXCL12/stromal cell-derived factor 1 is a potent HIV-1 Inhibitor with weak chemotaxis and cell survival activities. Journal of Virology 81(15): 8140-8148.

Agrawal, L., VanHorn-Ali, Berger, EA and Alkhatib G. 2004. Specific Inhibition of HIV-1 Coreceptor activity by synthetic peptides corresponding to the predicted extracellular loops of CCR5. BLOOD 103(4): 1211-1217.

Alkhatib, G., C. Combadiere, C.C. Boder, Y, Feng, P. Murphy & E.A. Berger. 1996. CCKR5: a RANTES, MIP-1, MIP-1 receptor as a fusion cofactor for Macrophage-Tropic HIV-1. SCIENCE 272: 1955-1958.