Full Name
Mohammed Eltalkhawy
Job Title
Ph.D. student
Kumamoto University, Joint Research Center for Human Retrovirus Infection
City (Work Address)
State/Province/County (Work Address)
Speaker Bio
• Ph.D. graduate student, Kumamoto University, Joint Research Center for Human Retrovirus Infection, Japan.
• Assistant Lecturer of Microbiology, Medical Research Institute, Alexandria University, Egypt
• Master’s degree in Microbiology, Medical Research Institute, Alexandria University, Egypt 2017.
• MBBCh, Faculty of Medicine, Alexandria University, Egypt 2011.
Scope of Research Interest: Viral pathogenesis, especially Emerging viruses as HIV-1, SARS CoV-2, ZKV and Ebola virus.

• Hiyoshi M, Takahashi N, Eltalkhawy YM, Noyori O, Lotfi S, Panaampon J, Okada S, Tanaka Y, Ueno T, Fujisawa JI, Sato Y. M-Sec induced by HTLV-1 mediates an efficient viral transmission. PLoS Pathogens. 2021 Nov 29;17(11):e1010126.
• Naga IS, Elsawaf GE, Elzalabany M, Eltalkhawy MY, Kader O. Human coronavirus OC43 and other respiratory viruses from acute respiratory infections of Egyptian children. Acta microbiologica et immunologica Hungarica. 2020 Jun;67(2):112-9.
Abstract Title
A novel macrophage model to study interaction with HIV-1
Abstract Summary
Recent studies have revealed that macrophages developed at the embryonic stage are still present in adult tissues because they have a potent proliferative capacity. Thus, to fully understand the role and significance of macrophages in HIV-1 infection, not only the non-proliferating MDMs but also another model that mimics the proliferating macrophages is important. In this study, we show that iPS-derived immortalized myeloid cell line (iPS-ML; Haruta M et al, Gene Ther 2013) is a useful model. iPS-ML stably proliferated in a cytokine-dependent manner and was phenotypically and functionally fully differentiated macrophages. In fact, iPS-ML cells shared many infection-related phenotypes with MDMs, such as the formation of tunneling nanotubes, enhanced cell motility, and up-regulation of several inhibitory factors. MDMs and iPS-ML exhibited differences in phenotypes in which cell cycling is critical. SAMHD1 loses its HIV-1 restrictive activity when phosphorylated by cell cycling. Vpr and Vif cause cell cycle arrest and thereby maximize viral gene expression. Consistent with this, the replication of mutant viruses lacking Vpr or Vif was more severely impaired in iPS-ML. Also, the appearance of defective proviruses, such as those with large internal deletion, was more rapid in iPS-ML. Interestingly, the suppression of viral gene expression by latency-promoting agents, filgotinib, spironolactone, and mycophenolic acid, was more obvious in iPS-ML. Collectively, HIV-1-related phenotypes of iPS-ML are overlapping but not identical with those of MDMs. The parallel use of MDMs and iPS-ML may recapitulate some of the heterogeneity of tissue-resident macrophages and help to understand the HIV-1 Kinetics in proliferating macrophages
Mohammed Eltalkhawy