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The department faculty in this area of research focus on mechanisms underlying virus-host interactions, virus assembly, gene regulation, oncogenesis and neurovirology. Work from our virology laboratories has provided novel insights into neuroinvasion, epithelial transformation, gene delivery and subversion of host cell function.

Labs in This Research Area

 Eva Gottwein Lab

Molecular biology of Kaposi's Sarcoma-associated herpesvirus and its associated cancers

Research Description

Viruses commonly modify their cellular environment to optimize viral replication and persistence. Much has been learned about the intervention of viral proteins with cellular pathways. More recently, it has become clear that herpesviruses also encode large numbers of microRNAs (miRNAs). The modest amount of space miRNA precursors occupy in the viral genome, their lack of immunogenicity and their potential as regulators of gene expression make miRNAs ideal candidates for viral effectors.

The lab’s research focuses on identifying targets and functions of miRNAs encoded by the human herpesvirus Kaposi’s sarcoma-associated herpesvirus (KSHV). KSHV causes cancer in immuno-compromised individuals. The clinically most relevant KSHV-induced disease is Kaposi’s sarcoma (KS), a complex tumor driven by KSHV-infected endothelial cells. Due to the AIDS epidemic, KS has become the most common cancer in parts of Africa. KSHV also infects B lymphocytes and can consequently cause B cell lymphomas, including primary effusion lymphoma (PEL). KSHV constitutively expresses viral miRNAs from 12 precursors, suggesting a role of these miRNAs in viral replication and pathogenesis.

My lab is currently pursuing the comprehensive identification of mRNA targets of these miRNAs in primary effusion lymphoma cell lines and KSHV-infected endothelial cells. Our data suggest that, together, the KSHV miRNAs directly target hundreds of cellular mRNAs encoding proteins with roles in several different biological pathways. Our goal is to use this knowledge to characterize the most important functions of the KSHV miRNAs.

For lab information and more, see Dr. Gottwein's faculty profile and lab website.


See Dr. Gottwein's publications on PubMed.


Contact Dr. Gottwein at 312-503-3075 or the lab at 312-503-3076.

Graduate Students: Shreya JambardiNeil KuehnleZiyan Liang, Aakaanksha MaddineniJesus Ortega

Technical Staff: Haocong MaScout Osborne

Research Staff: Xinquan Zhang

 Laimonis Laimins Lab

Molecular biology of human papillomaviruses (HPV) and their association with cervical cancer

Research Description

Our efforts are divided into two main categories:

  • An examination of how the viral oncoproteins E6 and E7 contribute to the development of malignancy
  • Studies on the mechanisms controlling the viral life cycle in differentiating epithelia

More than 100 distinct types of human papillomavirus have been identified and approximately one-third specifically target squamous epithelial cells in the genital tract. Of these genital papillomaviruses, a subset including types 16,18 and 31 have been shown to be the etiological agents of most cervical cancers.

One of our goals is to understand why infection by specific HPV types contributes to the development of malignancy. For these studies we have examined the interaction of the oncoproteins E6 and E7 with cellular proteins. In particular, E6 binds the p53 protein and facilitates its degradation by a ubiquitin-mediated pathway. It also activates telomerase as well as associates with PDZ-domain containing proteins. The interactions of the E6 and E7 proteins with these cellular proteins are being examined at both the biochemical and genetic level.

In examining the papillomavirus life cycle, we have used organotypic tissue culture systems to faithfully reproduce the differentiation program of epithelial cells in the laboratory. Using this system, the viral life cycle has been duplicated.  We are studying the mechanisms that regulate viral DNA replication, cell entry, immune evasion and gene expression. These studies should provide insight into viral pathogenesis as well as the mechanisms regulating epithelial differentiation.

For lab information and more, see Dr. Laimins' faculty profile and lab website.


See Dr. Laimins' publications on PubMed.


Contact Dr. Laimins at 312-503-0648 or the lab at 312-503-0650.

