Logo for University of Iowa Health Care This logo represents the University of Iowa Health Care

PhD candidate Masoudeh Masoud Bahnamiri successfully defends thesis

Masoudeh Masoud Bahnamiri successfully defends her Ph.D. thesis, "The role of viral protein kinases in herpes simplex virus type 1 nuclear egress" on June 29, 2022. His mentor is Professor Richard Roller, PhD. Masoudeh pictured with mentor. Masoudeh Masoud Bahnamiri and Richard Roller, PhD

About Masoudeh

I was born in the north of Iran, in a green nature beside the Caspian Sea. I grew up as the family's youngest child after my two elder brothers. My childhood was fun reading fiction books, playing in my family's orange orchard with my brothers and cousins, and gathering wild-flower collections to dry and archive. I loved biology from my first years of school, but I wanted to be a musician! However, during high school, I was sure I wanted to pursue science to make a vaccine someday! Meanwhile, I recognized my passion for painting and started to train myself, but later, I was trained by a professional art mentor for several years.

After being accepted in the nationwide exam for university entrance, I chose cell biology for my undergraduate study, where I was introduced more to microbiology. By the time I graduated with my bachelor's degree, I was sure I wanted to pursue microbiology as my higher degree. After a short master's degree in Microbiology at Shahid Beheshti University in Iran, which mainly focused on pseudomonas Aeruginosa, I found my extreme interest in virology. In pursuit of that, I applied to the Microbiology and Immunology program at the University of Iowa. I got admitted to the program in 2017, so I got my big flight to the USA and landed in Iowa City to pursue my Ph.D. journey in microbiology.

After several rotations, I decided to join Dr. Richard Roller's laboratory in 2018 to study herpesvirus genetics. Under Dr. Roller's mentorship, I experienced invaluable lessons of integrity in science, critical thinking, patience, and shaping my career perspective. My Ph.D. years were not just completing my degree to become a scientist. I found wonderful friends and colleagues in Iowa City who showed compassion during my difficult times. Additionally, I experienced big life events, including becoming a parent. Parenthood was a unique and challenging experience along with my Ph.D. training. I made many treasured memories with all the tears and smiles with my small family, my beloved husband, Mahmoud, and my little daughter, Anna, in Iowa City! I enjoyed painting in my spare time and had several fun art exhibitions in Iowa City. I am amazed by the fact how much Iowans appreciate art.

After completing my Ph.D., I am joining Dr. Vinay Pathak's laboratory in NIH at NCI in Frederick, MD, to study HIV post-entry events at the Department of HIV dynamics and replication. I am excited to move closer to my husband and reunite my family in the D.C. area. My goal is to work as an independent lead scientist eventually.


Herpesviruses translocate their nucleocapsids from the nucleus to the cytoplasm by capsid envelopment into the inner nuclear membrane and de-envelopment from the outer nuclear membrane, a process that is coordinated by energetically favorable self-association of nuclear egress complex (NEC) proteins, pUL34, and pUL31. Capsid envelopment is associated with alteration in the nuclear architecture and local redistribution of the nuclear lamina. NEC recruits protein kinases, including the virus-encoded protein kinase, pUS3, to the nuclear rim to regulate both lamina redistribution and NEC localization. Examining the role of capsid envelopment in the changes of the nuclear architecture suggests that disruption of the nuclear lamina is a preparation step prior to capsid envelopment. In the absence of capsid envelopment, lamin A/C becomes concentrated at the nuclear envelope in a pUL34-independent and cell type-specific manner, suggesting that ongoing nuclear egress may be required for the dispersal of lamins.

pUS3 catalytically-inactive mutants cause accumulation of perinuclear enveloped capsids, formation of NEC aggregates, and enhanced lamina disruption.  Interestingly, mutation of US3 in the absence of capsids results in identical NEC aggregation and lamina disruption phenotypes, and NEC aggregates correspond to multi-folded nuclear membrane structures, suggesting that pUS3’s specific role in nuclear egress is to control NEC self-association and membrane deformation.

pUS3 is also involved in many other viral and cellular functions, but its regulation is not understood. pUS3-mediated regulation of the NEC is suggested to be selectively regulated by another viral protein kinase, pUL13. However, the comparison of HSV-1 UL13 catalytically-inactive and US3 catalytically-inactive mutant revealed no defined classes of US3 substrates to be UL13-dependent, nor did mutation of UL13 induce a de-envelopment defect like that seen in US3 mutants. Accordingly, mutation of all UL13 kinase motifs in pUS3, individually or in aggregate, does not affect NEC localization, suggesting that pUL13-mediated regulation of the NEC is US3-independent.



Thursday, June 30, 2022