Dr. Al-Ghazali works at University College London. He obtained his PhD from the University of Sheffield in 2021 in the Department of Biomedical Science. He also worked as a postdoctoral research associate at the same university for two years.

The aged populations are generally more susceptible to infections. ElGhazaly's work uncovers methods by which a bacterium, known as Salmonella can promote premature ageing (senescence) within our cells in order to manipulate the host and establish infections. Aged cells tend to secrete an unusual profile of proteins depending on the stress. In his project, he examines the typhoid toxin, which is secreted by Salmonella Typhi to induce senescence. The project highlights how one bacterium, using one virulence factor can modulate our tissue microenvironment to establish a deadly infection.

ElGhazaly is very interested in aging research. Aging iscurrently not recognised as a disease, although it underlies many pathologies, including Alzheimer's, cardiovascular diseases, and infections. Whilst a lot of people would like to achieve immortality, the main priority in aging research is to extend healthy lifespan - i.e. reach an old age without the suffering of many diseases. ElGhazaly would like to establish his career in aging research in order to understand how we can promote healthy aging. In Sheffield, he investigated DNA damage and senescence host responses to the typhoid toxin of Salmonella Typhi, a bacterial pathogen that causes acute typhoid fever, chronic infections, and gallbladder carcinoma in low- and middle-income countries. His work was published in Nature Communications and Cell Reports. Since he developed a keen interest in host-pathogen interactions he decided to explore virology as a new research avenue. He is now working on understanding how our innate immunity functions against viruses by using HIV as a tool to understand the underlying mechanisms of innate immune sensing and evasion. His research particularly focuses on HIV accessory proteins Vpr/Vpx and their role in regulating host epigenetics in innate immune contexts.