Postdoctoral Fellows: Tazin FahmiConor Templeton, Arushi Vats

Lab Manager: Olga Rozhok

 Richard Longnecker Lab

Epstein-Barr virus (EBV) and herpes simplex virus (HSV) entry, replication and pathogenesis.

Research Description

Research in the Longnecker laboratory focuses on herpes simplex virus (HSV) and Epstein-Barr virus (EBV). These viruses typically cause self-limiting disease within the human population but both can be associated with serious complications. EBV is associated with variety of hematopoietic cancers such as African Burkitt lymphoma, Hodgkin Lymphoma and adult T-cell leukemia. EBV-associated lymphoproliferative disease occurs in individuals with congenital or acquired cellular immune deficiencies. The two notable epithelial diseases associated with EBV infection are nasopharyngeal cancer and oral hairy leukoplakia. Similar to EBV, HSV latent infections are very common in humans. HSV typically does not cause severe disease but is associated with localized mucocutaneous lesions, but in some cases can cause meningitis and encephalitis. The Longnecker laboratory focuses on several aspects of EBV and HSV replication and pathogenesis. First, the molecular basis EBV transformation and how it relates to cancer is being investigated. The laboratory is currently screening selective inhibitors that may be beneficial in EBV-associated cancers such as Hodgkin lymphoma, Burkitt lymphoma and proliferative disorders that occur in HIV/AIDS and transplant patients. Second, the laboratory is investigating herpesvirus latency in the human host and pathogenesis associated with infections in humans. In this regard, the laboratory is developing animal models for EBV and HSV infections. Finally, the laboratory is investigating the function of herpesvirus encoded proteins and the cellular receptors that are important for infection both using in vivo culture models as well as animal models. Ultimately, studies by the Longnecker laboratory may provide insight for the development of novel therapeutics for the treatment of herpesvirus infections in humans and better understanding of the herpesvirus life cycle in the human host

For lab information and more, see Dr. Longnecker's faculty profile.


See Dr. Longnecker's publications on PubMed.


Contact Dr. Longnecker at 312-503-0467 or the lab at 312-503-0468 or 312-503-9783.

Research Faculty: Jia Chen, Qing Fan, Masato Ikeda

Adjunct Faculty: Sarah Connolly

Graduate Students: Cooper Hayes, Daniel Giraldo Perez, Seo Jin Park

Technical Staff: Sarah KoppNanette Susmarski

 Mojgan Naghavi Lab

Microtubule regulation and function during infection by Human Immunodeficiency Virus (HIV)

Research Description

Our research focuses on infection by Human Immunodeficiency Virus type 1 (HIV-1), a retrovirus and causative agent of acquired immunodeficiency syndrome (AIDS). In addition to suppressing the immune system, rendering victims susceptible to opportunistic infections, HIV-1 can cross the blood-brain barrier and cause serious damage to the central nervous system, ultimately leading to HIV-associated dementia.

We are interested in how HIV-1 particles move within infected cells, including brain cell types such as microglia. Our work focuses on how the virus exploits host microtubules, the intracellular filaments that mediate cargo trafficking to different subcellular sites within the cell.

Our earlier work, employing a variety of screening approaches, identified a number of host proteins involved in cytoskeletal regulation and motor function as playing key roles in the early stages of HIV-1 infection. This includes Ezrin-Radixin-Moesin (ERM) proteins, which cross-link the actin and microtubule cytoskeletons. In exploring their role in HIV-1 infection, we identified the first biological function for the host protein, PDZD8, demonstrating that it binds ERMs to control microtubule stability. Furthermore, we uncovered that PDZD8 is a direct target for the HIV-1 protein, Gag.

Other work in our laboratory has shown that HIV-1 can induce the formation of highly stable microtubule subsets to facilitate early HIV-1 trafficking to the nucleus. We are interested in the role played in this process by proteins such as PDZD8, as well as a family of specialized microtubule regulatory proteins called +TIPs, which accumulate at the ends of dynamically growing microtubule filaments to control their growth and stability. We are also interested in the function of microtubule motors and cargo adaptor proteins in HIV-1 infection. In particular, we are exploring how Fasciculation and Elongation factor Zeta-1 (FEZ-1), a kinesin-1 adaptor protein that is highly expressed in neurons, functions to control HIV-1 infection. Our work employs a range of approaches, including biochemical characterization of protein-protein interactions as well as live imaging of fluorescently-labeled HIV-1 particles as they move within infected cells.

The ultimate goal of our work is to understand the molecular basis behind how microtubules, regulators of microtubule dynamics and microtubule motor proteins function to enable HIV-1 movement to and from the nucleus.

For lab information and more, see Dr. Naghavi's faculty profile and lab website.


See Dr. Naghavi's publications at PubMed.


Contact Dr. Naghavi at 312-503-4294.

Postdoctoral Fellows: Qingqing Chai, Feng Gu, Viacheslav Malikov, Sahana Mitra, Gina Pisano, Eveline Santos da Silva, Shanmugapriya Swamy

Technical Staff: Marie-Philipe Boisjoli, Kayla Schipper

 Pablo Penaloza-MacMaster Lab

Immune regulation and vaccines

Research Description

How can one improve immune responses during chronic infection or cancer? How can one improve the efficacy of viral vaccines? These are 2 main questions in the Penaloza lab. A unifying concept in the lab is how innate immune responses (TLRs and IFN-I) can be harnessed to treat immune exhaustion and improve vaccines.

Recently, the Penaloza group demonstrated a potent synergy between TLR4 signaling and PD-1 blockade at reinvigorating T cell function during chronic viral infection (Wang, PLOS Pathogens, 2019). This was the first demonstration that a specific microbiome component (LPS) can potentiate immune checkpoint therapy, via a B7 costimulation dependent mechanism. The group is now investigating whether other microbial components that target innate immune receptors can also improve immune checkpoint therapy, not only against chronic infections, but also against cancer. More recently, the Penaloza laboratory developed a novel strategy to improve viral vaccines by transiently blocking IFN-I (Palacio, JEM, 2020). Although IFN-I provides a rapid antiviral protection in the setting of natural infection, IFN-I can extinguish antigen prematurely following vaccination, impinging upon the priming of adaptive immune responses. By carefully downmodulating IFN-I at the time of vaccination, his group demonstrated an improvement in vaccine efficacy, using experimental HIV-1 and coronavirus vaccines.

Dr. Penaloza’s research has also investigated the mechanisms by which T regulatory cells suppress exhausted CD8 T cells (Penaloza-MacMaster, JEM, 2014), and how lack of these suppressive mechanisms can result in lethal immunopathology following viral infection (Penaloza-MacMaster, Science, 2015).

In summary, Dr. Penaloza's research is focused on immune regulation and vaccines, with a special emphasis on understanding how innate signals and immune checkpoints regulate adaptive immunity.

For lab information and more, see Dr. Penaloza-MacMaster's faculty profile and lab website.


See Dr. Penaloza-MacMaster's publications on PubMed.


Contact Dr. Penaloza-MacMaster at 312-503-0357.

Postdoctoral Fellows: Tanushree Dangi, Kelvin (Min Han) Lew

Graduate Students: Bakare AwakoaiyeYoung Rock Chung, Nicole Palacio, Sarah Sanchez

 Greg Smith Lab

Cell and molecular biology of herpesvirus invasion of the nervous system

Research Description

We investigate the relationship between infection of the nervous system by herpesviruses and disease outcome. Some of the most traumatic diseases – including polio, rabies and encephalitis – result from infections of the nervous system.  In contrast, herpesviruses are highly proficient at infecting the nervous system, yet normally do not cause neurological disease.  This is achieved in part by self-imposed restrictions encoded within the viruses that limit viral reproduction and prevent dissemination into the brain.  For the individual, this results in a relatively benign infection, yet the virus becomes a life-long occupant of the nervous system that will periodically reemerge at body surfaces to infect others. Unfortunately, this infectious cycle can go awry resulting in several forms of severe disease (i.e. keratitis and encephalitis).

We have pioneered methods to genetically manipulate herpesviruses and visualize individual viruses in living neurons. Using these methods, we are studying the mechanisms by which the virus achieves its stringently controlled infectious cycle. Current genetic manipulations are based on a full-length infectious clone of the herpesvirus genome. The clone was made as a bacterial artificial chromosome (BAC) in E. coli. Transfection of purified E. coli BAC plasmid into permissive eukaryotic cells is sufficient to initiate viral infection, allowing for immediate examination of viral mutant phenotypes in a variety of biological assays.  For example, by fusing the green fluorescent protein (GFP) to a structural component of the viral capsid, individual viral particles can be tracked within the axons of living neurons during both entry and egress phases of the infectious cycle. Studies in culture can be complemented by examining the pathogenesis of mutant viruses in rodent models of infection.

Using these methods, we have discovered key aspects of cellular infection, viral assembly and intracellular transport. Looking forward, we are continuing to pursue our multidisciplinary approach of combining neuroscience, cell biology, bacterial genetics and virology to better understand these important pathogens.

For lab information and more, see Dr. Smith's faculty profile.


See Dr. Smith's publications on PubMed.


Contact Dr. Smith at 312-503-3745 or the lab at 312-503-3744.

Research Faculty: Sarah Antinone

Postdoctoral Fellow: Oana Maier

Graduate Students: Kennen Hutchison, DongHo Kim, Caitlin Pegg, Jen Ai Quan

Technical Staff: John Miller, Austin Stults 

 Derek Walsh Lab

Mechanisms of poxvirus and herpesvirus infection; translational control of gene expression; virus trafficking

Research Description

Research in our laboratory focuses on two aspects of DNA virus biology:

1. The role of the host translation system during infection by poxviruses.

Members of the poxvirus family include Variola Virus (VarV), the causative agent of smallpox, and Vaccinia Virus (VacV), a close relative that was used as a vaccine against smallpox and which has become the laboratory prototype for poxvirus research. These large double-stranded DNA viruses exhibit an impressive level of self-sufficiency and encode many of the proteins required for transcription and replication of their DNA genomes. Indeed, unlike many other DNA viruses, poxviruses do not require access to the host nucleus and replicate exclusively in the cytoplasm of infected cells within compartments termed “viral factories”. However, like all viruses, they remain dependent on gaining access to host ribosomes in order to translate their mRNAs into proteins and must also counteract host antiviral responses aimed at crippling the translation system to prevent virus replication.

Our work focuses on the function of two eukaryotic translation initiation factor (eIF) complexes, eIF3 and eIF4F, that regulate ribosome recruitment to capped mRNAs and their role in VacV infection. We have found that VacV stimulates the assembly of eIF4F complexes and that this is important for both viral protein synthesis and control of host immune responses. Furthermore, we have found that eIF3 functionally communicates with eIF4F during translation initiation and that this plays an important role in VacV replication. We have also found that VacV redistributes key eIF4F subunits to specific regions within viral factories, a process that appears to involve the viral I3 protein.

We are currently exploring the compartmentalized replication of VacV as a means to better understand fundamental mechanisms of localized translational control and how this functions to regulate viral protein synthesis and host antiviral responses. We are also studying how the virus controls eIF4F activity by targeting upstream signaling pathways, with a particular emphasis on the metabolic sensor mammalian target of rapamycin (mTOR).

2. Microtubule regulation and function during herpes simplex virus infection.

We are also interested in how herpes simplex virus type 1 (HSV-1) exploits host signaling pathways and specialized microtubule regulatory proteins, called +TIPs, to facilitate virus movement within the cell at various stages of the viral lifecycle.

For lab information and more, see Dr. Walsh's faculty profile and the lab website.


See publications on PubMed.


Contact Dr. Walsh at 312-503-4292

Postdoctoral Fellows: Charles Hesser, Nathan Meade, Chorong Park

Graduate Students: Natalia KhalatyanCeleste Rosencrance

Technical Staff: Helen Astar